抄録
We tested whether pulmonary vascular effects of propofol depend on the level of vasomotor tone. We used the isolated perfused normal rat lung and monocrotaline (MCT)-induced pulmonary hypertension (PH) rat model. Rats were subcutaneously given MCT (PH group). On day 21 after injection, the rats were anesthetized, and the lungs were isolated and perfused. Pulmonary perfusion pressure (PPP) was measured. Changes in PPP during administration of propofol were compared between both groups in the absence or presence of phenylephrine (PE). Propofol had no effect on PPP in the absence of PE. Propofol caused dose-dependent pulmonary vasoconstriction in the presence of PE. To study effects of propofol on endothelial function or myofilament Ca2+ sensitivity, N-nitro-L-arginine methyl ester and indomethacin or an inhibitor of PKC, bisindolylmaleimide I (BIS) and calphostin C were administrated before PE treatment. BIS and Calphostin C significantly decreased propofol-induced PPP elevation in MCT rats. In contrast, indomethacin significantly decreased propofol-induced PPP elevation in normal rats. Propofol may exert pulmonary vascular contractility through PKC activation in MCT rats and through inhibition of cyclooxygenase pathway in normal rats. [J Physiol Sci. 2006;56 Suppl:S131]
