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



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.


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].


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.


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.



Vérifier si les effets metaboliques et circulatoires cérébraux provoqués par l’inhalation de N2O résultent de l’activation du système sympathico-surrénalien. Au cours de cette étude, on a étudié sur des chiens les effets de la sympathectomie chimique provoquée par l’administration intracistemale de 6-OHDA.


D’abord, les chiens ont negu des injections intracisternaJes de sol. phys. (Groupe factice) ou de 100 μg· kg−1 de 6-hydroxydopamine (groupe 6-OHDA). Sept jours plus tard, le débit sanguin cérébral (DSC) a été mesuré à l’aide d’un débitmètre électromagnétique; le métabolisme cérébral pour l’oxygène (CMRO2) a été calculé en multipliant le DSC par la différence artério-sinus sagittal du contenu en oxygène [C(a-v)O2].


Dans le groupe factice, le N2O (60%) a augmente le CRMO2 de 6,11 ± 0.21 ml· 100 g−1· min−1 à 7,10 ± 0,39 ml 100· g−1· min−1 et le DSC de 63 ± 5 ml· 100 g−1· min−1 à 173 ± 26 ml· 100 g−1· min−1. Dans le groupe 6-OHDA, le CMRO2 n’a pas varié pendant l’exposition au N2O, alors que le DSC augmentait de 61 ±3 ml· 100 g−1 · min−1 à 135 ± 19 ml· 100· g−1· min−1 mats moins que dans le groupe factice. Dans le groupe 6-OHDA, la concentration de la noradrenaline corticale baissait de 263,2 ± 35,6 ng· g−1 à 102,7 ± 16,5 ng·g−1, L’administration de 6-OHDA n’a pas affecté la concentration de la dopamine corticale.


Ces résultats suggèrent que, dans le groupe factice, pendant l’exposition au N2O, la presque totalité de l’augmentation du CMRO2 et, au moins une partie de l’augmentation du DSC, sont causées par la stimulation sympathico-surrénalienne.


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Correspondence to Osamu Nakanishi.

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Nakanishi, O., Ishikawa, T., Imarnura, Y. et al. Inhibition of cerebral metabolic and circulatory responses to nitrous oxide by 6-hydroxydopamine in dogs. Can J Anaesth 44, 1008–1013 (1997).

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  • Cerebral Blood Flow
  • Halothane
  • Mean Arterial Blood Pressure
  • Cerebral Metabolic Rate
  • Cerebral Blood Flow Measurement