Inhibition of cerebral metabolic and circulatory responses to nitrous oxide by 6-hydroxydopamine in dogs

Abstract

Purpose: To determine whether cerebral metabolic and circulatory consequences of N2O result from activation of the sympathoadrenal system. The effects of pretreatment with intracisternal injection of 6-OHDA, which produces chemical sympathectomy, were studied in dogs. Method: Seven days before measurement dogs were pretreated with intracisternal injection of either saline vehicle (sham-group) or 100 μg·kg-1 6-hydroxydopamine (6-OHDA group). Cerebral blood flow CBF) was measured using an electromagnetic flow-meter probe and cerebral metabolic rate for oxygen (CMRO2) was calculated as the product of CBF and arterial-sagittal sinus blood oxygen content difference [C(a-v)O2]. Results: In the sham group, N2O (60%) increased CMRO2 from 6.11 ± 0.21 ml·100 g-1·min-1 to 7.10 ± 0.39 ml·100 g-1·min-1 and CBF from 63 ± 5 ml·100 g-1·min-1 to 173 ± 26 ml·100 g-1·min-1. In the 6-OHDA group, CMRO2 did not change during N2O exposure, whereas CBF increased from 61 ± 3 ml·100 g-1·min-1 to 135 ± 19 ml·100 g-1·min-1 but less then in the sham group. The 6-OHDA group displayed a reduction in cortical noradrenaline (NA) concentration from 263.2 ± 35.6 ng·g-1 to 102.7 ± 16.5 ng·g-1. Cortical dopamine (DA) concentration was not affected by 6-OHDA administration. Conclusion: These results suggest that mos of the increase in CMRO2 and, at least a part of, the increase in CBF during N2O exposure in the sham-group are related to sympathoadrenal-stimulating effects of N2O.