Further Studies into the Pathogenesis and Treatment of Post-Traumatic Pulmonary Insufficiency with Special References to the Role of Banked Blood

摘要

The present report concerns studies into certain aspects of the pathogenesis and treatment of post-traumatic insufficiency (PTPI). It particularly emphasizes studies into the role of microaggregates from banked blood in the pathogenesis of PTPI. The studies were conducted in four parts: 1) A series of newly developed commercial transfusion filters were evaluated to determine efficiency of debris removal and resistance to blood flow. Studies were conducted using 21-day old stored human blood. The Pioneer filter proved the most effective filter in that it maintained high filtering efficiency with only modest resistance to blood flow. 2) Studies into the mechanism of debris formation have shown that it originates from spontaneous platelet aggregation in the blood with subsequent accumulation of fibrin. We have shown that platelets in stored blood continue to aggregate (although less rapidly and with smaller aggregate size) for the entire 21 days of storage. Further morphologic and ultrastructural studies on stored platelets has supported the possibility of residual functional capacity in stored platelets. In a separate series of experiments we showed that baboon blood and human blood share similar coagulation properties and platelet function. As a corollary to this, we have shown that patients taking aspirin, a platelet affecting drug, have greater intra-operative and post-operative blood loss than those not taking aspirin.