Vascular effects of ketamine in isolated rabbit aortic Smooth muscle

The precise mechanism by which ketamine induces relaxation of vascular smooth muscle is not clear. The goal of this study was to further characterize the vascular actions of ketamine in rabbitaortic smooth muscles. Ring segments (2mm) of rabbit aortae were suspended in 20ml organ baths containing physiological salt solution (PSS) and isometric contractions were recorded at 370C and pH7.4. The medium was bubbled with 95% O2, 5% CO2, and rings were given an initial load of 2g. An equilibration period of 90 minutes was allowed. Three protocols were examined: (a) Effect of ketamineon baseline tension (b) relaxation-responses to ketamine following precontractions induced by 10-7M phenylephrine or high K+ (40mM) PSS and (c) Influence of presence or absence of endothelium on therelaxation response to ketamine. Ketamine produced relaxation of contractile responses induced by both phenylephrine and High K+. The respective maximum relaxation responses induced by ketaminefollowing precontractions by phenylephrine and high-K+ were 76.8 ± 2.3 and 71.2 ± 8.0 (p > 0.05). Ach-induced relaxation was observed only in rings with intact endothelium whereas ketamine-induced relaxation was observed in intact as well as endothelium-denuded rings; this suggests that ketamineinduced relaxation of rabbit aortic smooth muscle is independent of vascular endothelium