Journal of Applied Physiology AJP: Gastrointestinal and Liver Physiology
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J Appl Physiol (February 1, 2007). doi:10.1152/japplphysiol.01291.2006
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Submitted on November 15, 2006
Accepted on January 26, 2007

Effects of intermittent hypoxia on oxidative stress-induced myocardial damage in mice

Ah-Mee Park1 and Yuichiro J. Suzuki1*

1 Pharmacology, Georgetown University, Washington, District of Columbia, United States

* To whom correspondence should be addressed. E-mail: ys82{at}georgetown.edu.

Obstructive sleep apnea is associated with increased risk for cardiovascular diseases. As obstructive sleep apnea is characterized by episodic cycles of hypoxia and normoxia during sleep, we investigated effects of intermittent hypoxia (IH) on ischemia/reperfusion-induced myocardial injury. C57BL/6 mice were subjected to IH (2 min 6% O2 and 2 min 21% O2) for 8 h/day for 1, 2 or 4 weeks; isolated hearts were then subjected to ischemia/reperfusion. IH for 1 or 2 weeks significantly enhanced ischemia/reperfusion-induced myocardial injury. However, enhanced cardiac damage was not seen in mice treated with 4 weeks of IH, suggesting that the heart has adapted to chronic IH. Ischemia/reperfusion-induced lipid peroxidation and protein carbonylation were enhanced with 2 weeks of IH; while with 4 weeks, oxidative stress was normalized to levels in animals without IH. H2O2 scavenging activity in adapted hearts was higher after ischemia/reperfusion, suggesting the increased antioxidant capacity. This might be due to the involvement of thioredoxin, as the expression level of this protein was increased; while levels of other antioxidant enzymes were unchanged. In the heart from mice treated with 2 weeks of IH, ischemia/reperfusion was found to decrease thioredoxin. Ischemia/reperfusion injury can also be enhanced when thioredoxin reductase was inhibited in control hearts. These results demonstrate that IH changes the susceptibility of the heart to oxidative stress in part via alteration of thioredoxin.




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