Enhancement of platelet aggregation by tranylcypromine in mouse cerebral microvessels.

Publisher Website
Google Scholar
Abstract
Tranylcypromine, given intraperitoneally at doses greater than or equal to 10 mg/kg, enhanced platelet aggregation in the arterioles on the cerebral surface in mice. Tranylcypromine inhibits prostacyclin synthesis in vitro. Iproniazid, which inhibits monoamine oxidase but not prostacyclin synthesis, failed to enhance platelet aggregation. The failure of iproniazid to enhance aggregation in this study rules out an effect on monoamine oxidase as the cause of tranylcypromine's action. That iproniazid inhibited aggregation indicates it has an effect opposite to that of tranylcypromine. Imidazole, a drug known to inhibit synthesis of both prostacyclin and thromboxane, failed to affect platelet aggregation. All of our data are compatible with the hypothesis that prostacyclin is an inhibitor of platelet aggregation. This hypothesis has been based largely on in vitro data, to which we now add in vivo support.