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

  • Huang-Tian YangEmail author
  • Yi Zhang
  • Zhi-Hua Wang
  • Zhao-Nian Zhou


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.


KATP Channel Cardioprotective Effect Mitochondrial Permeability Transition Pore Intermittent Hypoxia Mitochondrial Permeability Transition Pore 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



Action potential


Action potential duration


Angiotensin II type 1


Adenosine triphosphate


Intracellular free Ca2+ concentration


Ca2+/calmodulin-dependent kinase II


Coronary flow


Effective refractory period




Glycogen synthase I


ATP-sensitive potassium


High-altitude hypoxia


Intermittent hypoxia


L-type calcium channel


NCX currents


Outward potassium channel


Ischemic preconditioning




Mitochondrial permeability transition pore


Na+/Ca2+ exchanger


Obstructive sleep apnea


Protein kinase A


Protein kinase C




Resting potential


Ryanodine receptor


Sarcoplasmic reticulum Ca2+-ATPase isoforms 2


Sarcoplasmic reticulum


Vascular endothelial growth factor



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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Copyright information

© Springer-Verlag London 2012

Authors and Affiliations

  • Huang-Tian Yang
    • 1
    • 2
    Email author
  • Yi Zhang
    • 3
  • Zhi-Hua Wang
    • 1
  • Zhao-Nian Zhou
    • 4
  1. 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)ShanghaiChina
  2. 2.Key Laboratory of Stem Cell BiologyShanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS)ShanghaiChina
  3. 3.Department of PhysiologyHebei Medical UniversityShijiazhuangChina
  4. 4.Physiological Laboratory of HypoxiaSIBS, CASShanghaiChina

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