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Protective Effects of Chronic Intermittent Hypoxia Against Myocardial Ischemia/Reperfusion Injury

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Intermittent Hypoxia and Human Diseases

Abstract

Accumulated evidence has shown that adaptation to chronic hypobaric intermittent hypoxia (IH) increases myocardial tolerance to the subsequent severe hypoxia, Ca2+ overload, or ischemia/reperfusion (I/R) injury. Attractively, this form of protection is noninvasive, persists longer than ischemic preconditioning, and has less side effects such as right ventricular hypertrophy compared with the chronic continuous hypoxia. The cardioprotective effects are largely dependent on the degree and duration of IH. Therefore, to identify suitable cycle length, the number of hypoxic episodes per day, degree, and duration of chronic hypobaric IH is important for clinical application. In addition, elucidation of the mechanisms underlying chronic IH-induced cardioprotection is of basic and clinical importance. To address these issues, this chapter focuses primarily on the cardioprotective effects of chronic hypobaric IH in the improvement of myocardial contractile dysfunction and in the reduction of arrhythmias due to Ca2+ overload or I/R injury. The recent progresses in the understanding of the mechanisms, especially related to the cellular adaptation, are discussed. The knowledge we have got from this area should provide new insights into the understanding of the intrinsic defensive mechanism and have impact on the exploring of new therapeutic approaches in the protection of the heart against ischemic heart diseases and other stress.

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Abbreviations

AP:

Action potential

APD:

Action potential duration

AT1:

Angiotensin II type 1

ATP:

Adenosine triphosphate

[Ca2+]i :

Intracellular free Ca2+ concentration

CaMKII:

Ca2+/calmodulin-dependent kinase II

CF:

Coronary flow

ERP:

Effective refractory period

ET-1:

Endothelin-1

GS I:

Glycogen synthase I

KATP :

ATP-sensitive potassium

HAH:

High-altitude hypoxia

IH:

Intermittent hypoxia

Ica-L :

L-type calcium channel

INa/Ca :

NCX currents

Ito :

Outward potassium channel

IPC:

Ischemic preconditioning

I/R:

Ischemia/reperfusion

MPTP:

Mitochondrial permeability transition pore

NCX:

Na+/Ca2+ exchanger

OSA:

Obstructive sleep apnea

PKA:

Protein kinase A

PKC:

Protein kinase C

PLB:

Phospholamban

RP:

Resting potential

RyR:

Ryanodine receptor

SERCA2:

Sarcoplasmic reticulum Ca2+-ATPase isoforms 2

SR:

Sarcoplasmic reticulum

VEGF:

Vascular endothelial growth factor

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Acknowledgments

Some of the studies were supported partially by grants from Major State Basic Research Development Program of People’s Republic of China (2006CB504106; 2007CB512100) and Knowledge Innovation Program of the CAS (KSCX2-YW-R-75).

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Authors and Affiliations

  1. Laboratory of Molecular Cardiology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS) and Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, 200025, China

    Huang-Tian Yang & Zhi-Hua Wang

  2. Key Laboratory of Stem Cell Biology, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), Shanghai, China

    Huang-Tian Yang

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

    Yi Zhang

  4. Physiological Laboratory of Hypoxia, SIBS, CAS, Shanghai, 200031, China

    Zhao-Nian Zhou

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  1. Huang-Tian Yang
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Correspondence to Huang-Tian Yang .

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Editors and Affiliations

  1. , Division of Cardiology, Virginia Commonwealth University, Richmond, 23298, Virginia, USA

    Lei Xi

  2. Bogomoletz Institute of Physiology, Kiev, 01601, Ukraine

    Tatiana V. Serebrovskaya

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Yang, HT., Zhang, Y., Wang, ZH., Zhou, ZN. (2012). Protective Effects of Chronic Intermittent Hypoxia Against Myocardial Ischemia/Reperfusion Injury. In: Xi, L., Serebrovskaya, T. (eds) Intermittent Hypoxia and Human Diseases. Springer, London. https://doi.org/10.1007/978-1-4471-2906-6_4

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