A comparison was made between the effects of atheromatous and normal areas of the same aorta on coagulation, fibrinolytic, and platelet aggregating systems. In the thromboplastin generation test it was found that atheromatous aorta possessed significantly greater ability to generate intrinsic prothrombin activator than did normal aortic tissue. But, by the one-stage prothrombin time technique, the content of extrinsic thromboplastin in both types of aorta was similar. Aortic preparations, consisting of intimal and medial layers only, were not found to possess fibrinolytic ability and did not contain inhibitors of the fibrinolytic system. The adhesion of platelets to ulcerated atheromatous areas of aorta was significantly greater than to normal or non-ulcerated atheromatous areas. However, homogenates of atheromatous and normal aorta did not differ in their ability to accelerate platelet aggregation and fibrin clot formation when tested by a modified Chandler's tube technique. The significance of the findings is discussed and the suggestion made that the mechanisms by which atheromatous aortic tissue might predispose towards intravascular thrombosis in vivo are the ability of such tissue to enhance intrinsic prothrombin activator formation and platelet aggregation.

Aorta↗

PubMed1966

Effect of normal and atheromatous aortic tissue on platelet aggregation in vitro.

An investigation was made into the platelet-aggregating ability of human aortic tissue. It was found that potent aggregating substances are present in the vascular wall but that the degree and character of platelet aggregation produced was dependent on the method employed in the preparation of the tissue for study. The supernatants of aortic tissue homogenates were found to produce potent irreversible platelet aggregation that occurred after a latent period of one to two minutes. The activity was heat labile, destroyed by collagenase, sedimented by ultracentrifugation, and was considered to be identical or similar to collagen. An extract obtained by boiling aortic tissue with saline was found to cause less powerful reversible platelet aggregation that occurred within 15 to 30 seconds' contact with platelets; the activity was not affected by heating, incubation with collagenase, or ultracentrifugation, and was considered to be due to adenosine diphosphate. Atheromatous aortic tissue when extracted by either method was found to contain less than one half of the potency of normal tissue in causing platelet aggregation.

Aorta↗

PubMed1966