Mechanisms of lung vascular injury after intravascular coagulation.
Pulmonary intravascular coagulation and the resultant microembolization increase lung vascular permeability to proteins. The increase in permeability is mediated by the activation of cellular and humoral factors after intravascular coagulation. In particular, intravascular coagulation results in sequestration and activation of leukocytes, which appears to be of primary importance in mediating the lung vascular injury. In addition, fibrin entrapment and the generation of fibrin-degradation products after fibrinolysis also contribute to the vascular injury. The classical inflammatory agents, such as prostaglandin, histamine, bradykinin, and serotonin, may modulate the degree of injury after pulmonary vascular thrombosis, but they do not appear to be the primary mediators of the injury. Platelet aggregation did not mediate the lung vascular injury after intravascular coagulation, but was responsible for the pulmonary gas-exchange impairment that occurs with pulmonary vascular thrombosis.
D000818:Animals; D001777:Blood Coagulation; D002199:Capillary Permeability; D006439:Hemodynamics; D008196:Lymph / Q000502:physiology; D008833:Microcirculation; D008954:Models, Biological; D011506:Proteins / Q000502:physiology; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000097:blood / Q000503:physiopathology*; D011655:Pulmonary Embolism / Q000503:physiopathology*
D011506:Proteins