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Modification of disseminated intravascular coagulation by vasculoactive agents has been evaluated in rabbits infused with thrombin, measuring the extent of renal capillary thrombosis, suppression of creatinine clearance and elevation of plasma creatinine and pl. haemoglobin. Control studies included the administration of each agent without thrombin. The addition of angiotensin (0.1 μg/kg/min) consistently increased the extent of thrombosis and enhanced the other sequelae of thrombin infusion. Angiotensin was more potent than either norepinephrine or epinephrine (1 μg/kg/min). Intravenously, 5-hydroxytryptamine (1-10 μg/kg/min) decreased the severity of renal involvement and thrombosis. In contrast, if given intra-aortically 5-HT (1 yg per kg/min) enhanced all sequelae, being comparable to angiotensin. Propranolol, to blockade β-adrenoreceptors, did not significantly modify the response to thrombin, whether given alone or in addition to epinephrine. Blockade of α-adrenoreceptors with phenoxybenzamine variably decreased both renal lesions-and haemolysis produced by thrombin, and prevented the enhancement of these by epinephrine. Phenoxybenzamine blockade could be reversed by angiotensin. The addition of vasculoactive agents to thrombin only slightly influenced reductions in platelets and fibrinogen. While statistically significant, these small differences could not explain the differences in the pattern of thrombosis, α-adrenoreceptors in this model may be less critical than in the generalized Shwartzman reaction, but chemical mediators in general may be important in the expression of disseminated intravascular coagulation and thrombus localization.

Vasoconstrictor and Vasodilator Agents in Disseminated Intravascular Coagulation