Prostacyclin,Thromboplastin,and Antiheparin Activities of the Rat Aorta

Abstract

Abstract

We detected three “hemostasis-relevant” activities in an isotonic Tris-saline buffer in which fragments of normal rat aorta had been incubated for 10 min. One activity inhibited adenosine diphosphate-induced platelet aggregation, the other promoted clotting of citrated plasma and caused aggregation of platelets in heparinized piatelet-rich plasma, and the third suppressed the inhibitory effect of heparin on thrombin. These activities are represented by prostacyclin, thromboplastin, and an antiheparin of unknown nature. The platelet aggregation inhibiting activity in aorta-incubated buffer (AIB) disappeared upon storage or at high temperature, and was not present in AIB of aortas of aspirin-treated rats. Platelet aggregation of heparinized samples was inhibited by hirudin, citrate, high concentrations of heparin, and synthetic prostacyclin. The previously undescribed antiheparin activity appears to be distinct from both prostacyclin and thromboplastin.