Ruan J, Zhao X, Li Q
Department of Medicine, Beijing the 6th Hospital.
Zhonghua Nei Ke Za Zhi. 1995 Apr;34(4):253-5.
The degree of platelet activation and damage in 15 cases with acute myocardial infarction (AMI) receiving thrombolytic therapy and 15 cases with AMI receiving anticoagulant therapy were studied in vivo and in vitro by using specific monoclonal antibodies (SZ-51 & S12) against alpha-granule membrane protein 140 (GMP-140). Clinical indexes and myocardial enzyme changes in the two groups of patients were also observed. The results showed that the number of GMP-140 molecules on platelet surface and the concentration of GMP-140 in plasma were increased before treatment. The number of GMP-140 molecules on platelet surface began to decrease on the 1st day and returned to baseline on the 7th day after treatment. The concentration of GMP-140 in plasma reached a peak on the 1st day, began to fall on the 2nd day and returned to baseline on the 3rd day after treatment. There were no significant differences in the dynamic changes of number of GMP-140 molecules on platelet surface and the concentration of GMP-140 in plasma between groups of thrombolytic therapy and anticoagulant therapy. In vitro experiment showed that the thrombolytic medicine urokinase neither activated platelets nor inhibited platelet activation induced by thrombin. Significantly greater reperfusion rate and earlier appearance of CK and CK-MB peaks were found in the thrombolytic than in the anticoagulant group. LVEF determined by echocardiography, rate of return of ST segments to baseline and alleviation rate of chest pain were significantly greater and complications of AMI (ventricular fibrillation, left ventricular failure and angina) were less in the group receiving thrombolytic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)