Role of catalase and heat shock protein on recovery of cardiac endothelial and mechanical function after ischemia.

The aim of this study was to investigate the roles of heat shock proteins and catalase after heat shock stress in the recovery of cardiac mechanical and endothelial function following a prolonged ischemic, cardioplegic arrest. Isolated working rat hearts were subjected to an ischemic cardioplegic arrest for 4 hours at 4 degrees C. Six groups, each of 6 hearts, were studied: control; control treated with 3-aminotriazole, an inhibitor of catalase; sham; sham + 3-aminotriazole; heat-shocked rats; heat shocked rats + 3-aminotriazole. Postischemic recovery of cardiac output and endothelial function (as % of preischemic control values) were respectively 54.6 +/- 1.9 and 21.2 +/- 3.0 in the control group; 52.3 +/- 2.9 and 19.1 +/- 3.9 in the control + 3-aminotriazole group; 72.2 +/- 2.7 and 54.2 +/- 7.6 in the heat shocked group; and 68.0 +/- 4.0 and 21.0 +/- 5.8 in the heat shocked + 3-aminotriazole group. SDS PAGE and western blotting showed induction of heat shock proteins in the heat stressed animals. Measurement of catalase activity showed significant inhibition in the 3-aminotriazole treated groups. It is concluded that, following heat shock stress, the enhanced endothelial recovery after prolonged ischemic cardioplegic arrest is dependent on catalase activity but that this does not apply to the recovery of mechanical functional.