THE VASODILATORY EFFECTS OF KETAMINE ON ISOLATED RABBIT PORTAL VEINS

The vasodilation mechanism induced by ketamine was investigated in iso lated smooth muscle strips of rabbit portal veins. Ketamine inhibited both the phasic and tonic components of Ki-induced contraction at conc entrations greater than 500 mu M and 100 mu M, respectively. This effe ct was reversible anti concentration-dependent with concentrations up to 1 mM. These effects were similar to those producd by verapamil. In the presence of 60 mM K+, application of Ca2+ (2.5 mM) in the perfusin g solution caused tonic contraction of the smooth muscle, and ketamine at concentrations larger than 10 mu M strongly inhibited this Ca2+-in duced contraction. Ketamine (100 mu M) also inhibited the K+-induced c ontractions significantly in the absence and presence of guanethidine, tetrodotoxin and propranolol. Ketamine produced similar concentration -dependent relaxations in the tissues with and without endothelium. Th ese results indicate that in rabbit portal vein, vasodilation produced by ketamine is not endothelium-dependent but is likely to be due to b lockade of the voltage-gated influx of extracellular Ca2+.