Fibrinolytic activity of arterial tissues.

A MAJOR theory as to the pathogenesis of atherosclerosis considers the necrotic and calcine vascular changes to be secondary to repeated thromboses ineffectively neutralized by normal fibrinolytic processes. Duguid and Robertson have presented evidence indicating that many of the lesions we classify as atherosclerosis are arterial thrombi which, by the ordinary process of organization, have been transformed into fibrous thickenings. Willens* also noted that diffuse intimal thickening was more pronounced in arteries that commonly develop atherosclerosis than in those that are infrequently involved. The resolution of small thrombi and fibrin deposits in the vessels is considered to be a process occurring regularly in the normal organism because of the recurrent minor injuries produced during the stress of daily life and the consequent release of thromboplastic agents from the tissues. It seems quite possible, since atherosclerosis usually appears at points of stress and narrowing within the vascular system, that vascular tissue injury may initiate the deposition of fibrin upon the intima. In this respect, one might postulate that local tissue enzymes also function in the removal of the resultant fibrin deposits. Numerous human tissues are known to contain a tissue-activator of plasminogen, which is postulated to function in the removal of blood clots or other pathological fibrin deposits from tissue parenchyma. Until the recent studies of Astrup and co-workers,'" this activator had not been investigated within arterial tissues. The purpose of this paper is