Delayed cardioprotective effects of hyperoxia preconditioning prolonged by intermittent exposure

In our previous study, it was indicated that pre-exposing rats to normobaric hyperoxia could induce a late preconditioning against infarction and arrhythmia. In this study, attempts were made to know whether the intermittent pre-exposure to the same environment could prolong the late phase of hyperoxia preconditioning.

In the first series of experiments, rats were divided into five groups; group 1 was pre-exposed to normal air (NOR) and the other groups to hyperoxic air (O(2)>95%, 120 min once a d) 12, 24, 48, and 72 h (H12, H24, H48, and H72 groups) before 30 min ischemia. In the second series of experiments, rats were pre-exposed to intermittent hyperoxic air (1, 2, or 3 consecutive d) at different times before being subjected to ischemia (H48, H2-48, H2-72, H3-72, and H3-96 groups). The infarct size was measured by triphenyltetrazolium chloride staining, and lead II of electrocardiogram recorded to monitor ischemic-induced arrhythmia.

Compared with NOR group, the infarct size and incidence of arrhythmia were reduced significantly in H24 and H48 groups. When the exposure periods were enhanced to 2 d, the infarct size did not decrease significantly, but the incidence of arrhythmia reduced. When the pre-exposure times were enhanced to 3 d, both the infarct size and incidence of arrhythmia decreased significantly in H3-72 group, but not in H3-96 group.

These results show that the late phase of hyperoxia preconditioning may last for more than 48 h and prolong by intermittent per-exposure to the same environment.