HYDROGEN-PEROXIDE AS A PROTECTIVE AGENT DURING REPERFUSION - A STUDY IN THE ISOLATED-PERFUSED RABBIT HEART SUBJECTED TO REGIONAL ISCHEMIA

In spite of extensive research during the last decade it has not been possible to prove that endogenously generated hydrogen peroxide or any reduced oxygen species reaches sufficient concentration during reperf usion after myocardial ischemia to contribute significantly to irrever sible cell injury. In an attempt to further test this hypothesis we su bjected isolated perfused rabbit hearts to 30 min regional ischemia fo llowed by reperfusion and supplied hydrogen peroxide in low levels wit h or without catalase during the first 30 min of reperfusion and there after continued the reperfusion for a total of 120 min. Five different groups were studied: controls, and hearts supplied with 2 mu M H2O2, 1 mu M H2O2, 1 mu M H2O2 + catalase (IU/l) or catalase alone in the in itial part of the reperfusion. At the end of 120 min reperfusion, area at risk was measured with fluorescent particles and infarct zone size with tetrazolium staining. The results were: in the control group 32 +/- 5.0% of the risk zone infarcted, in the 2 mu M H2O2 group 16.3 +/- 5.6% and in the 1 mu M H2O2 group 6.9 +/- 0.8% (P < 0.05 compared to control). The reduction in infarct size was not present when catalase was added to the hydrogen peroxide-containing solution (26.4 +/- 4.5) or if catalase was present alone (22.9 +/- 1.8% infarction). In conclu sion, hydrogen peroxide, 1 mu M, protected the heart during reperfusio n and reduced the amount of cell death after 120 min of reperfusion, T he study demonstrated reduction or delay in infarction based only on t reatment in the reperfusion period. The mechanism behind this protecti on remains to be determined.