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* To whom correspondence should be addressed. E-mail: jbaker{at}mcw.edu.
Hypoxia from birth increases resistance to myocardial ischemia in infant rabbits. We hypothesized that increased cardioprotection in hearts chronically hypoxic from birth persists following development in a normoxic environment and involves increased activity of nitric oxide synthase (NOS) and KATP channels. Resistance to myocardial ischemia was determined in rabbits raised from birth to 10 days of age in a normoxic (FIO2=0.21) or hypoxic (FIO2=0.12) environment and subsequently exposed to normoxia for up to 60 days of age. Isolated hearts (n=8/group) were subjected to 30 min global ischemia, followed by 35 min of reperfusion. At 10 days of age, resistance to myocardial ischemia (percent recovery post-ischemic recovery left ventricular developed pressure) was higher in chronically hypoxic hearts (68±4%) than normoxic controls (43±4%). At 10 days of age, L-NAME (200 µM) and glibenclamide (3 µM) abolished the cardioprotective effects of chronic hypoxia (45±4% and 46±5% respectively) but had no effect on normoxic hearts. At 30 days of age resistance to ischemia in normoxic hearts declined (36±5%). However in hearts subjected to chronic hypoxia from birth to 10 days and then exposed to normoxia until 30 days of age, resistance to ischemia persisted (63±4%). L-NAME or glibenclamide abolished cardioprotection in previously hypoxic hearts (37±4% and 39±5% respectively) but had no effect on normoxic hearts. Increased cardioprotection was lost by 60 days. We conclude that cardioprotection conferred by adaptation to hypoxia from birth persists upon subsequent exposure to normoxia and is associated with enhanced NOS activity and activation of KATP channels.
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