Literature DB >> 11324449

Intermittent hypoxia exposure-induced heat-shock protein 70 expression increases resistance of rat heart to ischemic injury.

N Zhong1, Y Zhang, Q Z Fang, Z N Zhou.   

Abstract

AIM: To quantify the levels of HSP70 induced by different durations of intermittent (high altitude) hypoxia and to correlate them with the degree of protection of the rat heart from ischemic injury.
METHODS: Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the level of HSP70 mRNA expression in rat myocardium. Ischemia/reperfusion injury was presented as severity of arrhythmias induced by occlusion and reperfusion of the left anterior descending coronary artery of rat heart.
RESULTS: The level of HSP70 mRNA expression increased progressively along with the duration of intermittent hypoxia training. It was 2.6, 3.6, and 3.8 folds after 14-, 28-, and 42-d exposures compared to that of normoxia. The tolerance of rat heart to ischemia/reperfusion injury increased with hypoxia pretreatment. Such an effect was significant after rat were exposed to a 28-d intermittent hypoxia (IH). The scores for ischemia and reperfusion inducing arrhythmia for 28- and 42-d IH were 1.2 +/- 0.5, 1.0 +/- 0.5 and 1.0 +/- 0.5, 0.9 +/- 0.5 (P < 0.01 compared with 4.0 +/- 0.7, 3.3 +/- 0.6 in normoxia rats). The overexpression of HSP70 and the increased tolerance to subsequent acute ischemia/reperfusion injury could last for 2 wk after the rats (subjected to 28 d IH) returned to normoxia. Furthermore, there was a reverse correlation between the amount of HSP70 induced and the arrhythmia occurrence (r = -0.98, -0.92 for ischemia and reperfusion induced arrhythmia, P < 0.01).
CONCLUSION: These results suggest that increased resistance of rat heart to ischemia/reperfusion injury after intermittent hypoxia exposure may be related to the amount of HSP70 induced.

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Year:  2000        PMID: 11324449

Source DB:  PubMed          Journal:  Acta Pharmacol Sin        ISSN: 1671-4083            Impact factor:   6.150


  13 in total

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

Authors:  Wei-Zhong Zhu; Jian-Wen Dong; Hai-Lei Ding; Huang-Tian Yang; Zhao-Nian Zhou
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Review 2.  Cardioprotection by intermittent hypoxia conditioning: evidence, mechanisms, and therapeutic potential.

Authors:  Robert T Mallet; Eugenia B Manukhina; Steven Shea Ruelas; James L Caffrey; H Fred Downey
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4.  K(ATP) channels and MPTP are involved in the cardioprotection bestowed by chronic intermittent hypobaric hypoxia in the developing rat.

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5.  Chronic intermittent hypobaric hypoxia protects the heart against ischemia/reperfusion injury through upregulation of antioxidant enzymes in adult guinea pigs.

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Journal:  Acta Pharmacol Sin       Date:  2009-06-22       Impact factor: 6.150

6.  Ω3 Supplementation and intermittent hypobaric hypoxia induce cardioprotection enhancing antioxidant mechanisms in adult rats.

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Review 7.  Efficacy of Acute Intermittent Hypoxia on Physical Function and Health Status in Humans with Spinal Cord Injury: A Brief Review.

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Review 9.  Hypoxic Conditioning as a New Therapeutic Modality.

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10.  Enhancement of Glucose Metabolism via PGC-1α Participates in the Cardioprotection of Chronic Intermittent Hypobaric Hypoxia.

Authors:  Xuyi Li; Yan Liu; Huijie Ma; Yue Guan; Yue Cao; Yanming Tian; Yi Zhang
Journal:  Front Physiol       Date:  2016-06-08       Impact factor: 4.566

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