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-PGF1αlevel following iv administration of d-tubocurarine (dTc), with or without prior administration of aspirin and H1antagonist. 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-PGF1α(P< 0.05 in both). The maximum MAP decrease and plasma 6-keto-PGF1αincrease 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< 0.05 in both) and plasma 6-keto-PGF1αlevel (P< 0.01 for aspirin group,P< 0.05 for diphenhydramine group). There was a significant correlation between the changes in plasma 6-keto-PGF1αand those in MAP (Kendall tau (τ) = −0.504,P< 0.01). These findings suggest that a bolus injection of dTc induces a release of prostacyclin through H1receptor, which is responsible for the dTc-induced transient decrease of blood pressure in humans.