Ac. Hegstad et al., LOW CONCENTRATIONS OF HYDROGEN-PEROXIDE IMPROVE POSTISCHEMIC METABOLIC AND FUNCTIONAL RECOVERY IN ISOLATED-PERFUSED RAT HEARTS, Journal of Molecular and Cellular Cardiology, 29(10), 1997, pp. 2779-2787
The aim of the present study was to test the hypothesis that low conce
ntrations of hydrogen peroxide (H2O2) have a beneficial effect on post
-ischaemic myocardial recovery. Functional and metabolic measurements
were performed in isolated buffer-perfused rat hearts exposed to 30 mi
n perfusion with 0 (control group A), 25, 50, 100 or 200 mu M H2O2 or
30 min global ischaemia followed by 30 min reperfusion with 0 (control
group B), 25, 50 or 100 mu M H2O2. Catalase (200 U/ml) was added as s
cavenger during reperfusion with 25 mu M H2O2. Non-ischaemic perfusion
: All concentrations of H2O2 induced an immediate vasodilatation, whic
h was maintained in the 50 mu M group, but it was followed by vasocons
triction in the 100 and 200 mu M group. Left ventricular developed pre
ssure (LVDP) was significantly increased at the end of perfusion in th
e 50 mu M group compared to the control, group. Exposure to 100 and 20
0 mu M H2O2 significantly decreased LVDP and increased end-diastolic p
ressure. ATP was reduced in the 100 mu M group. Post-ischaemic perfusi
on: Exposure to 25 mu M H2O2 caused improved coronary now during the f
irst 20 min of reperfusion compared to the control group (accumulated
coronary now; 235.5 +/- 10.8 v 172.7 +/- 8.6 ml). LVDP was significant
ly higher in the 25 mu M group compared to the control (59.8 +/- 10.2
v 22.1 +/- 7.3 mmHg), and end-diastolic pressure was significantly low
er (32.1 +/- 19.6 v 78.8 +/- 2.2 mmHg) at the end of reperfusion. Impr
oved recovery was not observed in the group exposed to 25 mu M H2O2 pl
us catalase. Treatment with 25 mu M H2O2 caused significantly improved
recovery of tissue ATP and creatine phosphate. In conclusion, the pre
sent study showed that exposure to 25 mu M H2O2 improved post-ischaemi
c recovery in hearts subjected to global ischaemia. (C) 1997 Academic
Press Limited.