THE ROLE OF NITRIC-OXIDE IN CEREBROCORTICAL LASER-DOPPLER FLOW RESPONSE TO HALOTHANE IN THE RAT

Laser Doppler flowmetry was utilized to investigate whether nitric oxi de (NO) plays a role in the cerebrocortical hyperemic effect of haloth ane in rats. A particular objective was to elucidate whether the incre ased vascular tone or the removal of basal NO secondary to NO synthase inhibition influenced the response to halothane. The animals were ane sthetized with i.p. pentobarbital for surgery and 90 min later were ve ntilated with 1.0 minimum alveolar concentration (MAC) halothane for 1 h to achieve a steady-state baseline. The control group was infused w ith either 1 ml of saline or 20 mg/kg of D-NAME, and the treatment gro up received 20 mg/kg of L-NAME intravenously. In a subset of the treat ment group, we restored baseline flow and vascular tone using i.v. sod ium nitroprusside (SNP). Mean arterial pressure (MAP) was maintained c onstant with an infusion of phenylephrine (0.5-5 mu g/ kg/min). Then, 30 to 45 min later, inspired halothane was raised to 1.7 MAC in each g roup, and the increase in laser Doppler flow (LDF) was measured. On in creasing halothane MAC in the control group, LDF increased by 28 +/- 4 %. L-NAME increased MAP by 21 +/- 4% and reduced baseline LDF by 26 +/ - 2%. In the L-NAME-only treated group, 1.7 MAC halothane increased LD F by 12 +/- 3%, significantly less than control. The decrease in cereb rovascular resistance induced by increasing inspired halothane MAC was similar in the control group and in the L-NAME treated group at 23 +/ - 6% and 22% +/- 7, respectively. In the L-NAME + SNP group, increasin g halothane MAC decreased cerebrovascular resistance by 30 +/- 2% and increased LDF by 37 +/- 2%, not statistically different from the contr ol group. Thus cerebrocortical vasodilation in response to increasing halothane MAC from 1.0 to 1.7 MAC was not attenuated by L-NAME when ba seline flow and tone were restored with an NO donor to control levels. These data suggest that (a) NO is not an obligatory mediator of halot hane-induced cerebrocortical vasodilatation, (b) altered vascular tone and NO level after NO synthase inhibition may influence the cerebral vasodilator response to halothane, and (c) NO may have a permissive ro le in halothane-induced cerebral vasodilatation.