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Inhibition of vasoactive substances in experimental endotoxin shock.

Using the endotoxin shock model in mongrel dogs, the effects of a cyclooxygenase antagonist (diclofenac sodium) and an antihistamine (chlorpheniramine) were evaluated. Both drugs significantly raised the mean arterial pressure and systemic vascular resistance. The vasomotor activity of histamine appeared to be independent from the one mediated by prostaglandins (cyclooxygenase pathway) since the effect was additive during the first 60 minutes. Yet at 120 minutes only diclofenac sodium continued to be effective, suggesting a sustained role of prostaglandins in the pathophysiology of endotoxin shock.