K. Ytrehus et al., HYDROGEN-PEROXIDE AS A PROTECTIVE AGENT DURING REPERFUSION - A STUDY IN THE ISOLATED-PERFUSED RABBIT HEART SUBJECTED TO REGIONAL ISCHEMIA, Cardiovascular Research, 30(6), 1995, pp. 1033-1037
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.