Prostaglandins and Defects in Vascular Function
Atherosclerotic arterial lesions have been reported to exhibit altered arachidonic acid metabolism (1–4). These alterations have consistently involved decreases in arterial prostacyclin (prostaglandin I2 or PGI2) synthesis; arterial thromboxane A2 (TXA2) formation (3) and increased PGE2 formation (2) have also been associated with atherosclerotic lesions. Conversely, it has been recently reported that total urinary excretion of 2,3-dinor-6-keto-PGFlα, one of the metabolites of PGI2 produced. in vivo, is higher in patients with severe atherosclerosis than normal subjects (5). It was suggested that there was an increase in PGI2 formation due to stimulation of PGI2 synthetase as there may be increased platelet-endothelial interactions in patients with severe atherosclerosis. The present study reports that there are graduated decreases in human arterial PGI2 synthetase activity within atherosclerotic plaque but that these decreases are focal, as the arterial regions immediately adjacent to the plaque exhibit normal PGI2 synthetase activity.
KeywordsCarotid Plaque Severe Atherosclerosis Arterial Region Carotid Artery Plaque Human Carotid Artery
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