Charles Diffang

Effect of Trasylol® on fibrin deposition and elimination in the lungs of rats with intravascular coagulation induced by thrombin or thromboplastin

Abstract The effect of Trasylol on the fibrin deposition and elimination in the lungs of rats with intravascular coagulation induced by thrombin or thromboplastin was studied quantitatively. Trasylol strongly reduced the precipitation of fibrin in the lungs after intravenous injection of thromboplastin, while the same effect was not obtained after injection of thrombin. The elimination of fibrin from the lungs was delayed after treatment with Trasylol. This effect was not observed in rats treated with a synthetic fibrinolysis inhibitor, tranexamic acid (AMCA), in addition to Trasylol.

Pulmonary Insufficiency in the Rat after Intravascular Coagulation and Inhibition of Fibrinolysis

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.

Effect of brinase (protease I from aspergillus oryzae) on the elimination of fibrin from the lungs and pulmonary damage in rats with induced intravascular coagulation and inhibited fibrinolysis

Abstract Pulmonary damage with oedema developed in rats in which intravascular coagulation and inhibition of fibrinolysis had been induced by infusion of thrombin and tranexamic acid (AMCA). Treatment with brinase (Protease I from Aspergillus oryzae) resulted in strongly improved elimination of fibrin from the lungs. The pulmonary damage was also reduced, supporting the theory that decreased elimination of fibrin from the lungs is an important factor in the pathogenesis of this pulmonary condition. The effect of brinase on fibrin elimination was not due to activation of the fibrinolytic system, but seemed to be exerted directly on the fibrin.

Effect of hydrocortisone on the elimination of fibrin from the pulmonary vessels in the rat.

Abstract Administration of hydrocortisone resulted in delayed fibrin elimination from the lungs in rats with thrombin induced intravascular coagulation. The fibrinolytic system was inhibited, with increased fibrinolysis inhibition activity and decreased fibrinolytic activity in the blood, and decreased fibrinolytic activity in the pulmonary vessels. This inhibition of the fibrinolytic system might explain the delayed fibrin elimination from the lungs.

Inhibitory Effect of Dextran 40 upon Thrombin-induced Fibrin Deposition in Rat Lungs

The effect of dextran 40 upon thrombin-induced fibrin deposition in rat lungs was studied. A quantitative method employing isotope-labelled fibrinogen was used to determine the amount of fibrin in the lungs. It was shown that pretreatment was dextran 40 suppressed the accumulation of fibrin in the lungs after injection of thrombin. This was not due to redistribution of the fibrin to other organs but appeared to be a result of decreased intravascular coagulation. It seemed unlikely that the finding could be explained by an effect of dextran upon fibrinolysis.