Thromb Haemost 1975; 34(01): 145-158
DOI: 10.1055/s-0038-1651363
Original Article
Schattauer GmbH

Patho-physiological Studies on Lactic Acid-induced Pulmonary Thrombosis in Rat

I. Effect of Heparin, Acetylsalicylic Acid, Urokinase and Tranexamic Acid
Munehiro Tomikawa
1   Research Institute, Daiichi Seiyaku Co., Ltd., Edogawa-ku, Tokyo, Japan
› Author Affiliations
Further Information

Publication History

Received 26 January 1975

Accepted 10 April 1975

Publication Date:
02 July 2018 (online)

Summary

The roles 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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