抄録
To observe platelet TXA2 synthesizing activities in acute myocardial infarction (AMI, 38 cases) and effort angina (EA, 23 cases), radioimmunoassay was used to measure the amount of synthesized TXB23 at 5 min after an addition of arachidonic acid or thrombin to the platelet suspension. The amount of TXB2 in AMI patients did not show a significant difference from that of 13 healthy controls. However, there were significant changes during thee time course of AMI. It increased in the super acute phase within the first 12 hrs from the onset of AMI. The activity decreased in 4 days, increased again in 10 days and then gradually recovered to the normal value. Platelet aggregation was elevated immediately after the onset of AMI and recovered during the time course. A significant negative correlation was observed between aggregation and TXA2 production in AMI, but not in the healthy controls, suggesting that platelets with hyper TXA2 synthesizing activity are consumed selectively in AMI. In EA, activity increased after treadmill exercise. Under ticlopidine-treatment, activity was depressed, and these patients were able to tolerate a longer exercise time than before ticlopidine. Since the pressure rate products did not change under treatment, changes in microcirculation such as the appearance of platelet aggregates may be important in the occurrence of anginal attacks.
