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 oxide (NO) plays a role in the cerebrocortical hyperemic effect of halothane in rats. A particular objective was to elucidate whether the increased vascular tone or the removal of basal NO secondary to NO synthase inhibition influenced the response to halothane. The animals were anesthetized with i.p. pentobarbital for surgery and 90 min later were ventilated with 1.0 minimum alveolar concentration (MAC) halothane for 1 h to achieve a steady-state baseline. The control group was infused with either 1 ml of saline or 20 mg/kg of D-NAME, and the treatment group received 20 mg/kg of L-NAME intravenously. In a subset of the treatment group, we restored baseline flow and vascular tone using i.v. sodium nitroprusside (SNP). Mean arterial pressure (MAP) was maintained constant with an infusion of phenylephrine (0.5-5 micrograms/kg/min). Then, 30 to 45 min later, inspired halothane was raised to 1.7 MAC in each group, and the increase in laser Doppler flow (LDF) was measured. On increasing 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 LDF by 12 +/- 3%, significantly less than control. The decrease in cerebrovascular 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.(ABSTRACT TRUNCATED AT 250 WORDS)