Effect of fibrinogen on ADP-induced platelet aggregation.
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Biomedical subjects
Publications and source records attributed to M Tomikawa.
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The dimerous three-chained protein fibrinogen has at its disposal different functional zones which are included in the process of polymerisation and which possess importance for the specific reaction of fibrinogen with certain cells. The present paper is particularly engaged with the activation of fibrinogen by thrombin and with the mechanism of the arrangement of the activated units of fibrinogen concerning the fibrin fibre. Finding concerning the interaction of the platelets with fibrinogen connected to sepharose plead for the fact that a change of conformation in the molecule of fibrinogen precedes the specific platelet reaction.
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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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A group of 1127 patients who underwent sclerotherapy for esophageal varices were compared for outcome in terms of age: over and under age 70 years. Esophageal varices were completely eradicated in 81 of 110 patients > 70 years (73.6%) and in 791 of 1017 patients < 70 years (77.8%). Gastrointestinal bleeding after sclerotherapy occurred in 9 patients > 70 years (8.2%) and in 84 of those < 70 years (8.3%). Complications occurred in 16 patients > 70 years (14.5%) and in 141 < 70 years (13.9%). Liver failure and hepatoma accounted for more than 80% of the causes of death in both groups (80.3% versus 83.8%). The 5-year cumulative survival rates in patients with bleeding esophageal varices (bleeders) without hepatoma were 21.8% in those > 70 years and 58.7% in those < 70 years (p < 0.01), the relative survivals being 25.3% versus 66.6%. Patients without hepatoma and treated by prophylactic sclerotherapy accounted for 66.2% of patients > 70 years and 61.7% of those < 70 years, the relative survivals being 75.9% versus 71.9%. As analyzed by the Cox proportional-hazards model, age > 70 years was a prognostic factor in the bleeders (p < 0.01) but not in the nonbleeders. We recommend that elderly patients with esophageal varices be given prophylactic sclerotherapy, as the outcome for these patients is poor once bleeding has occurred.
Continuous bleeding from a Mallory-Weiss tear required laparoscopic surgery to halt the bleeding. The oversewing of the laceration at the esophagogastric junction was readily performed under video control with endoscopic guidance and the bleeding ceased. To stop bleeding from such a tear, we prefer to use this modern approach.