Propofol relaxes extrapulmonary artery but not intrapulmonary artery through nitric oxide pathway.

The object of this study was to compare vasorelaxing responses to propofol by the intrapulmonary artery (IPA) and the extrapulmonary artery (EPA), and to identify the mechanisms of action. Rat pulmonary arterial rings were isolated and suspended in organ chambers where isometric tension development was measured under optimal resting tension. All pulmonary arterial rings were pre-contracted with phenylephrine. Propofol (Diprivan) and the vehicle (10% Intralipid) were administered cumulatively in the presence or absence of N(omega)-nitro-L-arginine methyl ester (L-NAME). Sodium nitroprusside (SNP), a nitric oxide donor, was administered cumulatively. Propofol relaxed both EPA and IPA in a dose dependent manner (p<0.05), while the vehicle alone showed no effect. The vasorelaxing responses to propofol were significantly higher in EPA than IPA at higher concentrations (10(-4) M and 10(-4.5) M) (p<0.05), and were decreased by L-NAME in EPA (p<0.05), though it had no effect in IPA. The concentration for SNP causing 50% relaxation was not significantly different between the two arteries. We concluded that the response of smooth muscle to nitric oxide was the same between EPA and IPA; however, the vasorelaxing mechanisms of propofol seemed to be different between them at higher doses, suggesting that a mechanism exists and operates through the nitric oxide pathway.