Thrombin-induced intravascular coagulation was followed by pulmonary dysfunction in rats treated with the fibrinolysis inhibitor AMCA (trans-4-aminoethyl-cyclohexane carboxylic acid). The pulmonary dysfunction developed after a latency period of about 60 min and led progressively to pulmonary insufficiency with a morphological and functional pattern similar to that in the human delayed microembolism syndrome. Neither activation of the kallikrein-kinin system nor inhibition of converting enzyme activity in the lungs was of major importance in the pathogenesis. Accumulation of fibrin degradation products (FDP) occurred in the lungs and may have played a casual role.

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