Inhibitory Effects of Halothane, Isoflurane, Sevoflurane, and Pentobarbital on the Constriction Induced by Hypocapnia and Bicarbonate in Isolated Canine Cerebral Arteries

The effects of halothane, isoflurane, sevoflurane (0.5, 1 and 2 MAC) and pentobarbital (10(-5) M, 10(-4) M and 3 x 10(-4) M) on hypocapnia- and bicarbonate-induced constriction of isolated dog middle cerebral arteries were investigated in vitro. The isometric tension of isolated cerebral arterial rings was measured in an organ bath containing Krebs bicarbonate solution, aerated with 5% CO2 and 95% O2. Hypocapnia, induced by replacing the bathing solution with one that had been equilibrated with 2.5% CO2 and 97.5% O2, produced a sustained vasoconstriction (268 +/- 36 mg, mean +/- SEM). Exposure of arterial rings to a bathing solution that contained double the concentration of NaHCO3 (50 mM) elicited a phasic constriction followed by a gradual decrease in tension (309 +/- 34 mg). Although halothane, isoflurane, and sevoflurane attenuated both hypocapnia- and bicarbonate-induced constrictions in a dose-dependent manner, the inhibition of these constrictions was greater in rings treated with halothane than in those treated with isoflurane or sevoflurane when compared at equipotent concentrations. These alkaline-induced constrictions were attenuated by pentobarbital only at the highest concentration of 3 x 10(-4) M. Halothane (1 and 2 MAC) attenuated the constriction induced by hypocapnia to a greater extent than that induced by 15 mM KCl, whereas pentobarbital (10(-4) M and 3 x 10(-4) M) attenuated hypocapnia-induced constriction less than KCl-induced constriction. These results indicate that alkaline-induced constriction is more vulnerable to halothane than other volatile anesthetics and pentobarbital. The mechanisms of the inhibitory effects of halothane and pentobarbital on alkaline-induced cerebral vasoconstriction seem to differ; the inhibitory effect of pentobarbital, but not of halothane may be, in part, ascribed to its inhibitory effect on the Ca++ influx.