The effects of topical and intravenous ropivacaine on canine pial microcirculation.

To assess the direct cerebrovascular effects of ropivacaine, we studied pharmacological responses to its topical and intravenous (IV) administration on vasomotor tone of pial vessels in in vivo experiments using a parietal cranial window in 24 dogs anesthetized with pentobarbital. We directly measured the diameters of pial arteries and veins after the administration of five different concentrations of ropivacaine solution (10(-7) to 10(-3) mol/L) randomly given into the window (n = 10). In six dogs, after pretreating the pial vessels with yohimbine (10(-5) mol/L), the inhibitory action of yohimbine was examined after the application of ropivacaine (10(-3) mol/L). The effects of IV ropivacaine (1 and 4 mg/kg) were also evaluated in the remaining eight dogs. Ropivacaine produced significant constriction of the pial arteries in a concentration-dependent manner (10(-7) to 10(-3) mol/L, P < 0.05) and only exerted a constrictive action on small veins (P < 0.05) at 10(-3) mol/L. Yohimbine had no effect on ropivacaine-induced constriction of pial vessels. IV ropivacaine, 4 mg/kg but not 1 mg/kg, caused pial vascular constriction (large arteries P < 0.005, small arteries P < 0.0001, large veins P < 0.01, small veins P < 0.005) associated with decrease in heart rate (P < 0.001). The results indicate that topical application of ropivacaine constricts pial arterial vessels in a concentration-dependent manner. A large dose of IV ropivacaine produced pial vasoconstriction associated with a decrease in heart rate and no decrease in mean arterial blood pressure. These effects do not appear to be mediated via the mechanism that depends on the activation of alpha2-adrenoceptors. We conclude that ropivacaine in high concentrations could, perhaps directly, cause significant constriction of the central nervous system vasculature.