Platelet-derived 5-hydroxytryptamine and thromboxane A2 activate vascular smooth muscle cells, blood platelets and myocardial cells, both directly and through mutual amplification. Such an activation triggers: (1) vascular smooth muscle cell mitogenic activity, connective tissue synthetic activity and contractile activity; (2) platelet aggregation, secretion and procoagulant activity; (3) myocardial rhythm disturbances and necrosis. By such mechanisms, these autocoids contribute to arterial vessel wall proliferation, vasospasms and arterial thrombus formation in response to interactions of platelets with a damaged vessel wall, reduce the efficacy of thrombolytic agents and modulate myocardial reperfusion injury. Compounds directed specifically against these autocoids thus may offer possibilities for treating human ischaemic heart disease.