Regional cerebral glucose utilization transiently increases during mild hypoxia

C. MacNeill, R. M. Bryan

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Regional cerebral glucose utilization (rCMR(glu)) was studied during mild hypoxic hypoxia in awake free-ranging rats. Rats were prepared with chronic arterial and venous catheters and placed in individual chambers for 4 days to recover from surgery before the experiments. The catheters were accessible by passing them through the top of the chambers. Hypoxia was induced by filling the chambers with a gas mixture consisting of 11% O2 in a balance of N2. Regional CMR(glu) and physiological parameters were measured in normoxic controls and in rats that had been hypoxic for 2 and 17 min before beginning the measurements. Regional CMR(glu) was measured in 17 brain regions using [6-14C]glucose. P(a)O2 decreased from 88 mm Hg in the controls to ~ 40 mm Hg during hypoxia. In the early stages of hypoxia (2-12 min), rCMR(glu) increased ~ 10-25% above the control rates. In later stages of hypoxia (17-27 min), rCMR(glu) was not different from that in the normoxic controls. The increase in rCMR(glu) in the early hypoxia was not blocked by propranolol (1.4 mg/kg), indicating that beta-adrenergic receptors were not involved with the increase in rCMR(glu). It was concluded that mild hypoxia is associated with an increased rate of cerebral glucose utilization; however, the increase is transitory, with glucose utilization returning to control rates before 17 min.

Original languageEnglish (US)
Pages (from-to)495-501
Number of pages7
JournalJournal of Cerebral Blood Flow and Metabolism
Volume8
Issue number4
DOIs
StatePublished - Jan 1 1988

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Glucose
Catheters
Hypoxia
Receptors, Adrenergic, beta
Propranolol
Gases
Brain

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Regional cerebral glucose utilization transiently increases during mild hypoxia",
abstract = "Regional cerebral glucose utilization (rCMR(glu)) was studied during mild hypoxic hypoxia in awake free-ranging rats. Rats were prepared with chronic arterial and venous catheters and placed in individual chambers for 4 days to recover from surgery before the experiments. The catheters were accessible by passing them through the top of the chambers. Hypoxia was induced by filling the chambers with a gas mixture consisting of 11{\%} O2 in a balance of N2. Regional CMR(glu) and physiological parameters were measured in normoxic controls and in rats that had been hypoxic for 2 and 17 min before beginning the measurements. Regional CMR(glu) was measured in 17 brain regions using [6-14C]glucose. P(a)O2 decreased from 88 mm Hg in the controls to ~ 40 mm Hg during hypoxia. In the early stages of hypoxia (2-12 min), rCMR(glu) increased ~ 10-25{\%} above the control rates. In later stages of hypoxia (17-27 min), rCMR(glu) was not different from that in the normoxic controls. The increase in rCMR(glu) in the early hypoxia was not blocked by propranolol (1.4 mg/kg), indicating that beta-adrenergic receptors were not involved with the increase in rCMR(glu). It was concluded that mild hypoxia is associated with an increased rate of cerebral glucose utilization; however, the increase is transitory, with glucose utilization returning to control rates before 17 min.",
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Regional cerebral glucose utilization transiently increases during mild hypoxia. / MacNeill, C.; Bryan, R. M.

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 8, No. 4, 01.01.1988, p. 495-501.

Research output: Contribution to journalArticle

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