Effects of common carotid artery damage on anti-platelet-aggregability and PGI2 production in rats.
The effects of vascular damage on platelet function were investigated in rats. Common carotid artery specimens 4 mm in length were dissected from male Wistar rats and exposed to ultrasonic treatment or rubbing of the intimal surface. In some cases, carotis was dissected after ligation for 4 hr. The specimens were fixed on a stirring bar and agitated in platelet-rich plasma added with ADP. After determining platelet aggregability, the plasma was subjected to radioimmunoassay for 6-keto-prostaglandin F1 alpha (6-K-PGF1 alpha). Anti-platelet-aggregability in the arterial specimens was significantly greater in the sonicated, rubbed or ligated specimens than in the intact group, probably due to the effect of prostacyclin (PGI2). The measurement of 6-K-PGF1 alpha levels yielded similar results. Endogenous arachidonic acid in the vessel wall seems to be utilized in the production of PGI2, which probably acts only on local platelets. The findings indicate the presence of a mechanism that inhibits the formation of platelet thrombi by the accelerated production of PGI2 under conditions favorable for the generation of thrombosis.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D001792:Blood Platelets / Q000378:metabolism; D002339:Carotid Arteries / Q000502:physiology*; D004727:Endothelium / Q000502:physiology; D011464:Epoprostenol / Q000096:biosynthesis*; D008297:Male; D010974:Platelet Aggregation; D051381:Rats; D011919:Rats, Inbred Strains
D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol