Contribution of Prostacyclin to D-tubocurarine-Induced Hypotension in Humans

Abstract

In order to evaluate the role of prostacyclin in d-tubocurarine-induced hypotension in human, the authors examined the relationship of changes of arterial blood pressure and plasma 6-keto-PGF1 alpha level following iv administration of d-tubocurarine (dTc), with or without prior administration of aspirin and H1 antagonist. The bolus injection of dTc 0.6 mg/kg caused a significant decrease in mean arterial pressure (MAP) that was associated with a significant increase in plasma 6-keto-PGF1 alpha (P less than 0.05 in both). The maximum MAP decrease and plasma 6-keto-PGF1 alpha increase were noted at 2 min after dTc administration. Pretreatment with aspirin DL-lysine (25 mg/kg) or diphenhydramine (1 mg/kg) significantly attenuated the responses of MAP (P less than 0.05 in both) and plasma 6-keto-PGF1 alpha level (P less than 0.01 for aspirin group, P less than 0.05 for diphenhydramine group). There was a significant correlation between the changes in plasma 6-keto-PGF1 alpha and those in MAP (Kendall tau (tau) = -0.504, P less than 0.01). These findings suggest that a bolus injection of dTc induces a release of prostacyclin through H1 receptor, which is responsible for the dTc-induced transient decrease of blood pressure in humans.