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  • ISSN 1674-8301
  • CN 32-1810/R
Volume 37 Issue 4
Jul.  2023
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Abstract
Acknowledgments
References
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Natalia V. Naryzhnaya, Leonid N. Maslov, Ivan A. Derkachev, Huijie Ma, Yi Zhang, N. Rajendra Prasad, Nirmal Singh, Feng Fu, Jianming Pei, Akpay Sarybaev, Akylbek Sydykov. The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion[J]. The Journal of Biomedical Research, 2023, 37(4): 230-254. DOI: 10.7555/JBR.36.20220125
Citation: Natalia V. Naryzhnaya, Leonid N. Maslov, Ivan A. Derkachev, Huijie Ma, Yi Zhang, N. Rajendra Prasad, Nirmal Singh, Feng Fu, Jianming Pei, Akpay Sarybaev, Akylbek Sydykov. The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion[J]. The Journal of Biomedical Research, 2023, 37(4): 230-254. DOI: 10.7555/JBR.36.20220125
shu

The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion

  • 1.

    Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Science, Tomsk, Tomsk Region 634012, Russia

  • 2.

    Department of Physiology, Hebei Medical University, Shijiazhuang, Hebei 050017, China

  • 3.

    Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar, Tamilnadu 608002, India

  • 4.

    Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjabi 147002, India

  • 5.

    Department of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, the Fourth Military Medical University, Xi'an, Shaanxi 710032, China

  • 6.

    Department of Mountain and Sleep Medicine and Pulmonary Hypertension, National Center of Cardiology and Internal Medicine, Bishkek 720040, Kyrgyzstan

  • 7.

    Kyrgyz-Indian Mountain Biomedical Research Center, Bishkek 720033, Kyrgyzstan

  • 8.

    Department of Internal Medicine, Excellence Cluster Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Justus Liebig University of Giessen, Giessen, Hessen 35392, Germany

  • 9.

    Department of Mountain and Sleep Medicine and Pulmonary Hypertension, National Center of Cardiology and Internal Medicine, Bishkek 720040, Kyrgyzstan

Funds: This work was supported by the Russian Science Foundation grant 22-15-00048. The section dedicated to the role of kinases in the cardioprotective effect of chronic hypoxia is framed within the framework of state assignments 122020300042-4.
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  • Corresponding author:

    Leonid N. Maslov, Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center of the RAS, Kievskaya 111A, Tomsk, Tomsk Region 634012, Russia. Tel: +7-3822-262174, E-mail: maslov@cardio-tomsk.ru

  • Received Date: May 25, 2022
  • Revised Date: August 30, 2022
  • Accepted Date: September 04, 2022
  • Available Online: October 27, 2022
    Graphical Abstract
    • Abstract
  • The acute myocardial infarction (AMI) and sudden cardiac death (SCD), both associated with acute cardiac ischemia, are one of the leading causes of adult death in economically developed countries. The development of new approaches for the treatment and prevention of AMI and SCD remains the highest priority for medicine. A study on the cardiovascular effects of chronic hypoxia (CH) may contribute to the development of these methods. Chronic hypoxia exerts both positive and adverse effects. The positive effects are the infarct-reducing, vasoprotective, and antiarrhythmic effects, which can lead to the improvement of cardiac contractility in reperfusion. The adverse effects are pulmonary hypertension and right ventricular hypertrophy. This review presents a comprehensive overview of how CH enhances cardiac tolerance to ischemia/reperfusion. It is an in-depth analysis of the published data on the underlying mechanisms, which can lead to future development of the cardioprotective effect of CH. A better understanding of the CH-activated protective signaling pathways may contribute to new therapeutic approaches in an increase of cardiac tolerance to ischemia/reperfusion.
    • FullText(HTML)

  • None.

    CLC number: R542.2, Document code: A

    The authors reported no conflict of interests.

    • References (243)
  • [1]
    Musil J, Procházka J, Krofta K, et al. Effect of chronic systemic hypoxia of the methaemoglobin type on the rat myocardium and its resistance to anoxia[J]. Physiol Bohemoslov, 1966, 15(4): 357–361. https://pubmed.ncbi.nlm.nih.gov/4224277/
    [2]
    Poupa O, Krofta K, Prochazka J, et al. The resistance of the myocardium to anoxia in animals acclimated to simulated altitude[J]. Physiol Bohemoslov, 1965, 14: 233–237. https://pubmed.ncbi.nlm.nih.gov/14330883/
    [3]
    Poupa O, Krofta K, Rakusan K, et al. Myoglobin content of the heart and resistance of the isolated myocardium to anoxia in vitro during adaptation to high altitude hypoxia[J]. Physiol Bohemoslov, 1966, 15(5): 450–453. https://pubmed.ncbi.nlm.nih.gov/4230152/
    [4]
    Poupa O, Krofta K, Prochazka J, et al. Acclimation to simulated high altitude and acute cardiac necrosis[J]. Fed Proc, 1966, 25(4): 1243–1246. https://pubmed.ncbi.nlm.nih.gov/5913895/
    [5]
    Meerson FZ, Gomzakov OA, Shimkovich MV. Adaptation to high altitude hypoxia as a factor preventing development of myocardial ischemic necrosis[J]. Am J Cardiol, 1973, 31(1): 30–34. doi: 10.1016/0002-9149(73)90806-0
    [6]
    Meerson FZ, Ustinova EE, Orlova EH. Prevention and elimination of heart arrhythmias by adaptation to intermittent high altitude hypoxia[J]. Clin Cardiol, 1987, 10(12): 783–789. doi: 10.1002/clc.4960101202
    [7]
    Kronenberg RS, Safar P, Lee J, et al. Pulmonary artery pressure and alveolar gas exchange in man during acclimatization to 12, 470 ft[J]. J Clin Invest, 1971, 50(4): 827–837. doi: 10.1172/JCI106554
    [8]
    Pen̄aloza D, Sime F. Chronic cor pulmonale due to loss of altitude acclimatization (chronic mountain sickness)[J]. Am J Med, 1971, 50(6): 728–743. doi: 10.1016/0002-9343(71)90181-1
    [9]
    Sime F, Peñaloza D, Ruiz L. Bradycardia, increased cardiac output, and reversal of pulmonary hypertension in altitude natives living at sea level[J]. Br Heart J, 1971, 33(5): 647–657. doi: 10.1136/hrt.33.5.647
    [10]
    Yellon DM, Downey JM. Preconditioning the myocardium: from cellular physiology to clinical cardiology[J]. Physiol Rev, 2003, 83(4): 1113–1151. doi: 10.1152/physrev.00009.2003
    [11]
    Heusch G. Myocardial ischaemia-reperfusion injury and cardioprotection in perspective[J]. Nat Rev Cardiol, 2020, 17(12): 773–789. doi: 10.1038/s41569-020-0403-y
    [12]
    Neckář J, Ošťádal B, Kolář F. Myocardial infarct size-limiting effect of chronic hypoxia persists for five weeks of normoxic recovery[J]. Physiol Res, 2004, 53(6): 621–628. https://pubmed.ncbi.nlm.nih.gov/15588130/
    [13]
    Zhang Y, Zhong N, Zhu H, et al. Antiarrhythmic and antioxidative effects of intermittent hypoxia exposure on rat myocardium[J]. Acta Physiol Sin, 2000, 52(2): 89–92. https://pubmed.ncbi.nlm.nih.gov/11961574/
    [14]
    Meerson FZ, Boev VM, Kots II, et al. The effect of adaptation to periodic hypoxia on the tolerance of untrained subjects for physical loading and idiopathic cardiac arrhythmias[J]. Fiziol Cheloveka (in Russian), 1990, 16(1): 94–105. https://pubmed.ncbi.nlm.nih.gov/2358161/
    [15]
    Aleshin IA, Tin’kov AN, Kots II, et al. Experience in treating patients with cardiovascular diseases by means of adaptation to periodic barochamber hypoxia[J]. Ter Arkh (in Russian), 1997, 69(1): 54–58. https://pubmed.ncbi.nlm.nih.gov/9163053/
    [16]
    Uskina EV, Maslov LN, Lishmanov YB. Antiarrhythmic effect of hypoxic preconditioning is mediated by activation of μ- and δ-opioid receptors[J]. Bull Exp Biol Med, 1998, 125(3): 239–241. doi: 10.1007/BF02496869
    [17]
    Li J, Xu J, Xiao J, et al. Preservation of TSPO by chronic intermittent hypobaric hypoxia confers antiarrhythmic activity[J]. J Cell Mol Med, 2011, 15(1): 134–140. doi: 10.1111/j.1582-4934.2009.00949.x
    [18]
    Zhou J, Ma H, Liu Y, et al. The anti-arrhythmic effect of chronic intermittent hypobaric hypoxia in rats with metabolic syndrome induced with fructose[J]. Can J Physiol Pharmacol, 2015, 93(4): 227–232. doi: 10.1139/cjpp-2014-0343
    [19]
    Estrada JA, Williams AG Jr, Sun J, et al. δ-Opioid receptor (DOR) signaling and reactive oxygen species (ROS) mediate intermittent hypoxia induced protection of canine myocardium[J]. Basic Res Cardiol, 2016, 111(2): 17. doi: 10.1007/s00395-016-0538-5
    [20]
    Barbé C, Rochetaing A, Kreher P. Ischemic tolerance of the heart by adaptation to chronic hypoxia is suppressed by high subchronic carbon monoxide exposure[J]. Inhal Toxicol, 2001, 13(3): 219–232. doi: 10.1080/08958370150502458
    [21]
    Morand J, Arnaud C, Pepin JL, et al. Chronic intermittent hypoxia promotes myocardial ischemia-related ventricular arrhythmias and sudden cardiac death[J]. Sci Rep, 2018, 8(1): 2997. doi: 10.1038/s41598-018-21064-y
    [22]
    Manukhina EB, Belkina LM, Terekhina OL, et al. Normobaric, intermittent hypoxia conditioning is cardio- and vasoprotective in rats[J]. Exp Biol Med, 2013, 238(12): 1413–1420. doi: 10.1177/1535370213508718
    [23]
    Mallet RT, Ryou MG, Williams AG, et al. β1-Adrenergic receptor antagonism abrogates cardioprotective effects of intermittent hypoxia[J]. Basic Res Cardiol, 2006, 101(5): 436–446. doi: 10.1007/s00395-006-0599-y
    [24]
    Naryzhnaya NV, Mukhamedzyanov AV, Lasukova TV, et al. Involvement of autonomic nervous system in antiarrhythmic effect of intermittent hypobaric hypoxia[J]. Bull Exp Biol Med, 2017, 163(3): 299–301. doi: 10.1007/s10517-017-3789-8
    [25]
    Kohutova J, Elsnicova B, Holzerova K, et al. Anti-arrhythmic cardiac phenotype elicited by chronic intermittent hypoxia is associated with alterations in connexin-43 expression, phosphorylation, and distribution[J]. Front Endocrinol, 2019, 9: 789. doi: 10.3389/fendo.2018.00789
    [26]
    Asemu G, Neckár J, Szárszoi O, et al. Effects of adaptation to intermittent high altitude hypoxia on ischemic ventricular arrhythmias in rats[J]. Physiol Res, 2000, 49(5): 597–606. https://pubmed.ncbi.nlm.nih.gov/11191364/
    [27]
    Neckár J, Borchert GH, Hlousková P, et al. Brief daily episode of normoxia inhibits cardioprotection conferred by chronic continuous hypoxia. Role of oxidative stress and BKCa channels[J]. Curr Pharm Des, 2013, 19(39): 6880–6889. doi: 10.2174/138161281939131127115154
    [28]
    Lishmanov IB, Naryzhnaia NV, Maslov LN, et al. The opiatergic link between the antiarrhythmic effect of adaptation and hypoxia in the model of ischemia and reperfusion in vivo[J]. Patol Fiziol Eksp Ter (in Russian), 2003, (1): 19–21. https://pubmed.ncbi.nlm.nih.gov/12652938/
    [29]
    Wolfe BB, Voelkel NF. Effects of hypoxia on atrial muscarinic cholinergic receptors and cardiac parasympathetic responsiveness[J]. Biochem Pharmacol, 1983, 32(13): 1999–2002. doi: 10.1016/0006-2952(83)90418-5
    [30]
    De Ferrari GM, Vanoli E, Curcuruto P, et al. Prevention of life-threatening arrhythmias by pharmacologic stimulation of the muscarinic receptors with oxotremorine[J]. Am Heart J, 1992, 124(4): 883–890. doi: 10.1016/0002-8703(92)90968-2
    [31]
    Bober SL, Ciriello J, Jones DL. Atrial arrhythmias and autonomic dysfunction in rats exposed to chronic intermittent hypoxia[J]. Am J Physiol Heart Circ Physiol, 2018, 314(6): H1160–H1168. doi: 10.1152/ajpheart.00173.2017
    [32]
    Wu W, Lu Z. Loss of anti-arrhythmic effect of vagal nerve stimulation on ischemia-induced ventricular tachyarrhythmia in aged rats[J]. Tohoku J Exp Med, 2011, 223(1): 27–33. doi: 10.1620/tjem.223.27
    [33]
    Vanoli E, De Ferrari GM, Stramba-Badiale M, et al. Vagal stimulation and prevention of sudden death in conscious dogs with a healed myocardial infarction[J]. Circ Res, 1991, 68(5): 1471–1481. doi: 10.1161/01.RES.68.5.1471
    [34]
    Wang S, Han H, Jiang Y, et al. Activation of cardiac M3 muscarinic acetylcholine receptors has cardioprotective effects against ischaemia-induced arrhythmias[J]. Clin Exp Pharmacol Physiol, 2012, 39(4): 343–349. doi: 10.1111/j.1440-1681.2012.05672.x
    [35]
    Lin M, Liu R, Gozal D, et al. Chronic intermittent hypoxia impairs baroreflex control of heart rate but enhances heart rate responses to vagal efferent stimulation in anesthetized mice[J]. Am J Physiol Heart Circ Physiol, 2007, 293(2): H997–H1006. doi: 10.1152/ajpheart.01124.2006
    [36]
    Stembridge M, Ainslie PN, Hughes MG, et al. Ventricular structure, function, and mechanics at high altitude: chronic remodeling in Sherpa vs. short-term lowlander adaptation[J]. J Appl Physiol, 2014, 117(3): 334–343. doi: 10.1152/japplphysiol.00233.2014
    [37]
    Herrera EA, Farías JG, González-Candia A, et al. Ω3 Supplementation and intermittent hypobaric hypoxia induce cardioprotection enhancing antioxidant mechanisms in adult rats[J]. Mar Drugs, 2015, 13(2): 838–860. doi: 10.3390/md13020838
    [38]
    Wu S, Li Y, Shi Z, et al. Alteration of cholinergic anti-inflammatory pathway in rat with ischemic cardiomyopathy-modified electrophysiological function of heart[J]. J Am Heart Assoc, 2017, 6(9): e006510. doi: 10.1161/JAHA.117.006510
    [39]
    Zhang Y, Zhong N, Zhou Z. Effects of intermittent hypoxia on action potential and contraction in non-ischemic and ischemic rat papillary muscle[J]. Life Sci, 2000, 67(20): 2465–2471. doi: 10.1016/S0024-3205(00)00832-8
    [40]
    Naryzhnaia NV, Neckar J, Maslov LN, et al. The role of sarcolemmal and mitochondrial K(ATP)-channels in realization of the cardioprotection and antiarrhythmic effect of different regimens of hypobaric adaptation[J]. Ross Fiziol Zh Im I M Sechenova (in Russian), 2009, 95(8): 837–849. https://pubmed.ncbi.nlm.nih.gov/19803213/
    [41]
    Neckář J, Papoušek F, Nováková O, et al. Cardioprotective effects of chronic hypoxia and ischaemic preconditioning are not additive[J]. Basic Res Cardiol, 2002, 97(2): 161–167. doi: 10.1007/s003950200007
    [42]
    Tsibulnikov SY, Maslov LN, Naryzhnaya NV, et al. Role of protein kinase C, PI3 kinase, tyrosine kinases, NO-synthase, KATP channels and MPT pore in the signaling pathway of the cardioprotective effect of chronic continuous hypoxia[J]. Gen Physiol Biophys, 2018, 37(5): 537–547. doi: 10.4149/gpb_2018013
    [43]
    Neckář J, Sźárszoi O, Herget J, et al. Cardioprotective effect of chronic hypoxia is blunted by concomitant hypercapnia[J]. Physiol Res, 2003, 52(2): 171–175. https://pubmed.ncbi.nlm.nih.gov/12678659/
    [44]
    Neckář J, Marková I, Novák F, et al. Increased expression and altered subcellular distribution of PKC-δin chronically hypoxic rat myocardium: involvement in cardioprotection[J]. Am J Physiol Heart Circ Physiol, 2005, 288(4): H1566–H1572. doi: 10.1152/ajpheart.00586.2004
    [45]
    Kolář F, Neckář J, Ošťádal B. MCC-134, a blocker of mitochondrial and opener of sarcolemmal ATP-sensitive K+ channels, abrogates cardioprotective effects of chronic hypoxia[J]. Physiol Res, 2005, 54(4): 467–471. https://pubmed.ncbi.nlm.nih.gov/16117602/
    [46]
    Meng X, Yu H, Zhang W, et al. ZFP580, a novel zinc-finger transcription factor, is involved in cardioprotection of intermittent high-altitude hypoxia against myocardial ischemia-reperfusion injury[J]. PLoS One, 2014, 9(4): e94635. doi: 10.1371/journal.pone.0094635
    [47]
    Xu W, Yu Z, Xie Y, et al. Therapeutic effect of intermittent hypobaric hypoxia on myocardial infarction in rats[J]. Basic Res Cardiol, 2011, 106(3): 329–342. doi: 10.1007/s00395-011-0159-y
    [48]
    Bourdier G, Flore P, Sanchez H, et al. High-intensity training reduces intermittent hypoxia-induced ER stress and myocardial infarct size[J]. Am J Physiol Heart Circ Physiol, 2016, 310(2): H279–H289. doi: 10.1152/ajpheart.00448.2015
    [49]
    Milano G, Abruzzo PM, Bolotta A, et al. Impact of the phosphatidylinositide 3-kinase signaling pathway on the cardioprotection induced by intermittent hypoxia[J]. PLoS One, 2013, 8(10): e76659. doi: 10.1371/journal.pone.0076659
    [50]
    Maslov LN, Naryzhnaia NV, Tsibulnikov SY, et al. Role of endogenous opioid peptides in the infarct size-limiting effect of adaptation to chronic continuous hypoxia[J]. Life Sci, 2013, 93(9–11): 373–379. doi: 10.1016/j.lfs.2013.07.018
    [51]
    Moulin S, Arnaud C, Bouyon S, et al. Curcumin prevents chronic intermittent hypoxia-induced myocardial injury[J]. Ther Adv Chronic Dis, 2020, 11: 2040622320922104. doi: 10.1177/2040622320922104
    [52]
    Wang Z, Si L. Hypoxia-inducible factor-1α and vascular endothelial growth factor in the cardioprotective effects of intermittent hypoxia in rats[J]. Ups J Med Sci, 2013, 118(2): 65–74. doi: 10.3109/03009734.2013.766914
    [53]
    Kasparova D, Neckar J, Dabrowska L, et al. Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems[J]. Physiol Genomics, 2015, 47(12): 612–620. doi: 10.1152/physiolgenomics.00058.2015
    [54]
    Kolář F, Ježková J, Balková P, et al. Role of oxidative stress in PKC-δupregulation and cardioprotection induced by chronic intermittent hypoxia[J]. Am J Physiol Heart Circ Physiol, 2007, 292(1): H224–H230. doi: 10.1152/ajpheart.00689.2006
    [55]
    Hrdlička J, Neckář J, Papoušek F, et al. Beneficial effect of continuous normobaric hypoxia on ventricular dilatation in rats with post-infarction heart failure[J]. Physiol Res, 2016, 65(5): 867–870. doi: 10.33549/physiolres.933308
    [56]
    Zhu W, Xie Y, Chen L, et al. Intermittent high altitude hypoxia inhibits opening of mitochondrial permeability transition pores against reperfusion injury[J]. J Mol Cell Cardiol, 2006, 40(1): 96–106. doi: 10.1016/j.yjmcc.2005.09.016
    [57]
    Ma H, Li Q, Ma H, et al. Chronic intermittent hypobaric hypoxia ameliorates ischemia/reperfusion-induced calcium overload in heart via Na+/Ca2+ exchanger in developing rats[J]. Cell Physiol Biochem, 2014, 34(2): 313–324. doi: 10.1159/000363001
    [58]
    Maslov LN, Naryzhnaya NV, Prokudina ES, et al. Preserved cardiac mitochondrial function and reduced ischaemia/reperfusion injury afforded by chronic continuous hypoxia: role of opioid receptors[J]. Clin Exp Pharmacol Physiol, 2015, 42(5): 496–501. doi: 10.1111/1440-1681.12383
    [59]
    Prokudina ES, Naryzhnaya NV, Mukhomedzyanov AV, et al. Effect of chronic continuous normobaric hypoxia on functional state of cardiac mitochondria and tolerance of isolated rat heart to ischemia and reperfusion: role of µ and δ2 opioid receptors[J]. Physiol Res, 2019, 68(6): 909–920. doi: 10.33549/physiolres.933945
    [60]
    Naryzhnaya NV, Prokudina ES, Nesterov EA, et al. The role of cardiac opioid receptors in the cardioprotective effect of continuous normobaric hypoxia[J]. Bull Exp Biol Med, 2020, 168(6): 727–729. doi: 10.1007/s10517-020-04789-7
    [61]
    Naryzhnaya NV, Khaliulin I, Lishmanov YB, et al. Participation of opioid receptors in the cytoprotective effect of chronic normobaric hypoxia[J]. Physiol Res, 2019, 68(2): 245–253. https://www.biomed.cas.cz/physiolres/pdf/2019/68_245.pdf
    [62]
    Borchert GH, Yang C, Kolář F. Mitochondrial BKCa channels contribute to protection of cardiomyocytes isolated from chronically hypoxic rats[J]. Am J Physiol Heart Circ Physiol, 2011, 300(2): H507–H513. doi: 10.1152/ajpheart.00594.2010
    [63]
    Holzerová K, Hlaváčková M, Žurmanová J, et al. Involvement of PKCε in cardioprotection induced by adaptation to chronic continuous hypoxia[J]. Physiol Res, 2015, 64(2): 191–201. https://www.biomed.cas.cz/physiolres/pdf/64/64_191.pdf
    [64]
    Xu S, Jia L, Liu X, et al. Effect of chronic intermittent hypobaric hypoxia on cardiac function in female metabolic syndrome rats[J]. Adapt Med, 2021, 13: 8–15. doi: 10.4247/AM.2021.ACB257
    [65]
    Dong J, Zhu H, Zhu W, et al. Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression[J]. Cell Res, 2003, 13(5): 385–391. doi: 10.1038/sj.cr.7290184
    [66]
    Kolar D, Gresikova M, Waskova-Arnostova P, et al. Adaptation to chronic continuous hypoxia potentiates Akt/HK2 anti-apoptotic pathway during brief myocardial ischemia/reperfusion insult[J]. Mol Cell Biochem, 2017, 432(1–2): 99–108. doi: 10.1007/s11010-017-3001-5
    [67]
    Xie S, Deng Y, Pan Y, et al. Chronic intermittent hypoxia induces cardiac hypertrophy by impairing autophagy through the adenosine 5’-monophosphate-activated protein kinase pathway[J]. Arch Biochem Biophys, 2016, 606: 41–52. doi: 10.1016/j.abb.2016.07.006
    [68]
    Chang JC, Hu W, Lee WS, et al. Intermittent hypoxia induces autophagy to protect cardiomyocytes from endoplasmic reticulum stress and apoptosis[J]. Front Physiol, 2019, 10: 995. doi: 10.3389/fphys.2019.00995
    [69]
    Gyongyosi A, Terraneo L, Bianciardi P, et al. The impact of moderate chronic hypoxia and hyperoxia on the level of apoptotic and autophagic proteins in myocardial tissue[J]. Oxid Med Cell Longev, 2018, 2018: 5786742. doi: 10.1155/2018/5786742
    [70]
    Nedvedova I, Kolar D, Elsnicova B, et al. Mitochondrial genome modulates myocardial Akt/Glut/HK salvage pathway in spontaneously hypertensive rats adapted to chronic hypoxia[J]. Physiol Genomics, 2018, 50(7): 532–541. doi: 10.1152/physiolgenomics.00040.2017
    [71]
    Rathod KS, Koganti S, Jain AK, et al. Complete versus culprit only revascularisation in patients with cardiogenic shock complicating acute myocardial infarction: incidence and outcomes from the London heart attack group[J]. Cardiovasc Revasc Med, 2020, 21(3): 350–358. doi: 10.1016/j.carrev.2019.06.007
    [72]
    Kopylov YN, Golubeva LY. Effect of adaptation to periodic hypoxia on stability of myocardial energy metabolism and contractility parameters in the presence of acute anoxia and reoxygenation[J]. Bull Exp Biol Med, 1991, 111(1): 27–30. doi: 10.1007/BF00841231
    [73]
    Krylatov AV, Tsibulnikov SY, Mukhomedzyanov AV, et al. The role of natriuretic peptides in the regulation of cardiac tolerance to ischemia/reperfusion and postinfarction heart remodeling[J]. J Cardiovasc Pharmacol Ther, 2021, 26(2): 131–148. doi: 10.1177/1074248420952243
    [74]
    Casserly B, Pietras L, Schuyler J, et al. Cardiac atria are the primary source of ANP release in hypoxia-adapted rats[J]. Life Sci, 2010, 87(11–12): 382–389. doi: 10.1016/j.lfs.2010.07.013
    [75]
    Lordick F, Hauck RW, Senekowitsch R, et al. Atrial natriuretic peptide in acute hypoxia-exposed healthy subjects and in hypoxaemic patients[J]. Eur Respir J, 1995, 8(2): 216–221. doi: 10.1183/09031936.95.08020216
    [76]
    Winter RJD, Meleagros L, Pervez S, et al. Atrial natriuretic peptide levels in plasma and in cardiac tissues after chronic hypoxia in rats[J]. Clin Sci (Lond), 1989, 76(1): 95–101. doi: 10.1042/cs0760095
    [77]
    Bullard AJ, Govewalla P, Yellon DM. Erythropoietin protects the myocardium against reperfusion injury in vitro and in vivo[J]. Basic Res Cardiol, 2005, 100(5): 397–403. doi: 10.1007/s00395-005-0537-4
    [78]
    Piperno A, Galimberti S, Mariani R. Modulation of hepcidin production during hypoxia-induced erythropoiesis in humans in vivo: data from the HIGHCARE project[J]. Blood, 2011, 117(10): 2953–2959. doi: 10.1182/blood-2010-08-299859
    [79]
    Feizi H, Rajaee K, Keyhanmanesh R, et al. Effect of ghrelin on renal erythropoietin production in chronic hypoxic rats[J]. Endocr Regul, 2014, 48(1): 3–8. doi: 10.4149/endo_2014_01_3
    [80]
    Schmidt W, Spielvogel H, Eckardt KU, et al. Effects of chronic hypoxia and exercise on plasma erythropoietin in high-altitude residents[J]. J Appl Physiol, 1993, 74(4): 1874–1878. doi: 10.1152/jappl.1993.74.4.1874
    [81]
    Zhang S, Ma K, Liu Y, et al. Stabilization of hypoxia-inducible factor by DMOG inhibits development of chronic hypoxia-induced right ventricular remodeling[J]. J Cardiovasc Pharmacol, 2016, 67(1): 68–75. doi: 10.1097/FJC.0000000000000315
    [82]
    Asimakis GK, Inners-McBride K, Conti VR, et al. Transient β adrenergic stimulation can precondition the rat heart against postischaemic contractile dysfunction[J]. Cardiovasc Res, 1994, 28(11): 1726–1734. doi: 10.1093/cvr/28.11.1726
    [83]
    Ravingerová T, Pancza D, Ziegelhoffer A, et al. Preconditioning modulates susceptibility to ischemia-induced arrhythmias in the rat heart: the role of α-adrenergic stimulation and K(ATP) channels[J]. Physiol Res, 2002, 51(2): 109–119. https://www.biomed.cas.cz/physiolres/pdf/51/51_109.pdf
    [84]
    Shin MK, Han W, Joo H, et al. Effect of adrenal medullectomy on metabolic responses to chronic intermittent hypoxia in the frequently sampled intravenous glucose tolerance test[J]. J Appl Physiol, 2017, 122(4): 767–774. doi: 10.1152/japplphysiol.00975.2016
    [85]
    Zoccal DB, Bonagamba LGH, Oliveira FRT, et al. Increased sympathetic activity in rats submitted to chronic intermittent hypoxia[J]. Exp Physiol, 2007, 92(1): 79–85. doi: 10.1113/expphysiol.2006.035501
    [86]
    Oštádal B, Ressl J, Urbanová D, et al. The effect of beta adrenergic blockade on pulmonary hypertension, right ventricular hypertrophy and polycythaemia, induced in rats by intermittent high altitude hypoxia[J]. Basic Res Cardiol, 1978, 73(5): 422–432. doi: 10.1007/BF01906523
    [87]
    Zhu B, Simonis U, Cecchini G, et al. Comparison of pyrroloquinoline quinone and/or metoprolol on myocardial infarct size and mitochondrial damage in a rat model of ischemia/reperfusion injury[J]. J Cardiovasc Pharmacol Ther, 2006, 11(2): 119–128. doi: 10.1177/1074248406288757
    [88]
    Hu A, Jiao X, Gao E, et al. Chronic β-adrenergic receptor stimulation induces cardiac apoptosis and aggravates myocardial ischemia/reperfusion injury by provoking inducible nitric-oxide synthase-mediated nitrative stress[J]. J Pharmacol Exp Ther, 2006, 318(2): 469–475. doi: 10.1124/jpet.106.102160
    [89]
    Du X, Gao X, Kiriazis H, et al. Transgenic α1A-adrenergic activation limits post-infarct ventricular remodeling and dysfunction and improves survival[J]. Cardiovasc Res, 2006, 71(4): 735–743. doi: 10.1016/j.cardiores.2006.06.015
    [90]
    León-Velarde F, Bourin MC, Germack R, et al. Differential alterations in cardiac adrenergic signaling in chronic hypoxia or norepinephrine infusion[J]. Am J Physiol Regul Integr Comp Physiol, 2001, 280(1): R274–R281. doi: 10.1152/ajpregu.2001.280.1.R274
    [91]
    Wang P, Gallagher KP, Downey JM, et al. Pretreatment with endothelin-1 mimics ischemic preconditioning against infarction in isolated rabbit heart[J]. J Mol Cell Cardiol, 1996, 28(3): 579–588. doi: 10.1006/jmcc.1996.0054
    [92]
    Bugge E, Ytrehus K. Endothelin-1 can reduce infarct size through protein kinase C and KATP channels in the isolated rat heart[J]. Cardiovasc Res, 1996, 32(5): 920–929. doi: 10.1016/S0008-6363(96)00129-0
    [93]
    Duda M, Konior A, Klemenska E, et al. Preconditioning protects endothelium by preventing ET-1-induced activation of NADPH oxidase and xanthine oxidase in post-ischemic heart[J]. J Mol Cell Cardiol, 2007, 42(2): 400–410. doi: 10.1016/j.yjmcc.2006.10.014
    [94]
    Zhang M, Gu W, Hong X. Involvement of endothelin 1 in remote preconditioning-induced cardioprotection through connexin 43 and Akt/GSK-3β signaling pathway[J]. Sci Rep, 2018, 8(1): 10941. doi: 10.1038/s41598-018-29196-x
    [95]
    Tamareille S, Terwelp M, Amirian J, et al. Endothelin-1 release during the early phase of reperfusion is a mediator of myocardial reperfusion injury[J]. Cardiology, 2013, 125(4): 242–249. doi: 10.1159/000350655
    [96]
    Blumberg FC, Wolf K, Arzt M, et al. Effects of ET-A receptor blockade on eNOS gene expression in chronic hypoxic rat lungs[J]. J Appl Physiol, 2003, 94(2): 446–452. doi: 10.1152/japplphysiol.00239.2002
    [97]
    Pan P, Zhang X, Qian H, et al. Effects of electro-acupuncture on endothelium-derived endothelin-1 and endothelial nitric oxide synthase of rats with hypoxia-induced pulmonary hypertension[J]. Exp Biol Med, 2010, 235(5): 642–648. doi: 10.1258/ebm.2010.009353
    [98]
    Wang N, Chang Y, Chen L, et al. Tanshinone IIA protects against chronic intermittent hypoxia-induced myocardial injury via activating the endothelin 1 pathway[J]. Biomed Pharmacother, 2017, 95: 1013–1020. doi: 10.1016/j.biopha.2017.08.036
    [99]
    Hamid SA, Baxter GF. Adrenomedullin limits reperfusion injury in experimental myocardial infarction[J]. Basic Res Cardiol, 2005, 100(5): 387–396. doi: 10.1007/s00395-005-0538-3
    [100]
    Nishida H, Sato T, Miyazaki M, et al. Infarct size limitation by adrenomedullin: protein kinase A but not PI3-kinase is linked to mitochondrial KCa channels[J]. Cardiovasc Res, 2008, 77(2): 398–405. https://academic.oup.com/cardiovascres/article/77/2/398/432211
    [101]
    Gong Y, Fan X, Wu X, et al. Changes of intermedin/adrenomedullin 2 and its receptors in the right ventricle of rats with chronic hypoxic pulmonary hypertension[J]. Acta Physiol Sin, 2007, 59(2): 210–214. https://kns.cnki.net/KCMS/detail/detail.aspx?dbcode=CJFD&dbname=CJFD2007&filename=SLXU200702015
    [102]
    Wang S, Yu Z, Liu K, et al. Synthesis and release of pulmonary tissue adrenomedullin on hypoxic pulmonary hypertension in rats and its significance[J]. Chin J Tuberc Respir Dis, 2001, 24(12): 725–727. https://pubmed.ncbi.nlm.nih.gov/11930700/
    [103]
    Cheng Y, Dai L, Xia G. The alterations and clinical significance of serum thyroid hormone levels in patients with acute exacerbation of chronic obstructive pulmonary disease[J]. Chin J Tuberc Respir Dis, 2016, 39(12): 939–943. http://rs.yiigle.com/resource_static.jspx?contentId=931446
    [104]
    Tsibulnikov S, Maslov L, Voronkov N, et al. Thyroid hormones and the mechanisms of adaptation to cold[J]. Hormones, 2020, 19(3): 329–339. doi: 10.1007/s42000-020-00200-2
    [105]
    Jeddi S, Zaman J, Zadeh-Vakili A, et al. Involvement of inducible nitric oxide synthase in the loss of cardioprotection by ischemic postconditioning in hypothyroid rats[J]. Gene, 2016, 580(2): 169–176. doi: 10.1016/j.gene.2016.01.014
    [106]
    Maslov LN, Khaliulin I, Oeltgen PR, et al. Prospects for creation of cardioprotective and antiarrhythmic drugs based on opioid receptor agonists[J]. Med Res Rev, 2016, 36(5): 871–923. doi: 10.1002/med.21395
    [107]
    Naryzhnaya NV, Maslov LN, Prokudina ES, et al. Contribution of opioid receptors to the cytoprotective effect of the adaptation to chronic hypoxia at anoxia/reoxygenation of isolated cardiomyocytes[J]. Bull Exp Biol Med, 2015, 159(2): 209–212. doi: 10.1007/s10517-015-2924-7
    [108]
    Pei J, Zhou J, Bian J, et al. Impaired [Ca2+]i and pHiresponses to κ-opioid receptor stimulation in the heart of chronically hypoxic rats[J]. Am J Physiol Cell Physiol, 2000, 279(5): C1483–C1494. doi: 10.1152/ajpcell.2000.279.5.C1483
    [109]
    Yuan F, Li H, Song S, et al. Opioid receptors mediate enhancement of ACh-induced aorta relaxation by chronic intermittent hypobaric hypoxia[J]. Acta Physiol Sin, 2013, 65(3): 269–275. https://kns.cnki.net/KCMS/detail/detail.aspx?dbcode=CJFD&dbname=CJFD2013&filename=SLXU201303005
    [110]
    Wu J, Li P, Wu X, et al. Chronic intermittent hypoxia decreases pain sensitivity and increases the expression of HIF1α and opioid receptors in experimental rats[J]. Sleep Breath, 2015, 19(2): 561–568. doi: 10.1007/s11325-014-1047-0
    [111]
    Li C, Chen L, Song M, et al. Ferulic acid protects cardiomyocytes from TNF-α/cycloheximide-induced apoptosis by regulating autophagy[J]. Arch Pharm Res, 2020, 43(8): 863–874. doi: 10.1007/s12272-020-01252-z
    [112]
    Degterev A, Hitomi J, Germscheid M, et al. Identification of RIP1 kinase as a specific cellular target of necrostatins[J]. Nat Chem Biol, 2008, 4(5): 313–321. doi: 10.1038/nchembio.83
    [113]
    Gao C, Liu Y, Yu Q, et al. TNF-α antagonism ameliorates myocardial ischemia-reperfusion injury in mice by upregulating adiponectin[J]. Am J Physiol Heart Circ Physiol, 2015, 308(12): H1583–H1591. doi: 10.1152/ajpheart.00346.2014
    [114]
    Chytilová A, Borchert GH, Mandíková-Alánová P, et al. Tumour necrosis factor-α contributes to improved cardiac ischaemic tolerance in rats adapted to chronic continuous hypoxia[J]. Acta Physiol, 2015, 214(1): 97–108. doi: 10.1111/apha.12489
    [115]
    Alánová P, Chytilová A, Neckář J, et al. Myocardial ischemic tolerance in rats subjected to endurance exercise training during adaptation to chronic hypoxia[J]. J Appl Physiol, 2017, 122(6): 1452–1461. doi: 10.1152/japplphysiol.00671.2016
    [116]
    Bilenko MV. Ischemic and reperfusion injury to organs[M]. Editors: Medicine, Moscow, 1989.
    [117]
    Krylatov AV, Maslov LN, Voronkov NS, et al. Reactive oxygen species as intracellular signaling molecules in the cardiovascular system[J]. Curr Cardiol Rev, 2018, 14(4): 290–300. doi: 10.2174/1573403X14666180702152436
    [118]
    Lien CF, Lee WS, Wang IC, et al. Intermittent hypoxia-generated ROS contributes to intracellular zinc regulation that limits ischemia/reperfusion injury in adult rat cardiomyocyte[J]. J Mol Cell Cardiol, 2018, 118: 122–132. doi: 10.1016/j.yjmcc.2018.03.014
    [119]
    Chang JC, Lien CF, Lee WS, et al. Intermittent hypoxia prevents myocardial mitochondrial Ca2+ overload and cell death during ischemia/reperfusion: the role of reactive oxygen species[J]. Cells, 2019, 8(6): 564. doi: 10.3390/cells8060564
    [120]
    Mrakic-Sposta S, Gussoni M, Dellanoce C, et al. Effects of acute and sub-acute hypobaric hypoxia on oxidative stress: a field study in the Alps[J]. Eur J Appl Physiol, 2021, 121(1): 297–306. doi: 10.1007/s00421-020-04527-x
    [121]
    Mallet RT, Burtscher J, Richalet JP, et al. Impact of high altitude on cardiovascular health: current perspectives[J]. Vasc Health Risk Manag, 2021, 17: 317–335. doi: 10.2147/VHRM.S294121
    [122]
    Balková P, Hlaváčková M, Milerová M, et al. N-acetylcysteine treatment prevents the up-regulation of MnSOD in chronically hypoxic rat hearts[J]. Physiol Res, 2011, 60(3): 467–474. https://www.biomed.cas.cz/physiolres/pdf/60/60_467.pdf
    [123]
    Heusch G. Molecular basis of cardioprotection: signal transduction in ischemic pre-, post-, and remote conditioning[J]. Circ Res, 2015, 116(4): 674–699. doi: 10.1161/CIRCRESAHA.116.305348
    [124]
    Fabian MR, Sonenberg N, Filipowicz W. Regulation of mRNA translation and stability by microRNAs[J]. Annu Rev Biochem, 2010, 79: 351–379. doi: 10.1146/annurev-biochem-060308-103103
    [125]
    McCreight JC, Schneider SE, Wilburn DB, et al. Evolution of microRNA in primates[J]. PLoS One, 2017, 12(6): e0176596. doi: 10.1371/journal.pone.0176596
    [126]
    Tsibulnikov SY, Maslov LN, Gorbunov AS, et al. A review of humoral factors in remote preconditioning of the heart[J]. J Cardiovasc Pharmacol Ther, 2019, 24(5): 403–421. doi: 10.1177/1074248419841632
    [127]
    Chen Y, Ye X, Yan F. MicroRNA 3113-5p is a novel marker for early cardiac ischemia/reperfusion injury[J]. Diagn Pathol, 2019, 14(1): 121. doi: 10.1186/s13000-019-0894-1
    [128]
    He S, Liu P, Jian Z, et al. miR-138 protects cardiomyocytes from hypoxia-induced apoptosis via MLK3/JNK/c-Jun pathway[J]. Biochem Biophys Res Commun, 2013, 441(4): 763–769. doi: 10.1016/j.bbrc.2013.10.151
    [129]
    Chen Q, Huang J, Wang H, et al. Effects of chronic intermittent hypoxia on regulation of miRNA-214 in myocardial apoptosis in rats[J]. Natl Med J China, 2015, 95(16): 1214–1217. http://rs.yiigle.com/CN112137201516/146750.htm
    [130]
    Huang J, Li X, Li H, et al. Down-regulation of microRNA-184 contributes to the development of cyanotic congenital heart diseases[J]. Int J Clin Exp Pathol, 2015, 8(11): 14221–14227. https://pubmed.ncbi.nlm.nih.gov/26823736/
    [131]
    Zhou Y, Jia W, Jian Z, et al. Downregulation of microRNA-199a-5p protects cardiomyocytes in cyanotic congenital heart disease by attenuating endoplasmic reticulum stress[J]. Mol Med Rep, 2017, 16(3): 2992–3000. doi: 10.3892/mmr.2017.6934
    [132]
    He W, Che H, Jin C, et al. Effects of miR-23b on hypoxia-induced cardiomyocytes apoptosis[J]. Biomed Pharmacother, 2017, 96: 812–817. doi: 10.1016/j.biopha.2017.09.148
    [133]
    Ren J, Liu W, Li G, et al. Atorvastatin attenuates myocardial hypertrophy induced by chronic intermittent hypoxia in vitro partly through miR-31/PKCε pathway[J]. Curr Med Sci, 2018, 38(3): 405–412. doi: 10.1007/s11596-018-1893-2
    [134]
    Zhang K, Ma Z, Wang W, et al. Beneficial effects of tolvaptan on atrial remodeling induced by chronic intermittent hypoxia in rats[J]. Cardiovasc Ther, 2018, 36(6): e12466. doi: 10.1111/1755-5922.12466
    [135]
    Santolini J. What does "NO-synthase" stand for ?[J]. Front Biosci, 2019, 24(1): 133–171. doi: 10.2741/4711
    [136]
    Cohen MV, Downey JM. Signalling pathways and mechanisms of protection in pre- and postconditioning: historical perspective and lessons for the future[J]. Br J Pharmacol, 2015, 172(8): 1913–1932. doi: 10.1111/bph.12903
    [137]
    Ferreiro CR, Chagas ACP, Carvalho MHC, et al. Influence of hypoxia on nitric oxide synthase activity and gene expression in children with congenital heart disease: a novel pathophysiological adaptive mechanism[J]. Circulation, 2001, 103(18): 2272–2276. doi: 10.1161/01.CIR.103.18.2272
    [138]
    Grilli A, De Lutiis MA, Patruno A, et al. Inducible nitric oxide synthase and heme oxygenase-1 in rat heart: direct effect of chronic exposure to hypoxia[J]. Ann Clin Lab Sci, 2003, 33(2): 208–215. http://www.annclinlabsci.org/content/33/2/208.long
    [139]
    Jung F, Palmer LA, Zhou N, et al. Hypoxic regulation of inducible nitric oxide synthase via hypoxia inducible factor-1 in cardiac myocytes[J]. Circ Res, 2000, 86(3): 319–325. doi: 10.1161/01.RES.86.3.319
    [140]
    Rouet-Benzineb P, Eddahibi S, Raffestin B, et al. Induction of cardiac nitric oxide synthase 2 in rats exposed to chronic hypoxia[J]. J Mol Cell Cardiol, 1999, 31(9): 1697–1708. doi: 10.1006/jmcc.1999.1005
    [141]
    Yuan X, Zhu D, Guo X, et al. Telmisartan attenuates myocardial apoptosis induced by chronic intermittent hypoxia in rats: modulation of nitric oxide metabolism and inflammatory mediators[J]. Sleep Breath, 2015, 19(2): 703–709. doi: 10.1007/s11325-014-1081-y
    [142]
    Thompson LP, Dong Y. Chronic hypoxia decreases endothelial nitric oxide synthase protein expression in fetal guinea pig hearts[J]. J Soc Gynecol Investig, 2005, 12(6): 388–395. doi: 10.1016/j.jsgi.2005.04.011
    [143]
    La Padula PH, Etchegoyen M, Czerniczyniec A, et al. Cardioprotection after acute exposure to simulated high altitude in rats. Role of nitric oxide[J]. Nitric Oxide, 2018, 73: 52–59. doi: 10.1016/j.niox.2017.12.007
    [144]
    Felaco M, Grilli A, Gorbunov N, et al. Endothelial NOS expression and ischemia-reperfusion in isolated working rat heart from hypoxic and hyperoxic conditions[J]. Biochim Biophys Acta, 2000, 1524(2-3): 203–211. doi: 10.1016/S0304-4165(00)00159-8
    [145]
    Forkel J, Chen X, Wandinger S, et al. Responses of chronically hypoxic rat hearts to ischemia: KATP channel blockade does not abolish increased RV tolerance to ischemia[J]. Am J Physiol Heart Circ Physiol, 2004, 286(2): H545–H551. doi: 10.1152/ajpheart.00022.2003
    [146]
    Quing M, Görlach A, Schumacher K, et al. The hypoxia-inducible factor HIF-1 promotes intramyocardial expression of VEGF in infants with congenital cardiac defects[J]. Basic Res Cardiol, 2007, 102(3): 224–232. doi: 10.1007/s00395-007-0639-2
    [147]
    Shi Y, Pritchard KA, Holman P, et al. Chronic myocardial hypoxia increases nitric oxide synthase and decreases caveolin-3[J]. Free Radic Biol Med, 2000, 29(8): 695–703. doi: 10.1016/S0891-5849(00)00364-6
    [148]
    La Padula P, Bustamante J, Czerniczyniec A, et al. Time course of regression of the protection conferred by simulated high altitude to rat myocardium: correlation with mtNOS[J]. J Appl Physiol, 2008, 105(3): 951–957. doi: 10.1152/japplphysiol.90400.2008
    [149]
    Ghafourifar P, Cadenas E. Mitochondrial nitric oxide synthase[J]. Trends Pharmacol Sci, 2005, 26(4): 190–195. doi: 10.1016/j.tips.2005.02.005
    [150]
    Thompson L, Dong Y, Evans L. Chronic hypoxia increases inducible NOS-derived nitric oxide in fetal guinea pig hearts[J]. Pediatr Res, 2009, 65(2): 188–192. doi: 10.1203/PDR.0b013e31818d6ad0
    [151]
    Milano G, Corno AF, Samaja M, et al. Daily reoxygenation decreases myocardial injury and improves post-ischaemic recovery after chronic hypoxia[J]. Eur J Cardiothorac Surg, 2010, 37(4): 942–949. doi: 10.1016/j.ejcts.2009.10.030
    [152]
    Yu X, Ge L, Niu L, et al. The dual role of inducible nitric oxide synthase in myocardial ischemia/reperfusion injury: friend or foe?[J]. Oxid Med Cell Longev, 2018, 2018: 8364848. doi: 10.1155/2018/8364848
    [153]
    Baker JE, Holman P, Kalyanaraman B, et al. Adaptation to chronic hypoxia confers tolerance to subsequent myocardial ischemia by increased nitric oxide production[J]. Ann N Y Acad Sci, 1999, 874: 236–253. doi: 10.1111/j.1749-6632.1999.tb09239.x
    [154]
    Earley S, Walker BR. Increased nitric oxide production following chronic hypoxia contributes to attenuated systemic vasoconstriction[J]. Am J Physiol Heart Circ Physiol, 2003, 284(5): H1655–H1661. doi: 10.1152/ajpheart.00964.2002
    [155]
    Fitzpatrick CM, Shi Y, Hutchins WC, et al. Cardioprotection in chronically hypoxic rabbits persists on exposure to normoxia: role of NOS and KATP channels[J]. Am J Physiol Heart Circ Physiol, 2005, 288(1): H62–H68. doi: 10.1152/ajpheart.00701.2004
    [156]
    Rafiee P, Shi Y, Kong X, et al. Activation of protein kinases in chronically hypoxic infant human and rabbit hearts: role in cardioprotection[J]. Circulation, 2002, 106(2): 239–245. doi: 10.1161/01.CIR.0000022018.68965.6D
    [157]
    Morel OE, Buvry A, Le Corvoisier P, et al. Effects of nifedipine-induced pulmonary vasodilatation on cardiac receptors and protein kinase C isoforms in the chronically hypoxic rat[J]. Pflugers Arch, 2003, 446(3): 356–364. doi: 10.1007/s00424-003-1034-y
    [158]
    Naryzhnaya NV, Maslov IN, Khaliulin IG, et al. Chronic continuous nor-Mobaric hypoxia augments cell tolerance to anoxia (reoxyge-nation: the role of protein kinases[J]. Ross Fiziol Zh Im I M Sechenova (in Russian), 2016, 102(12): 1462–1471. https://pubmed.ncbi.nlm.nih.gov/30198641/
    [159]
    El Alwani M, Usta J, Nemer G, et al. Regulation of the sphingolipid signaling pathways in the growing and hypoxic rat heart[J]. Prostaglandins Other Lipid Mediat, 2005, 78(1–4): 249–263. doi: 10.1016/j.prostaglandins.2005.09.002
    [160]
    Hlaváčková M, Kožichová K, Neckář J, et al. Up-regulation and redistribution of protein kinase C-δ in chronically hypoxic heart[J]. Mol Cell Biochem, 2010, 345(1-2): 271–282. doi: 10.1007/s11010-010-0581-8
    [161]
    Hlavácková M, Neckár J, Jezková J, et al. Dietary polyunsaturated fatty acids alter myocardial protein kinase C expression and affect cardioprotection induced by chronic hypoxia[J]. Exp Biol Med, 2007, 232(6): 823–832. https://pubmed.ncbi.nlm.nih.gov/17526775/
    [162]
    Su Z, Liu Y, Zhang H. Adaptive cardiac metabolism under chronic hypoxia: mechanism and clinical implications[J]. Front Cell Dev Biol, 2021, 9: 625524. doi: 10.3389/fcell.2021.625524
    [163]
    de Miranda DC, de Oliveira Faria G, Hermidorff MM, et al. Pre- and post-conditioning of the heart: an overview of cardioprotective signaling pathways[J]. Curr Vasc Pharmacol, 2021, 19(5): 499–524. doi: 10.2174/1570161119666201120160619
    [164]
    Micova P, Hahnova K, Hlavackova M, et al. Chronic intermittent hypoxia affects the cytosolic phospholipase A2α/cyclooxygenase 2 pathway via β2-adrenoceptor-mediated ERK/p38 stimulation[J]. Mol Cell Biochem, 2016, 423(1-2): 151–163. doi: 10.1007/s11010-016-2833-8
    [165]
    Zeng C, Liang B, Jiang R, et al. Protein kinase C isozyme expression in right ventricular hypertrophy induced by pulmonary hypertension in chronically hypoxic rats[J]. Mol Med Rep, 2017, 16(4): 3833–3840. doi: 10.3892/mmr.2017.7098
    [166]
    Ling H, Gray CBB, Zambon AC, et al. Ca2+/calmodulin-dependent protein kinase II δ mediates myocardial ischemia/reperfusion injury through nuclear factor-κB[J]. Circ Res, 2013, 112(6): 935–944. doi: 10.1161/CIRCRESAHA.112.276915
    [167]
    Yang Y, Jiang K, Liu X, et al. CaMKII in regulation of cell death during myocardial reperfusion injury[J]. Front Mol Biosci, 2021, 8: 668129. doi: 10.3389/fmolb.2021.668129
    [168]
    Zhao P, Pan J, Li F, et al. Effects of chronic hypoxia on the expression of calmodulin and calcicum/calmodulin-dependent protein kinase II and the calcium activity in myocardial cells in young rats[J]. Chin J Contemp Pediatr, 2008, 10(3): 381–385. https://d.wanfangdata.com.cn/periodical/zgddekzz200803028
    [169]
    Nehra S, Bhardwaj V, Kar S, et al. Chronic hypobaric hypoxia induces right ventricular hypertrophy and apoptosis in rats: therapeutic potential of nanocurcumin in improving adaptation[J]. High Alt Med Biol, 2016, 17(4): 342–352. doi: 10.1089/ham.2016.0032
    [170]
    Xie Y, Zhu W, Zhu Y, et al. Intermittent high altitude hypoxia protects the heart against lethal Ca2+ overload injury[J]. Life Sci, 2004, 76(5): 559–572. doi: 10.1016/j.lfs.2004.09.017
    [171]
    Gui L, Guo X, Zhang Z, et al. Activation of CaMKIIδA promotes Ca2+ leak from the sarcoplasmic reticulum in cardiomyocytes of chronic heart failure rats[J]. Acta Pharmacol Sin, 2018, 39(10): 1604–1612. doi: 10.1038/aps.2018.20
    [172]
    Strnisková M, Ravingerová T, Neckár J, et al. Changes in the expression and/or activation of regulatory proteins in rat hearts adapted to chronic hypoxia[J]. Gen Physiol Biophys, 2006, 25(1): 25–41. http://www.gpb.sav.sk/2006_01_25.pdf
    [173]
    Milano G, von Segesser LK, Morel S, et al. Phosphorylation of phosphatidylinositol-3-kinase-protein kinase B and extracellular signal-regulated kinases 1/2 mediate reoxygenation-induced cardioprotection during hypoxia[J]. Exp Biol Med, 2010, 235(3): 401–410. doi: 10.1258/ebm.2009.009153
    [174]
    Ravingerová T, Matejíková J, Neckář J, et al. Differential role of PI3K/Akt pathway in the infarct size limitation and antiarrhythmic protection in the rat heart[J]. Mol Cell Biochem, 2007, 297(1-2): 111–120. doi: 10.1007/s11010-006-9335-z
    [175]
    Jia W, Jian Z, Li J, et al. Upregulated ATF6 contributes to chronic intermittent hypoxia-afforded protection against myocardial ischemia/reperfusion injury[J]. Int J Mol Med, 2016, 37(5): 1199–1208. doi: 10.3892/ijmm.2016.2535
    [176]
    Luo G, Jian Z, Ma R, et al. Melatonin alleviates hypoxia-induced cardiac apoptosis through PI3K/Akt pathway[J]. Int J Clin Exp Pathol, 2018, 11(12): 5840–5849. https://pubmed.ncbi.nlm.nih.gov/31949670/
    [177]
    García-Niño WR, Zazueta C, Buelna-Chontal M, et al. Mitochondrial quality control in cardiac-conditioning strategies against ischemia-reperfusion injury[J]. Life (Basel), 2021, 11(11): 1123. doi: 10.3390/LIFE11111123
    [178]
    Morel S, Milano G, Ludunge KM, et al. Brief reoxygenation episodes during chronic hypoxia enhance posthypoxic recovery of LV function: role of mitogen-activated protein kinase signaling pathways[J]. Basic Res Cardiol, 2006, 101(4): 336–345. doi: 10.1007/s00395-006-0596-1
    [179]
    Milano G, Morel S, Bonny C, et al. A peptide inhibitor of c-Jun NH2-terminal kinase reduces myocardial ischemia-reperfusion injury and infarct size in vivo[J]. Am J Physiol Heart Circ Physiol, 2007, 292(4): H1828–H1835. doi: 10.1152/ajpheart.01117.2006
    [180]
    Heidbreder M, Naumann A, Tempel K, et al. Remote vs. ischaemic preconditioning: the differential role of mitogen-activated protein kinase pathways[J]. Cardiovasc Res, 2008, 78(1): 108–115. doi: 10.1093/cvr/cvm114
    [181]
    Menon VP, Sudheer AR. Antioxidant and anti-inflammatory properties of curcumin[M]//Aggarwal BB, Surh YJ, Shishodia S. The Molecular Targets and Therapeutic Uses of Curcumin in Health and Disease. New York: Springer, 2007: 105–125.
    [182]
    Li Q, Xiang Y, Chen Y, et al. Ginsenoside Rg1 protects cardiomyocytes against hypoxia/reoxygenation injury via activation of Nrf2/HO-1 signaling and inhibition of JNK[J]. Cell Physiol Biochem, 2017, 44(1): 21–37. doi: 10.1159/000484578
    [183]
    He S, Liu S, Wu X, et al. Protective role of downregulated MLK3 in myocardial adaptation to chronic hypoxia[J]. J Physiol Biochem, 2016, 73(3): 371–380. doi: 10.1007/s13105-017-0561-5
    [184]
    Zhao Y, An J, Yang S, et al. Hydrogen and oxygen mixture to improve cardiac dysfunction and myocardial pathological changes induced by intermittent hypoxia in rats[J]. Oxid Med Cell Longev, 2019, 2019: 7415212. doi: 10.1155/2019/7415212
    [185]
    Wagner C, Tillack D, Simonis G, et al. Ischemic post-conditioning reduces infarct size of the in vivo rat heart: role of PI3-K, mTOR, GSK-3β, and apoptosis[J]. Mol Cell Biochem, 2010, 339(1-2): 135–147. doi: 10.1007/s11010-009-0377-x
    [186]
    Li W, Zhu L, Ruan Z, et al. Nicotinamide protects chronic hypoxic myocardial cells through regulating mTOR pathway and inducing autophagy[J]. Eur Rev Med Pharmacol Sci, 2019, 23(12): 5503–5511. https://www.europeanreview.org/wp/wp-content/uploads/5503-5511.pdf
    [187]
    Guan P, Sun ZM, Wang N, et al. Resveratrol prevents chronic intermittent hypoxia-induced cardiac hypertrophy by targeting the PI3K/AKT/mTOR pathway[J]. Life Sci, 2019, 233: 116748. doi: 10.1016/j.lfs.2019.116748
    [188]
    Wang J, Maimaitili Y, Zheng H, et al. The influence of rapamycin on the early cardioprotective effect of hypoxic preconditioning on cardiomyocytes[J]. Arch Med Sci, 2017, 13(4): 947–955. doi: 10.5114/aoms.2016.59712
    [189]
    Gu S, Hua H, Guo X, et al. PGC-1α Participates in the protective effect of chronic intermittent hypobaric hypoxia on cardiomyocytes[J]. Cell Physiol Biochem, 2018, 50(5): 1891–1902. doi: 10.1159/000494869
    [190]
    Zhang H, Liu B, Li T, et al. AMPK activation serves a critical role in mitochondria quality control via modulating mitophagy in the heart under chronic hypoxia[J]. Int J Mol Med, 2018, 41(1): 69–76. https://pubmed.ncbi.nlm.nih.gov/29115402/
    [191]
    Miura T, Miki T. GSK-3β, a therapeutic target for cardiomyocyte protection[J]. Circ J, 2009, 73(7): 1184–1192. doi: 10.1253/circj.CJ-09-0284
    [192]
    McCarthy J, Lochner A, Opie LH, et al. PKCε promotes cardiac mitochondrial and metabolic adaptation to chronic hypobaric hypoxia by GSK3β inhibition[J]. J Cell Physiol, 2011, 226(9): 2457–2468. doi: 10.1002/jcp.22592
    [193]
    Waskova-Arnostova P, Elsnicova B, Kasparova D, et al. Cardioprotective adaptation of rats to intermittent hypobaric hypoxia is accompanied by the increased association of hexokinase with mitochondria[J]. J Appl Physiol, 2015, 119(12): 1487–1493. doi: 10.1152/japplphysiol.01035.2014
    [194]
    Gross GJ, Peart JN. KATP channels and myocardial preconditioning: an update[J]. Am J Physiol Heart Circ Physiol, 2003, 285(3): H921–H930. doi: 10.1152/ajpheart.00421.2003
    [195]
    Grover GJ, Garlid KD. ATP-sensitive potassium channels: a review of their cardioprotective pharmacology[J]. J Mol Cell Cardiol, 2000, 32(4): 677–695. doi: 10.1006/jmcc.2000.1111
    [196]
    Peart JN, Gross GJ. Sarcolemmal and mitochondrial KATP channels and myocardial ischemic preconditioning[J]. J Cell Mol Med, 2002, 6(4): 453–464. doi: 10.1111/j.1582-4934.2002.tb00449.x
    [197]
    Baker JE, Contney SJ, Gross GJ, et al. KATP channel activation in a rabbit model of chronic myocardial hypoxia[J]. J Mol Cell Cardiol, 1997, 29(2): 845–848. doi: 10.1006/jmcc.1996.0361
    [198]
    Zhu Z, Burnett CM, Maksymov G, et al. Reduction in number of sarcolemmal KATP channels slows cardiac action potential duration shortening under hypoxia[J]. Biochem Biophys Res Commun, 2011, 415(4): 637–641. doi: 10.1016/j.bbrc.2011.10.125
    [199]
    Crawford RM, Jovanović S, Budas GR, et al. Chronic mild hypoxia protects heart-derived H9c2 cells against acute hypoxia/reoxygenation by regulating expression of the SUR2A subunit of the ATP-sensitive K+ channel[J]. J Biol Chem, 2003, 278(33): 31444–31455. doi: 10.1074/jbc.M303051200
    [200]
    Kolar F, Nekar J, Ostadal B, et al. Role of ATP-sensitive K+-channels in antiarrhythmic and cardioprotective action of adaptation to intermittent hypobaric hypoxia[J]. Bull Exp Biol Med, 2008, 145(4): 418–421. doi: 10.1007/s10517-008-0106-6
    [201]
    Neckář J, Szárszoi O, Koten L, et al. Effects of mitochondrial KATP modulators on cardioprotection induced by chronic high altitude hypoxia in rats[J]. Cardiovasc Res, 2002, 55(3): 567–575. doi: 10.1016/S0008-6363(02)00456-X
    [202]
    Lishmanov YB, Naryzhnaya NV, Tsibul’nikov SY, et al. Role of ATP-sensitive K+ channels in myocardial infarct size-limiting effect of chronic continuous normobaric hypoxia[J]. Bull Exp Biol Med, 2017, 163(1): 22–24. doi: 10.1007/s10517-017-3728-8
    [203]
    Testai L, Rapposelli S, Martelli A, et al. Mitochondrial potassium channels as pharmacological target for cardioprotective drugs[J]. Med Res Rev, 2015, 35(3): 520–553. doi: 10.1002/med.21332
    [204]
    Semenza GL. Pharmacologic targeting of hypoxia-inducible factors[J]. Annu Rev Pharmacol Toxicol, 2019, 59: 379–403. doi: 10.1146/annurev-pharmtox-010818-021637
    [205]
    Li J, Zhou W, Chen W, et al. Mechanism of the hypoxia inducible factor 1/hypoxic response element pathway in rat myocardial ischemia/diazoxide post-conditioning[J]. Mol Med Rep, 2020, 21(3): 1527–1536. doi: 10.3892/mmr.2020.10966
    [206]
    Lin C, Hsu KC, Huangfu W, et al. Investigating the potential effects of selective histone deacetylase 6 inhibitor ACY1215 on infarct size in rats with cardiac ischemia-reperfusion injury[J]. BMC Pharmacol Toxicol, 2020, 21(1): 21. doi: 10.1186/s40360-020-0400-0
    [207]
    Wang Z, Zhang Z, Zhao J, et al. Polysaccharides from enteromorpha prolifera ameliorate acute myocardial infarction in vitro and in vivo via up-regulating HIF-1α[J]. Int Heart J, 2019, 60(4): 964–973. doi: 10.1536/ihj.18-519
    [208]
    Wei Q, Bian Y, Yu F, et al. Chronic intermittent hypoxia induces cardiac inflammation and dysfunction in a rat obstructive sleep apnea model[J]. J Biomed Res, 2016, 30(6): 490–495. doi: 10.7555/JBR.30.20160110
    [209]
    Sarkar FH, Li Y, Wang Z, et al. NF-κB signaling pathway and its therapeutic implications in human diseases[J]. Int Rev Immunol, 2008, 27(5): 293–319. doi: 10.1080/08830180802276179
    [210]
    Morgan EN, Boyle EM, Yun W, et al. An essential role for NF-κB in the cardioadaptive response to ischemia[J]. Ann Thorac Surg, 1999, 68(2): 377–382. doi: 10.1016/S0003-4975(99)00646-3
    [211]
    Yuan C, Wang H, Yuan Z. Ginsenoside Rg1 inhibits myocardial ischaemia and reperfusion injury via HIF-1 α-ERK signalling pathways in a diabetic rat model[J]. Pharmazie, 2019, 74(3): 157–162. https://pubmed.ncbi.nlm.nih.gov/30961682/
    [212]
    Liu D, Zhang Y, Hu H, et al. Downregulation of microRNA-199a-5p attenuates hypoxia/reoxygenation-induced cytotoxicity in cardiomyocytes by targeting the HIF-1α-GSK3β-mPTP axis[J]. Mol Med Rep, 2019, 19(6): 5335–5344. https://www.spandidos-publications.com/mmr/19/6/5335
    [213]
    Dong J, Xu M, Zhang W, et al. Effects of sevoflurane pretreatment on myocardial ischemia-reperfusion injury through the Akt/hypoxia-inducible factor 1-alpha (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway[J]. Med Sci Monit, 2019, 25: 3100–3107. doi: 10.12659/MSM.914265
    [214]
    Jiang L, Zeng H, Ni L, et al. HIF-1α preconditioning potentiates antioxidant activity in ischemic injury: the role of sequential administration of dihydrotanshinone I and protocatechuic aldehyde in cardioprotection[J]. Antioxid Redox Signal, 2019, 31(3): 227–242. doi: 10.1089/ars.2018.7624
    [215]
    Tranter M, Ren X, Forde T, et al. NF-κB driven cardioprotective gene programs; Hsp70.3 and cardioprotection after late ischemic preconditioning[J]. J Mol Cell Cardiol, 2010, 49(4): 664–672. doi: 10.1016/j.yjmcc.2010.07.001
    [216]
    Wilhide ME, Tranter M, Ren X, et al. Identification of a NF-κB cardioprotective gene program: NF-κB regulation of Hsp70.1 contributes to cardioprotection after permanent coronary occlusion[J]. J Mol Cell Cardiol, 2011, 51(1): 82–89. doi: 10.1016/j.yjmcc.2011.03.011
    [217]
    Stein AB, Bolli R, Dawn B, et al. Carbon monoxide induces a late preconditioning-mimetic cardioprotective and antiapoptotic milieu in the myocardium[J]. J Mol Cell Cardiol, 2012, 52(1): 228–236. doi: 10.1016/j.yjmcc.2011.11.005
    [218]
    Qiao S, Xie H, Wang C, et al. Delayed anesthetic preconditioning protects against myocardial infarction via activation of nuclear factor-κB and upregulation of autophagy[J]. J Anesth, 2013, 27(2): 251–260. doi: 10.1007/s00540-012-1494-3
    [219]
    Haar L, Ren X, Liu Y, et al. Acute consumption of a high-fat diet prior to ischemia-reperfusion results in cardioprotection through NF-κB-dependent regulation of autophagic pathways[J]. Am J Physiol Heart Circ Physiol, 2014, 307(12): H1705–H1713. doi: 10.1152/ajpheart.00271.2014
    [220]
    Naryzhnaya NV, Maslov LN, Oeltgen PR. Pharmacology of mitochondrial permeability transition pore inhibitors[J]. Drug Dev Res, 2019, 80(8): 1013–1030. doi: 10.1002/ddr.21593
    [221]
    Armstrong SC, Liu GS, Downey JM, et al. Potassium channels and preconditioning of isolated rabbit cardiomyocytes: effects of glyburide and pinacidil[J]. J Mol Cell Cardiol, 1995, 27(8): 1765–1774. doi: 10.1016/S0022-2828(95)90986-9
    [222]
    Xu M, Wang Y, Ayub A, et al. Mitochondrial KATP channel activation reduces anoxic injury by restoring mitochondrial membrane potential[J]. Am J Physiol Heart Circ Physiol, 2001, 281(3): H1295–H1303. doi: 10.1152/ajpheart.2001.281.3.H1295
    [223]
    Hausenloy DJ, Schulz R, Girao H, et al. Mitochondrial ion channels as targets for cardioprotection[J]. J Cell Mol Med, 2020, 24(13): 7102–7114. doi: 10.1111/jcmm.15341
    [224]
    Ozcan C, Bienengraeber M, Dzeja PP, et al. Potassium channel openers protect cardiac mitochondria by attenuating oxidant stress at reoxygenation[J]. Am J Physiol Heart Circ Physiol, 2002, 282(2): H531–H539. doi: 10.1152/ajpheart.00552.2001
    [225]
    Ichinose M, Yonemochi H, Sato T, et al. Diazoxide triggers cardioprotection against apoptosis induced by oxidative stress[J]. Am J Physiol Heart Circ Physiol, 2003, 284(6): H2235–H2241. doi: 10.1152/ajpheart.01073.2002
    [226]
    Jung YS, Lee DH, Lim H, et al. KR-31378 protects cardiac H9c2 cells from chemical hypoxia-induced cell death via inhibition of JNK/p38 MAPK activation[J]. Jpn J Physiol, 2004, 54(6): 575–583. doi: 10.2170/jjphysiol.54.575
    [227]
    Obata T, Yamanaka Y. Block of cardiac atp-sensitive K+ channels reduces hydroxyl radicals in the rat myocardium[J]. Arch Biochem Biophys, 2000, 378(2): 195–200. doi: 10.1006/abbi.2000.1830
    [228]
    Pain T, Yang XM, Critz SD, et al. Opening of mitochondrial KATP channels triggers the preconditioned state by generating free radicals[J]. Circ Res, 2000, 87(6): 460–466. doi: 10.1161/01.RES.87.6.460
    [229]
    Carroll R, Gant VA, Yellon DM. Mitochondrial KATP channel opening protects a human atrial-derived cell line by a mechanism involving free radical generation[J]. Cardiovasc Res, 2001, 51(4): 691–700. doi: 10.1016/S0008-6363(01)00330-3
    [230]
    Forbes RA, Steenbergen C, Murphy E. Diazoxide-induced cardioprotection requires signaling through a redox-sensitive mechanism[J]. Circ Res, 2001, 88(8): 802–809. doi: 10.1161/hh0801.089342
    [231]
    Tsuchida A, Miura T, Tanno M, et al. Infarct size limitation by nicorandil: roles of mitochondrial KATP channels, sarcolemmal KATP channels, and protein kinase C[J]. J Am Coll Cardiol, 2002, 40(8): 1523–1530. doi: 10.1016/S0735-1097(02)02268-4
    [232]
    Wang Y, Hirai K, Ashraf M. Activation of mitochondrial ATP-sensitive K+ channel for cardiac protection against ischemic injury is dependent on protein kinase C activity[J]. Circ Res, 1999, 85(8): 731–741. doi: 10.1161/01.RES.85.8.731
    [233]
    Wang Y, Takashi E, Xu M, et al. Downregulation of protein kinase C inhibits activation of mitochondrial KATP channels by diazoxide[J]. Circulation, 2001, 104(1): 85–90. doi: 10.1161/01.CIR.104.1.85
    [234]
    Tsukamoto O, Asanuma H, Kim J, et al. A role of opening of mitochondrial ATP-sensitive potassium channels in the infarct size-limiting effect of ischemic preconditioning via activation of protein kinase C in the canine heart[J]. Biochem Biophys Res Commun, 2005, 338(3): 1460–1466. doi: 10.1016/j.bbrc.2005.10.109
    [235]
    Akao M, Teshima Y, Marbán E. Antiapoptotic effect of nicorandil mediated by mitochondrial atp-sensitive potassium channels in cultured cardiac myocytes[J]. J Am Coll Cardiol, 2002, 40(4): 803–810. doi: 10.1016/S0735-1097(02)02007-7
    [236]
    Gao Q, Pan H, Qiu S, et al. Atractyloside and 5-hydroxydecanoate block the protective effect of puerarin in isolated rat heart[J]. Life Sci, 2006, 79(3): 217–224. doi: 10.1016/j.lfs.2005.12.040
    [237]
    Gross ER, Hsu AK, Gross GJ. Delayed cardioprotection afforded by the glycogen synthase kinase 3 inhibitor SB-216763 occurs via a KATP- and MPTP-dependent mechanism at reperfusion[J]. Am J Physiol Heart Circ Physiol, 2008, 294(3): H1497–H1500. doi: 10.1152/ajpheart.01381.2007
    [238]
    Bu H, Yang C, Wang M, et al. KATP channels and MPTP are involved in the cardioprotection bestowed by chronic intermittent hypobaric hypoxia in the developing rat[J]. J Physiol Sci, 2015, 65(4): 367–376. doi: 10.1007/s12576-015-0376-5
    [239]
    Topsakal R, Eryol NK, Abacı A, et al. The relation between chronic obstructive pulmonary disease and coronary collateral vessels[J]. Angiology, 2005, 56(6): 651–656. doi: 10.1177/000331970505600601
    [240]
    Tin'kov AN, Aksenov VA. Effects of intermittent hypobaric hypoxia on blood lipid concentrations in male coronary heart disease patients[J]. High Alt Med Biol, 2002, 3(3): 277–282. doi: 10.1089/152702902320604250
    [241]
    del Pilar Valle M, García-Godos F, Woolcott OO, et al. Improvement of myocardial perfusion in coronary patients after intermittent hypobaric hypoxia[J]. J Nucl Cardiol, 2006, 13(1): 69–74. doi: 10.1016/j.nuclcard.2005.11.008
    [242]
    Syrkin AL, Glazachev OS, Kopylov FY, et al. Adaptation to intermittent hypoxia-hyperoxia in the rehabilitation of patients with ischemic heart disease: exercise tolerance and quality of life[J]. Kardiologiia (in Russian), 2017, 57(5): 10–16. https://pubmed.ncbi.nlm.nih.gov/28762914/
    [243]
    Glazachev O, Kopylov P, Susta D, et al. Adaptations following an intermittent hypoxia-hyperoxia training in coronary artery disease patients: a controlled study[J]. Clin Cardiol, 2017, 40(6): 370–376. doi: 10.1002/clc.22670
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