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Postnatal development in intermittent hypoxia enhances resistance to myocardial ischemia/reperfusion in male rats.

作者信息

Zhu Wei-Zhong, Dong Jian-Wen, Ding Hai-Lei, Yang Huang-Tian, Zhou Zhao-Nian

机构信息

Physiological Laboratory of Hypoxia, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue Yang Road, 200031 Shanghai, China.

出版信息

Eur J Appl Physiol. 2004 May;91(5-6):716-22. doi: 10.1007/s00421-003-0939-7. Epub 2004 Feb 17.

DOI:10.1007/s00421-003-0939-7
PMID:14985993
Abstract

To assess the tolerance of rats that developed from birth in intermittent hypoxia (IH) to myocardial ischemia and reperfusion, we set up a reproducible model in our laboratory. IH rats were raised 60 days from birth in a hypobaric chamber at 5000 m for 6 h daily, while controls were in continuous normoxic conditions. At 60 days after birth, the antioxidant capacity of the heart was determined; arterial and venous partial pressures of oxygen were measured at sea level and 5000 m altitude. In addition, isolated hearts of each group were perfused in Langendorff mode and submitted to 30 min global ischemia followed by 30 min reperfusion to compare functional recovery and lactate dehydrogenase release. For the IH rats, recovery of left ventricular developed pressure (DP), the maximum of the positive or negative first derivative of left ventricular pressure with respect to time (+/-LV d P/d t), end-diastolic pressure (EDP), and pressure-rate product (PRP) were all superior ( P<0.05) to those of control rats. The myocardial antioxidant capacity was also significantly increased in the left ventricle of IH rats. Further, at 5000 m altitude the arterio-venous oxygen gradient ( Pa-vO(2)) was significantly ( P<0.01) higher in the IH rats than in the controls. These data indicate that IH from birth enhances the tolerance of the heart to ischemia/reperfusion, elevates the myocardial antioxidant capacity, and increases oxygen extraction.

摘要

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本文引用的文献

1
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Comp Biochem Physiol C Toxicol Pharmacol. 2002 Dec;133(4):537-56. doi: 10.1016/s1532-0456(02)00080-7.
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Cardioprotective effects of chronic hypoxia and ischaemic preconditioning are not additive.慢性缺氧与缺血预处理的心脏保护作用并非相加的。
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[Antiarrhythmic and antioxidative effects of intermittent hypoxia exposure on rat myocardium].
Ω-3补充剂和间歇性低压缺氧可诱导成年大鼠产生心脏保护作用,增强抗氧化机制。
Mar Drugs. 2015 Feb 4;13(2):838-60. doi: 10.3390/md13020838.
4
Chronic intermittent hypobaric hypoxia protects the heart against ischemia/reperfusion injury through upregulation of antioxidant enzymes in adult guinea pigs.慢性间歇性低压缺氧通过上调成年豚鼠抗氧化酶来保护心脏免受缺血/再灌注损伤。
Acta Pharmacol Sin. 2009 Jul;30(7):947-55. doi: 10.1038/aps.2009.57. Epub 2009 Jun 22.
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Hypoxic conditioning suppresses nitric oxide production upon myocardial reperfusion.缺氧预处理可抑制心肌再灌注时一氧化氮的产生。
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间歇性低氧暴露对大鼠心肌的抗心律失常和抗氧化作用
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4
Intermittent hypoxia exposure prevents mtDNA deletion and mitochondrial structure damage produced by ischemia/reperfusion injury.间歇性低氧暴露可预防缺血/再灌注损伤所导致的线粒体DNA缺失和线粒体结构损伤。
Sheng Li Xue Bao. 2000 Oct;52(5):375-80.
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Reactive oxygen species, antioxidants, and the mammalian thioredoxin system.活性氧、抗氧化剂与哺乳动物硫氧还蛋白系统
Free Radic Biol Med. 2001 Dec 1;31(11):1287-312. doi: 10.1016/s0891-5849(01)00724-9.
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Reactive oxygen species as intracellular messengers during cell growth and differentiation.活性氧作为细胞生长和分化过程中的细胞内信使。
Cell Physiol Biochem. 2001;11(4):173-86. doi: 10.1159/000047804.
7
Intermittent hypoxia exposure-induced heat-shock protein 70 expression increases resistance of rat heart to ischemic injury.间歇性低氧暴露诱导热休克蛋白70表达增加大鼠心脏对缺血性损伤的抗性。
Acta Pharmacol Sin. 2000 May;21(5):467-72.
8
Mitochondrial DNA damage and dysfunction associated with oxidative stress in failing hearts after myocardial infarction.心肌梗死后衰竭心脏中与氧化应激相关的线粒体DNA损伤和功能障碍。
Circ Res. 2001 Mar 16;88(5):529-35. doi: 10.1161/01.res.88.5.529.
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Life Sci. 2000 Oct 6;67(20):2465-71. doi: 10.1016/s0024-3205(00)00832-8.
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