INTRACELLULAR CATALASE INHIBITION DOES NOT PREDISPOSE RAT-HEART TO ISCHEMIA-REPERFUSION AND HYDROGEN PEROXIDE-INDUCED INJURIES

The objective of this study was to determine whether inhibition of int racellular catalase would decrease the tolerance of the heart to ische mia-reperfusion and hydrogen peroxide-induced injuries. Isolated bicar bonate buffer-perfused rat hearts were used in the study. Intracellula r catalase was inhibited with 3-amino-1,2,4-triazole (ATZ, 1.5 g/kg bo dy weight, two hours prior to heart perfusion). In the ischemia-reperf usion protocol, hearts were arrested with St. Thomas' II cardioplegic solution, made ischemic for 35 min at 37 degrees C, and reperfused wit h Krebs-Henseleit buffer for 30 min. The extent of ischemic injury was assessed using postischemic contractile recovery and lactate dehydrog enase (LDH) leakage into reperfusate. In the hydrogen peroxide infusio n protocol, hearts were perfused with increasing concentrations of hyd rogen peroxide (inflow rates 0.05-1.25 mu mol/min). Inhibition of cata lase activity (30.4 +/- 1.8 mU/mg protein in control vs 2.4 +/- 0.3 mU /mg in ATZ-treated hearts) affected neither pre-ischemic aerobic cardi ac function nor post-ischemic functional recovery and LDH release in h earts subjected to 35 min cardioplegic ischemic arrest. Myocardial con tents of lipid hydroperoxides were similar in control and ATZ-treated animals after 20 min aerobic perfusion, ischemia, and ischemia-reperfu sion. During hydrogen peroxide perfusion, there was an increase in cor onary flow rate followed by an elevation in diastolic pressure and inh ibition of contractile function in comparison with control hearts. The functional parameters between control and ATZ-treated groups remained unchanged. The concentrations of myocardial lipid hydroperoxides were the same in both groups. We conclude that inhibition of myocardial ca talase activity with ATZ does not predispose the rat heart to ischemia -reperfusion and hydrogen peroxide-induced injury.