Experimental studies show that detrimental effects of ischemia-reperfusion (I/R) injury can be
attenuated by hyperoxic preconditioning in normal hearts, however, there are few studies
about hyperoxia effects in diseased myocardium. The present study was designed to assess the
cardioprotective effects of hyperoxia pretreatment (≥ 95 % O2) in acute diabetic rat hearts.
Normal and one week acute diabetic rats were either exposed to 60 (H60) and 180 (H180)
min of hyperoxia or exposed to normal atmospheric air (21 % O2). Then hearts were isolated
immediately and subjected to 30 min of regional ischemia followed by 120 min of reperfusion.
Infarct size, cardiomyocyte apoptosis, enzymes release and ischemia induced arrhythmias
were determined. Heart of diabetic control rats had less infarct size and decreased LDH and
CK-MB release compared to normal hearts. 60 and 180 min of hyperoxia reduced myocardial
infarct size and enzymes release in normal hearts. 180 min of hyperoxia also decreased cardiomyocytes
apoptosis in normal state. On the other hand, protective values of hyperoxia
were not significantly different in diabetic hearts. Moreover, hyperoxia reduced severity of
ventricular arrhythmias in normal rat hearts whereas; it did not confer any additional antiarrhythmic
protection in diabetic hearts. These findings suggest that diabetic hearts are less
susceptible to ischemia-induced arrhythmias and infarction. Hyperoxia greatly protects rat
hearts against I/R injury in normal hearts, however, it could not provide added cardioprotective
effects in acute phase of diabetes