Pulmonary insufficiency in the rat after intravascular coagulation and inhibition of fibrinolysis. II. Investigations on oedema formation and morphology.

Solute and fluid compartments in the lungs were investigated following thrombin-induced intravascular coagulation in rats treated with the fibrinolysis inhibitor, Trans-4-(amino-methyl) cyclohexanecarboxalic acid. The lung weight was increased to almost three times normal due to accumulation of extravascular water with albumin and chloride concentrations similar to those in plasma. The blood content and dry weight were doubled. Microscopic sections were characterized by widespread fibrin-rich microemboli, thickened alveolar walls, distension of peribronchiolar and perivascular spaces with fluid, dilated lymph vessels and protein-rich alveolar oedema. An increased microvascular permeability to protein explains the findings. When the dose of thrombin was decreased to a point where no pulmonary oedema developed, supplementary infusion of low molecular weight fibrinogen degradation products induced oedema formation as verified microscopically.