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

Purpose

To determine whether cerebral metabolic and circulatory consequences of N₂O result from activation of the sympathoadrenal system. The effects of pretreatment with intracistemal 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· 100g^?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 most 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.