Pulmonary Insufficiency in the Rat After Intravascular Coagulation and Inhibition of Fibrinolysis - Studies on Pulmonary Microcirculation and Pathophysiology

Abstract

In posttraumatic pulmonary insufficiency microembolism of fibrin to the lungs and inhibited fibrinolysis have been given key-roles and the term "the delayed microembolism syndrome" has been designated to those cases. The pathogenetic mechanisms involved are only to a limited extent known. Those were investigated in a rat model. Fibrinolysis was inhibited with AMCA and intravascular coagulation induced by a 5-min injection of thrombin, 500 NIH/kg b.w.. Within 5 min a profound consumption of fibrinogen occurred and 125-la- belled fibrin was embolized to the lungs. At that time the alveolar circulation was decreased, vasoconstriction and platelet-red cell aggragates appeared as seen by in vivo microscopy and arterial P02 was diminished irrespective of fibrinolysis. After restitution for 1 h a progressive pulmonary insufficiency with P02 decrease and PC02 retention occurred. Trasylol® did not influence on pulmonary damage. Converting enzyme activity was not diminished. A retention of fibrin degradation products (fdp) occurred in the lungs and infusion of low molecular weight fdp aggravated pulmonary oedema. Lung mast cells were partly degranulated and mepyramine maleate slightly counteracted pulmonary oedema. It is concluded that release of vasoactive low molecular weight fdp probably plays a causal role in oedema formation; probably in part by releasing histamine from lung mast cells.