Stenosis and Vascular Damage as an Experimental Model of Arterial Thrombosis: A Role for Prostanoids

Abstract

Arachidonic acid, a membrane bound fatty acid, is released following a variety of stimuli. Upon release the fatty acid undergoes a series of reactions which may yield prostanoids. Prostanoids are potent agents capable of eliciting profound effects within their immediate environment. One such effect, the formation of an arterial thrombus, is regulated by the interaction of the endothelium and subendothelium of the blood vessel wall with platelets and white blood cells (de Gaetano et al., 1986; Dejana, 1987; Prosdocimi et al., 1988a). Once activated, platelets may aggregate to generate the thrombus, often formed in patients with coronary atherosclerosis. This process may, in turn, lead to an active phase of unstable angina or to a myocardial infarction (see for review Fuster et al., 1988). In addition, it has been suggested that the thrombotic procest plays a major role in provoking cerebral and peripheral ischemic pathology (Folts, 1980; Born et al., 1983; Kistler et al., 1984; Fitzgerald et al. 1984; Hess et al., 1985). Thus, the study of prostanoids in arterial thrombosis is an area of intensive investigation. This article will focus on the role of two arachidonate metabolites, prostacyclin and thromboxane, and the application of an experimental model of arterial thrombosis induced by vessel wall damage and flow alterations.