Hypoxia, α2-adrenergic, and nitric oxide-dependent interactions on canine cerebral blood flow

R. W. McPherson, Raymond C Koehler, R. J. Traystman

Research output: Contribution to journalArticle

Abstract

We tested the hypothesis that NO synthase inhibition with N(ω)-nitro-L- arginine methyl ester (L-NAME) and α2-adrenoreceptor stimulation with dexmedetomidine (Dex) decreases the cerebral blood flow (CBF) response to hypoxia. In isoflurane-anesthetized dogs, CBF was measured during two episodes of hypoxic hypoxia. In a control group (n = 6), CBF increased similarly from 83 ± 4 to 210 ± 30 ml · min-1 · 100 g-1 and from 88 ± 7 to 205 ± 27 (±SE) ml · min-1 · 100 g-1 during two hypoxic episodes. In a second group (n = 6), hypoxia increased CBF from 88 ± 15 to 204 ± 38 ml · min-1 · 100 g-1. Dex (10 μg/kg iv) reduced normoxic CBF to 54 ± 8 ml · min-1 · 100 g-1, and subsequent hypoxia increased CBF to 97 ± 14 ml · min-1 · 100 g-1. In a third group pretreated with L-NAME (40 mg/kg iv) 1 h before anesthesia (n = 6), normoxic CBF was less than in the control group (52 ± 2 vs. 83 ± 4 ml · min-1 · 100 g-1). Hypoxia increased CBF to 177 ± 13 ml · min-1 · 100 g-1. Dex after L-NAME further decreased normoxic CBF to 37 ± 3 ml · min-1 · 100 g-1, and subsequent hypoxia increased CBF to 106 ± 18 ml · min-1 · 100 g-1. Dex, L-NAME, and Dex + L-NAME each reduced cerebral O2 transport (CBF x arterial O2 content) during normoxia, but the increase in CBF during hypoxia was sufficient to prevent further decreases in O2 transport. Thus the response to hypoxia remained proportional to normoxic levels of CBF. These results indicate that 1) CBF responsivity to hypoxia is intact during isoflurane anesthesia despite the relative hyperemia during normoxia, and 2) mediators of hypoxic vasodilation, NO-dependent vasodilation, and α2- adrenergic vasoconstriction act via additive mechanisms on cerebrovascular tone in the presence of isoflurane anesthesia.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume266
Issue number2 35-2
StatePublished - 1994

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Cerebrovascular Circulation
Adrenergic Agents
blood flow
nitric oxide
Canidae
hypoxia
Nitric Oxide
dogs
dexmedetomidine
Dexmedetomidine
NG-Nitroarginine Methyl Ester
Isoflurane
isoflurane
anesthesia
normoxia
Anesthesia
vasodilation
Hypoxia
Vasodilation
Control Groups

Keywords

  • dexmedetomidine
  • hypoxic hypoxia
  • isoflurane
  • N(ω)-nitro-L-arginine methyl ester

ASJC Scopus subject areas

  • Physiology
  • Agricultural and Biological Sciences(all)

Cite this

Hypoxia, α2-adrenergic, and nitric oxide-dependent interactions on canine cerebral blood flow. / McPherson, R. W.; Koehler, Raymond C; Traystman, R. J.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 266, No. 2 35-2, 1994.

Research output: Contribution to journalArticle

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N2 - We tested the hypothesis that NO synthase inhibition with N(ω)-nitro-L- arginine methyl ester (L-NAME) and α2-adrenoreceptor stimulation with dexmedetomidine (Dex) decreases the cerebral blood flow (CBF) response to hypoxia. In isoflurane-anesthetized dogs, CBF was measured during two episodes of hypoxic hypoxia. In a control group (n = 6), CBF increased similarly from 83 ± 4 to 210 ± 30 ml · min-1 · 100 g-1 and from 88 ± 7 to 205 ± 27 (±SE) ml · min-1 · 100 g-1 during two hypoxic episodes. In a second group (n = 6), hypoxia increased CBF from 88 ± 15 to 204 ± 38 ml · min-1 · 100 g-1. Dex (10 μg/kg iv) reduced normoxic CBF to 54 ± 8 ml · min-1 · 100 g-1, and subsequent hypoxia increased CBF to 97 ± 14 ml · min-1 · 100 g-1. In a third group pretreated with L-NAME (40 mg/kg iv) 1 h before anesthesia (n = 6), normoxic CBF was less than in the control group (52 ± 2 vs. 83 ± 4 ml · min-1 · 100 g-1). Hypoxia increased CBF to 177 ± 13 ml · min-1 · 100 g-1. Dex after L-NAME further decreased normoxic CBF to 37 ± 3 ml · min-1 · 100 g-1, and subsequent hypoxia increased CBF to 106 ± 18 ml · min-1 · 100 g-1. Dex, L-NAME, and Dex + L-NAME each reduced cerebral O2 transport (CBF x arterial O2 content) during normoxia, but the increase in CBF during hypoxia was sufficient to prevent further decreases in O2 transport. Thus the response to hypoxia remained proportional to normoxic levels of CBF. These results indicate that 1) CBF responsivity to hypoxia is intact during isoflurane anesthesia despite the relative hyperemia during normoxia, and 2) mediators of hypoxic vasodilation, NO-dependent vasodilation, and α2- adrenergic vasoconstriction act via additive mechanisms on cerebrovascular tone in the presence of isoflurane anesthesia.

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