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 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 micrograms.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 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.