Abstract
Platelets are belleved to play a role in the pathologic sequelae of acute myocardial ischemia. Several of the compounds generated and released by activated platelets during cardiac ischemia may contribute to the production of cellular necrosis (free oxygen radicals), coronary vasoconstriction (thromboxane, serotonin, catecholamines), and perpetuation of the platelet aggregatory reaction (thromboxane, serotonin, adenosine diphosphate). In the present study, it was demonstrated that platelet serotonin uptake function is markedly depressed following the induction of myocardial ischemia in cats. The possible mechanism through which the depression occurs and the resulting pathologic sequelae are discussed. The results of the present study illustrate another mechanism by which platelets can potentially mediate the severity and perpetuation of cellular events during acute myocardial ischemic insult.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
