Streptokinase Alters Myocardial Creatine Kinase Depletion After Ischaemia and Reperfusion in Rabbits

The efficacy of streptokinase as an intracoronary thrombolytic agent is well-recognized. The effect of streptokinase, distinct from its thrombolytic action, on ischaemic myocardium distal to an area of coronary artery occlusion when reperfusion occurs has not been well-defined. In order to do this, myocardial creatine kinase depletion and the histopathology of infarctions produced in rabbits after 1 h of circumflex coronary artery occlusion and mechanical release of the occlusion were assessed. Streptokinase or saline was infused intravenously for 1 h beginning 0.5 h after occlusion. Rabbits were divided into two time intervals: early (less than 10 h) and late (24 h) after release of coronary artery occlusion. When streptokinase was infused in early infarctions, haemorrhage did not correlate with infarction cross-sectional area or myocardial creatine kinase depletion. However, myocardial creatine kinase depletion was 40% less when streptokinase was infused than when saline was infused, suggesting that streptokinase might limit infarct size. In late infarctions, the degree of haemorrhage, infarction cross-sectional area, and myocardial creatine kinase depletion were similar after reperfusion with streptokinase or saline. By 24 h, the beneficial effect of a single dose of streptokinase given early in the course of occlusion-reperfusion myocardial injury was no longer evident in limiting infarct size.