Increased platelet aggregability is associated with increased prostacyclin production by vessel walls in hypercholesterolemic rabbits.
The influences of experimental hypercholesterolemia in the rabbit on platelet-vessel wall interactions have been studied by evaluating the aggregatory response of platelet rich plasma (PRP) to arachidonic acid (AA) stimulation and levels of 6-keto-PGF1 alpha in PRP from normal (N) and hypercholesterolemic (HC) animals prior and after perfusion through the corresponding aortas. In addition, the responses of N PRP to aggregation after perfusion through HC aortas and those of HC PRP perfused through N aortas, and the platelet response to the inhibitory effect of exogenous prostacyclin have been evaluated. The data indicate that in HC rabbits, on one side platelets are hyperreactive to AA and less sensitive to the inhibitory activity of prostacyclin and, on the other, the antiaggregatory activity and prostacyclin production of vessel walls is higher, suggesting compensatory mechanisms in the haemostatic balance.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism*; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology; D002784:Cholesterol / Q000097:blood; D011464:Epoprostenol / Q000096:biosynthesis*; D006937:Hypercholesterolemia / Q000378:metabolism*; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000096:biosynthesis*; D011817:Rabbits
D001095:Arachidonic Acids; D011453:Prostaglandins; D016718:Arachidonic Acid; D015121:6-Ketoprostaglandin F1 alpha; D002784:Cholesterol; D011464:Epoprostenol