Prostaglandin Endoperoxide Metabolism by the Human Carotid Artery
Prostacyclin (PGI2) synthesis is associated with maintenance of normal vascular function, and a fall in human vascular PGI2 synthesis has been associated with atherosclerosis (1,2). It has been proposed that a decrease in PGI2 production results in the loss or impairment of the vascular defense mechanism against platelet deposition which might favor thrombosis and the progression of atherosclerosis (1). A decrease in bioassayable PGI2 production by vascular sections from fatty streak (pre-atherosclerotic) and advanced atherosclerotic lesions has been reported (3). Little if any information is available concerning the activity of prostacyclin synthetase in vascular tissue immediately adjacent to advanced atherosclerotic plaques. An increase or decrease in the PGI2 generating capacity of these adjacent areas could represent a protective mechanism against or a predisposing factor for, respectively, the progression of atherosclerotic disease into these areas.
KeywordsSynthetase Activity Fatty Streak Vascular Segment External Elastic Lamina Human Carotid Artery
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- 3.Sinzinger H, Feigl W, Silberbauer K, Oppolzer R, Winter M, Auerswald W: Prostacyclin (PGI2)-generation by different types of human atherosclerotic lesions. Exp. Pathol. (Jena) (18):175–180, 1980.Google Scholar
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