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Articles in PresS, published online ahead of print December 13, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00920.2001
Submitted on October 22, 2001
Accepted on December 11, 2001
1 Cardiology Division, Medical College of Virginia, Virginia Commonwealth University, Richmond, Va, USA
* To whom correspondence should be addressed. E-mail: rakesh{at}hsc.vcu.edu.
Chronic systemic hypoxia (SH) enhances myocardial ischemic tolerance in mammals. We studied the delayed cardioprotection caused by acute SH and associated signaling mechanism. Conscious adult male mice were exposed to one or two cycles of hypoxia (H; 10%O2) or normoxia (21%O2) for various durations (30 min, 2h, 4h) followed by 24h reoxygenation. Hearts were isolated 24h later and subjected to ischemia-reperfusion in Langendorff model. Infarct size was reduced in mice pretreated with one (H4h) or two cycles (H4hx2) of 4 hrs SH as compared to normoxia (P<0.05), which was abolished by NOS2 inhibitor (S-methylisothiourea, 3 mg/kg), given prior to SH or ischemia. H4hx2 also failed to reduce infarct size in NOS2 knockout mice. COX-2 inhibitor (NS398, 10 mg/kg) did not block the protection given either before H4hx2 or ischemia. A 2-3 fold increase in myocardial NOS2 expression was observed in H4h, H2hx2, and H4hx2 (P<0.05), whereas NOS3 or COX-2 remained unchanged. We conclude that acute SH induces delayed cardioprotection, which is triggered and mediated by NOS2, but not NOS3 or COX-2.
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