Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats

Brain ischemia followed by reperfusion causes neuronal death related to oxi dative damage. Furthermore, it has been reported that subjects suffering fr om ischemic cerebrovascular disorders exhibit changes in circulating platel et aggregation, a characteristic that might be important for their clinical outcome. In the present investigation we studied tert-butyl hydroperoxide- initiated plasma chemiluminescence and thiol content as measures of periphe ral oxidative damage in naive and preconditioned rats submitted to forebrai n ischemia produced by the 4-vessel occlusion method. Rats were submitted t o 2 or 10 min of global transient forebrain ischemia followed by 60 min or 1, 2, 5, 10 or 30 days of reperfusion. Preconditioned rats were submitted t o a 10-min ischemic episode 1 day after a 2-min ischemic event (2 + 10 min) , followed by 60 min or 1 or 2 days of reperfusion. It has been demonstrate d that such preconditioning protects against neuronal death in rats and ger bils submitted to a lethal (10 min) ischemic episode. The results show that both 2 and 10 min of ischemia cause an increase of plasma chemiluminescenc e when compared to control and sham rats. In the 2-min ischemic group, the effect was not present after reperfusion. In the 10-min ischemic group, the increase was present up to 1 day after recirculation and values returned t o control levels after 2 days. However, rats preconditioned to ischemia (2 + 10 min) and reperfusion showed no differences in plasma chemiluminescence when compared to controls. We also analyzed plasma thiol content since it has been described that sulfhydryl (SH) groups significantly contribute to the antioxidant capacity of plasma. There was a significant decrease of pla sma thiol content after 2, 10 and 2 + 10 min of ischemia followed by reperf usion when compared to controls. We conclude that ischemia may cause, along with brain oxidative damage and cell death, a peripheral oxidative damage that is reduced by the preconditioning phenomenon.