Effects of hypoxia and normocarbia on cerebral blood flow and metabolism in conscious man.

Cohen, Peter J.; Alexander, S. Craighead; Smith, Timothy M.; Reivich, M.; Wollman, Harry

doi:10.1152/jappl.1967.23.2.183

Cited by 350 publications

(151 citation statements)

References 27 publications

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“…1 /Lmol 100 g-l min-1 (mean ± SD, n = 40) are similar to glucose utilization values of 29 ± 6/Lmol 100 g-l min-1 (mean ± SD, n = 39) found by Gottstein et aI. (1963) and 29 ± 8/Lmol 100 g-l min-1 (mean ± SD, n = 59) found by Cohen et a!. (1967), who used the method of Kety and Schmidt (1948).…”

Section: Figsupporting

confidence: 84%

Effects of Human Aging on Patterns of Local Cerebral Glucose Utilization Determined by the [¹⁸F] Fluorodeoxyglucose Method

et al. 1982

J Cereb Blood Flow Metab

318

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Summary:The [IHF]fluorodeoxyglucose (FDG) scan method with positron emission computed tomography was used to determine patterns of local cere bral glucose utilization (LCMRg1u) in 40 normal volunteer subjects aged 18 to 78 years. Throughout all the studies. each subject was quiet, without movement, with eyes open and ears unplugged, exposed only to ambient room light and sound. For the entire group, whole brain mean CMRglu was 26.1 ± 6. I /Lmol 100 g-l min-1 (mean ± SD, n = 40). At age 78, mean CMRglu was, on the average, 26% less than at age 18, an alteration of the same order as the variance among subjects at any age. The gradual decline of mean CMRglu with advancing age occurred at a faster rate than was reported for mean cerebral oxygen utilization, possibly due to increasingly altered pathways for glucose utilization, or to increasing oxidation of ketone bodies or other alternative substrates. Glucose utilization in the hemispheres was symmetrical and mean CMRglU of overall cortex, caudate, and thalamus was equal in individuals at all ages. The slopes of decline with age were similar when LCM Rglu was averaged over zones corresponding to centrum semiovale, caudate, putamen, and fron tal, temporal, parietal, occipital, and primary visual cortex. However, the met abolic ratio of superior frontal cortex to superior parietal cortex declined with age, possibly due to selective degeneration of superior frontal cortex or to differences between age groups in the sensory and cognitive response to the study. These results should be useful in distinguishing age from disease effects when the FDG scan method is used. 163 koloff et aI., 1977) used in animals, but emission computed tomography is substituted for the au toradiography. After intravenous injection, FDG enters the brain, is phosphorylated by brain hexokinase, and the metabolic product, FDG-6-P0 4 , remains fixed with only slow dephosphoryla tion. The time course of specific activity is mea sured in plasma, brain activity is determined by scanning, and with knowledge of predetermined rate constants, an operational equation allows cal culations of LCMRglu that are distributed in a cross-

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Section: Figsupporting

confidence: 84%

Effects of Human Aging on Patterns of Local Cerebral Glucose Utilization Determined by the [¹⁸F] Fluorodeoxyglucose Method

et al. 1982

J Cereb Blood Flow Metab

318

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“…The effect of hypoxia may be related to less central ventilatory drive (40) as result of medullary hypocapnia due to hypoxia-induced hyperventilation and increased cerebral blood flow. Thus hypoxia may enhance periodic breathing and apnea through a combination of its stimulating effect on the peripheral chemoreceptor and its suppressive effect on central respiratory drive (26,41) and via increased cerebral blood flow (12). In other words, even though peripheral chemoreceptor presence is necessary for the manifestation of a rapid-onset posthyperventilation apnea, additional central influences are required to produce periodic breathing.…”

Section: Discussionmentioning

confidence: 99%

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Xie¹,

Skatrud²,

Puleo³

et al. 2006

Journal of Applied Physiology

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Xie, Ailiang, James B. Skatrud, Dominic S. Puleo, and Jerome A. Dempsey. Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep. J Appl Physiol 100: 171-177, 2006. First published September 22, 2005 doi:10.1152/japplphysiol.00440.2005.-To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired PO 2. We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O 2 saturation ϭ 78 -80%), and hyperoxia (inspired O2 fraction ϭ 50 -52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sighlike breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 Ϯ 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 Ϯ 0.8 s; P Ͻ 0.05), whereas hyperoxia prolonged it (71.5 Ϯ 13.8 s; P Ͻ 0.01). The apneic threshold end-tidal PCO 2 (PETCO 2 ) was defined as the PETCO 2 at the onset of apnea. During hypoxia, the apneic threshold PET CO 2 was higher (38.9 Ϯ 1.7 Torr; P Ͻ 0.01) compared with normoxia (35.8 Ϯ 1.1; Torr); during hyperoxia, it was lower (33.0 Ϯ 0.8 Torr; P Ͻ 0.05). Furthermore, the difference between the eupneic PET CO 2 and apneic threshold PET CO 2 was smaller during hypoxia (3.0 Ϯ 1.0 Torr P Ͻ 001) and greater during hyperoxia (10.6 Ϯ 0.8 Torr; P Ͻ 0.05) compared with normoxia (8.0 Ϯ 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO 2 below the eupneic PETCO 2 was increased by hypoxia (3.44 Ϯ 0.63 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ; P Ͻ 0.05) and decreased by hyperoxia (0.63 Ϯ 0.04 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ; P Ͻ 0.05) compared with normoxia (0.79 Ϯ 0.05 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors. apnea threshold THE RELATIVE CONTRIBUTION of peripheral vs. central chemoreception in initiating the posthyperventilation apneas remains an unresolved question. The importance of peripheral chemoreception in mediating the rapid ventilatory response to hypocapnia has been supported using animal models. Carotid body denervation either eliminated or prolonged the time course for the development of apnea after the administration of augmented breaths (6, 39). However, carotid body denervation profoundly alters central chemoreception as indicated by the substantial CO 2 retention after denervation. Our laboratory has previously demonstrated the complex effect of hypoxia in t...

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“…First, ex treme hypoxia can elevate CMRglc (28% for Pa02 = 34.6 mm Hg) (Cohen et al 1967) by stimulating anaerobic glycolysis (Siesj61978). Furthermore, although elevated CO2 can reduce cerebral glucose metabolism by inhibit ing hexokinase and phosphofructokinase (Siesj61978), preliminary studies in our laboratory have shown that hypercapnia at a level similar to that seen in the current study did not reduce CMRglc (J .M.…”

Section: Buprenorphine and Cerebral Glucose Metabolism 165mentioning

confidence: 99%

Buprenorphine Reduces Cerebral Glucose Metabolism in Polydrug Abusers

Walsh

Gilson

Jasinski

et al. 1994

Neuropsychopharmacol

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Buprenorphine is a mixed opioid agonist-antagonist, which acts as a partial mu agonist and a kappa antagonist. The present study evaluated the acute effects of buprenorphine on cerebral glucose metabolism (CMRglc) in six human substance abusers using a double-blind, placebo-controlled, counterbalanced, crossover design. Each subject participated in two positron emission tomographic (PET) studies, 1 week apart, following the injection of buprenorphine (1 mg, intramuscularly) and placebo. Buprenorphine significantly reduced CMRglc and the regional cerebral KEY WORDS: Opioid; Buprenorphine; Glucose metabolism; Drug abuse; Human brain imaging Buprenorphine, a semi-synthetic opioid drug derived from thebaine, is currently marketed in the United States as an analgesic, and is approximately 25 to 50 times as potent as morphine (Cowan et al. 1977). In hu man subjects, it produces effects that are typical of opi oid agonists (Heel et al. 1979). These include analge-

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Effects of hypoxia and normocarbia on cerebral blood flow and metabolism in conscious man.

Cited by 350 publications

References 27 publications

Effects of Human Aging on Patterns of Local Cerebral Glucose Utilization Determined by the [¹⁸F] Fluorodeoxyglucose Method

Effects of Human Aging on Patterns of Local Cerebral Glucose Utilization Determined by the [¹⁸F] Fluorodeoxyglucose Method

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Buprenorphine Reduces Cerebral Glucose Metabolism in Polydrug Abusers

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Effects of hypoxia and normocarbia on cerebral blood flow and metabolism in conscious man.

Cited by 350 publications

References 27 publications

Effects of Human Aging on Patterns of Local Cerebral Glucose Utilization Determined by the [18F] Fluorodeoxyglucose Method

Effects of Human Aging on Patterns of Local Cerebral Glucose Utilization Determined by the [18F] Fluorodeoxyglucose Method

Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep

Buprenorphine Reduces Cerebral Glucose Metabolism in Polydrug Abusers

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Product

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Effects of Human Aging on Patterns of Local Cerebral Glucose Utilization Determined by the [¹⁸F] Fluorodeoxyglucose Method

Effects of Human Aging on Patterns of Local Cerebral Glucose Utilization Determined by the [¹⁸F] Fluorodeoxyglucose Method

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep