BACKGROUND: Previous studies have shown that pretreatment with normobaric hyperoxia has cardioprotective effect in isolated rat heart. The present study was designed to test the hypothesis that pretreatment normobaric hyperoxia could induce delayed cardioprotection effect in an in vivo regional heart ischemia. MATERIALS AND METHODS: Experiment 1: Rats were exposed to normobaric normoxia or to normobaric hyperoxia (O(2) > 95%) for 15, 30, 60, 120, and 180 min (H15, H30, H60, H120, and H180 groups, respectively). After 24 h, they were subjected to 30 min regional ischemia and 90 min reperfusion. Then, the hearts were harvested for measurement of infarct size. Lead II of electrocardiogram was continuously recorded for analysis of ischemic arrhythmias. Experiment 2: Different oxygen concentrations were tested in the same model of heart ischemia. RESULTS: Compared with normoxia group, infarct size significantly reduced in H120 and H180 groups (from 48.1 +/- 4 to 31.4 +/- 3.3 and 30 +/- 2.4, respectively); 120 and 180 min of >95% hyperoxia significantly reduced the number of ventricular beats (from 314 +/- 34.9 to 173 +/- 20.3 and 178 +/- 15.7, respectively) and incidence of ventricular fibrillation (from 66.8% to 30% and 22.2%, respectively). When the oxygen concentration decreased to 80%, its effect on infarct size was abolished; however, its antiarrhythmic effect persisted. Further reduction of oxygen concentration eliminated both the effects. CONCLUSION: These results show that hyperoxia pretreatment may induce delayed anti-infarct and antiarrhythmic effects in anesthetized rats. These effects are dependent on the exposure time and oxygen concentration.
BACKGROUND: Previous studies have shown that pretreatment with normobaric hyperoxia has cardioprotective effect in isolated rat heart. The present study was designed to test the hypothesis that pretreatment normobaric hyperoxia could induce delayed cardioprotection effect in an in vivo regional heart ischemia. MATERIALS AND METHODS: Experiment 1: Rats were exposed to normobaric normoxia or to normobaric hyperoxia (O(2) > 95%) for 15, 30, 60, 120, and 180 min (H15, H30, H60, H120, and H180 groups, respectively). After 24 h, they were subjected to 30 min regional ischemia and 90 min reperfusion. Then, the hearts were harvested for measurement of infarct size. Lead II of electrocardiogram was continuously recorded for analysis of ischemic arrhythmias. Experiment 2: Different oxygen concentrations were tested in the same model of heart ischemia. RESULTS: Compared with normoxia group, infarct size significantly reduced in H120 and H180 groups (from 48.1 +/- 4 to 31.4 +/- 3.3 and 30 +/- 2.4, respectively); 120 and 180 min of >95% hyperoxia significantly reduced the number of ventricular beats (from 314 +/- 34.9 to 173 +/- 20.3 and 178 +/- 15.7, respectively) and incidence of ventricular fibrillation (from 66.8% to 30% and 22.2%, respectively). When the oxygen concentration decreased to 80%, its effect on infarct size was abolished; however, its antiarrhythmic effect persisted. Further reduction of oxygen concentration eliminated both the effects. CONCLUSION: These results show that hyperoxia pretreatment may induce delayed anti-infarct and antiarrhythmic effects in anesthetized rats. These effects are dependent on the exposure time and oxygen concentration.