Propofol, 2,6-diisopropyl phenol, is a short-acting, potent intravenous anesthetics agent. In both general anesthetic care and the anesthetic care of patients undergoing cardiovascular surgery, the unique characteristics of propofol might make it a logical part of the anesthetic plan for patients such as pulmonary hypertension. But there are limited experimental and clinical data on the effects of propofol on pulmonary vascular resistance, and they are somewhat contradictory. the purpose of this study was to investigated.the effect and mechanism of vasodilation induced by propofol using isolated rat pulmonary artery rings.

Cumulative dose-response curves for propofol(10(-6)~10(-3)M) were obtained from tension measurements of rings that contracted with phenylephrine(10(-6)M) and KCI(40 mM) in the presence and absence of endothelium, and in the pretreatment of L-NAME(3x10(-4)M) and substance P(3x10(-4)M). Thereafter the effect of propofol(10(-4)M) on vascular smooth muscle contration in response to Ca++ mobilization in vscular rings were investigated.

Propofol(10(-6)~10(-3)M) produced dose-dependent relaxation and had no signficant effect from endothelium. Pretreatment of L-NAME and substance P failed to have influence on cumulative dose-respose curves. Therefore vasodilator effect of propofol was not endothelium-dependent. And 10(-4)M propofol attenuated a contraction in response to CaCl2 in vascular rings depolarized by KCI, and vasoconstraction in response to calcium entry in the presence of phenylephine was attenuated by 10(-4)M propofol. Ryanodine preteament had not influence on contractile response.

These results suggest that vasodilation produced by propofol is not endothelium-dependent but is probably due to nonspecific intracellular Ca++ influx blockade through voltage-operated calcium channels and receptor-operated channels.