Increased vascular permeability in the delayed microembolism syndrome: Experimental and human findings

Abstract

Intravenous infusion of thrombin and a fibrinolysis inhibitor, tranexamic acid (AMCA), in dogs caused an increase in pulmonary vascular permeability with increased leakage of protein and high molecular weight dextran-rich fluid from the circulation into the pulmonary interstitial space and into the lung lymph, with consequent pulmonary oedema. Ultrastructural studies showed that the leakage occurred across the endothelial cells by means of micropinocytosis, as well as through endothelial cell junctions. Typical changes were observed at the junctional level. The endothelial cell matrix adjacent to the tight junctions appeared dense and granular; cystic gaps were found and fibrin was seen within them. Similar ultrastructural changes were found in the lungs from patients suffering from the delayed microembolism syndrome indicating a common pathogenesis in the experimental and clinical conditions.