The role of platelets in post-traumatic pulmonary insufficiency

It is suggested that pulmonary microembolism, due to intravascular platelet aggregation, is an important pathogenetic factor in the development of acute post-traumatic pulmonary insufficiency. Changes in blood flow, vessel wall injury and/or changes in the composition of the blood may all induce aggregation of the circulating platelets. Platelet aggregates are then trapped in the pulmonary microcirculation. Experimentally induced intravascular platelet aggregation causes pulmonary vasoconstriction and increases pulmonary vascular resistance. The vasoconstriction has predominantly a precapillary localization. It has also been demonstrated that intravascular platelet aggregation will increase transiently the hydraulic conductivity of pulmonary exchange vessels. Thus, edema development is facilitated, although platelet aggregation per se cannot induce fulminant lung edema. In parallel with the vascular changes, platelet aggregation causes constriction of both peripheral and central airways, as reflected in a decreased dynamic compliance and an increased pulmonary resistance. The central airways are at least partly constricted secondary to nervous reflexes mediated through bronchomotor, parasympathetic nerve fibres in the vagal nerve. If a persistent and long-lasting intravascular aggregation of platelets is induced, the changes in respiratory mechanics described will impair gas exchange and precipitate a severe respiratory insufficiency. This pulmonary insufficiency is, however, dependent on an ongoing activation and aggregation of platelets. When the experimentally induced platelet aggregation is stopped, gas exchange function returns rapidly to normal.