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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of platelet aggregation and coagulo-fibrinolytic systems in thrombogenesis of lactic acid-induced pulmonary thrombosis in rat were studied using an anti-coagulant, platelet aggregation inhibitor, fibrinolytic or anti-fibrinolytic agents. In normal rat, heparin (2.5 mg/kg), acetylsalicylic acid (30 mg/kg) and tranexamic acid (100 mg/kg) suppressed specifically coagulation, platelet aggregation induced by collagen or thrombin and fibrinolysis respectively. Urokinase (10,000 units/kg) activated powerfully fibrinolytic system in addition to suppressing slightly platelet aggregation. The pretreatment with heparin, acetylsalicylic acid or urokinase markedly prevented the formation of thrombus initiated by the infusion of lactic acid at the doses used. Additive effect was also obtained by combined administration of these agents. On the other hand, it was interesting to note that tranexamic acid (100 mg/kg) did not affect the thrombus formation at all despite a potent anti-fibrinolytic effect of this agent. These results indicate that both platelet aggregation and enhancement of coagulation activity are important factors responsible for the formation of thrombi in DIC, while the fibrinolytic activity in blood seems not to be involved in it. On the basis of the findings, mechanism for triggering activation of coagulation and platelet aggregation is also discussed here.
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PMID:Patho-physiological studies on lactic acid-induced pulmonary thrombosis in rat. I. Effect of heparin, acetylsalicylic acid, urokinase and tranexamic acid. 118 8

Balloon occlusion pulmonary angiography was used to assess the frequency of pulmonary vascular thrombosis in five patients suffering from ARDS of diverse causes. Pulmonary hypertension, elevated pulmonary vascular resistance and disseminated intravascular coagulation were observed in all patients. Pulmonary artery filling defects (PAFD) were found in four of five patients. The results suggest that PAFD can be detected in a large proportion of patients in ARDS. It was therefore speculated that the detection of PAFD is a sign of severe lung injury. Urokinase, heparin and protease inhibitor were infused to test the potential reversibility of pulmonary vascular thrombosis in four patients. After infusion, we found angiographic evidence of clearing of obstruction in arteries in three of four patients. We conclude that anticoagulant-antithrombotic therapy can improve hemodynamics in ARDS-associated pulmonary vascular thrombosis.
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PMID:[Balloon occlusion pulmonary angiography and anticoagulant-antithrombotic therapy in ARDS-associated pulmonary vascular thrombosis]. 190 95

Previous work has shown that disseminated intravascular coagulation (DIC) may produce multiple organ failure, including adult respiratory distress syndrome, by obstruction of visceral micro circulation by microclots DIC can be produced by sepsis. This study tests the ability of a plasminogen activator to prevent death from an intravenous injection of killed Escherichia coli by causing lysis of the microclots. Subjects were two groups of 8 pigs each with body weight of 60-70 lbs. Killed Escherichia coli were injected IV in 16 pigs. Invasive monitoring was used to record physiologic data during the 5.0-hr experimental period. Urokinase injected 20 min after the injection of Escherichia coli organisms significantly prevented mortality, acidosis, and development of blood incoagulability. We conclude that plasminogen activator can significantly prevent fatal Escherichia coli (septic) shock without causing bleeding.
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PMID:A new approach to the treatment of experimental septic shock. 865 1

Our study evaluated the possible therapeutic effect of urokinase in treating the microthrombiotic effects of disseminated intravascular coagulation by assisting the activation of endogenous plasminogen. Twenty-six pigs were anesthetized, intubated, mechanically ventilated, and surgically catheterized. Septic shock was induced in all 26 pigs by an intravenous infusion of heat-killed Escherichia coli. The pigs were divided into two sets of experiments: in experiment 2 (n = 14), one-half received an intravenous dose of urokinase 1 h after heat-killed E. coli infusion and in experiment 3 (n = 12) one-half received an intravenous bolus dose and a continuous drip of urokinase 2 h after heat-killed E. coli infusion. The untreated pigs served as controls. Hemodynamic parameters, blood chemistries, and blood gases were analyzed. Urokinase given 1 h after bacterial toxin infusion significantly restored blood flow, resulting in an increase in cardiovascular and pulmonary function and improved survival rate (43% control vs. 100% treated, 24-h experimental period). Treatment given after 2 h showed some significant effect on pulmonary function; however, within 10 h of E. coli infusion, mortality rates in control and treated groups were 100 and 83%, respectively. Early administration of urokinase after onset of disseminated intravascular coagulation restored blood flow and helped resolve organ damage.
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PMID:Effect of urokinase on disseminated intravascular coagulation. 976 Mar 36