Local oxygen tension and spike activity of the cerebral grey matter of the rat and its response to short intervals of O2 deficiency or CO2 excess

Metzger, Hermann; Heuber, S.

doi:10.1007/bf00581695

Cited by 46 publications

(27 citation statements)

References 25 publications

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“…This experimental setting is not necessarily analogous to the physiologic situation in which oxygen is continuously supplied into a tissue micro-environment that may be poised at a very low Po2 (9,10). The role of oxygen in the control of mitochondrial behavior has been explored from a number of perspectives; for example, the kinetics of cellular respiration (11), the redox state of respiratory chain carriers (12), the preservation of energetic function (13), and the thermodynamic relationship between the mitochondrial oxidation-reduction reactions and the extramitochondrial phosphorylation state (14).…”

mentioning

confidence: 99%

Reversible uncoupling of oxidative phosphorylation at low oxygen tension.

Kramer¹,

Pearlstein²

1983

Proc. Natl. Acad. Sci. U.S.A.

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The stoichiometry of oxidative phosphorylation at low oxygen tension (< 3 torr; 02 < 5 aiM) has been measured in rat liver mitochondria. In a steady-state model in which respiration rate was experimentally controlled by either oxygen or substrate (succinate) limitation, flux-dependent variation in the phosphorylation efficiency (P/O ratio) of stimulated mitochondrial respiration was evaluated. P/O ratio remained constant over a wide range of respiration rates in mitochondria limited only by substrate availability. In contrast, oxygen-limited mitochondria demonstrated a continuous decline in P/O ratio as respiration was increasingly restricted. Significant differences in the two test conditions were demonstrated throughout the range of analysis. The effect of oxygen limitation on phosphorylation efficiency was shown to be completely reversed by restoring zero-order kinetics associated with high oxygen tension. These findings are discussed in regard to a proposed uncoupling of mitochondrial coupling site II at low oxygen tension arising as a consequence of energy-dissipating electron flux through the ubiquinone-cytochrome b-cl region of the respiratory chain (complex III).Living cells utilize and conserve energy in various forms. In this regard, the cell shares with other mixed-energy-domain systems the ability to convert energy internally from one physical form to another. For aerobic organisms, the existence of one such biological energy transduction has been extensively documented: the coupling of electron transport in the mitochondrial respiratory chain (cellular respiration) to the synthesis of ATP. Indeed, so effectively does oxidative phosphorylation support the many energy-requiring reactions of aerobic cells that there is a tendency to assume that mitochondrial ATP synthesis proceeds with maximum stoichiometric efficiency under nearly all physiologic conditions. However, it is well established that mitochondrial respiration is not obligatorily linked to the formation of high-energy phosphate bonds (1-4). The phenomenon of uncoupling has been demonstrated routinely in the laboratory by using chemical agents that direct the energy released by electron transport into mitochondrial energetic activities other than phosphorylation. The possibility of intrinsic mitochondrial uncoupling has been considered by several investigators and is predicated on the hypothetical existence of energy-dissipating pathways of electron flux through the respiratory chain. In this connection, Trumpower (5) commented on a potential uncoupling of Mitchell's proposed "Q-cycle" (6) related to the disposition of the unpaired electron of ubisemiquinone interacting with the Rieske iron-sulfur protein at coupling site II. An explicit separation of energy-transducing and energy-dissipating electron transport pathways in submitochondrial particles is described in the dual respiratory chain model of Norling et al. (7). Chance (8) proposed energy-dissipating electron flux between quasi-equipotential carrier groups to explain the init...

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confidence: 99%

Reversible uncoupling of oxidative phosphorylation at low oxygen tension.

Kramer¹,

Pearlstein²

1983

Proc. Natl. Acad. Sci. U.S.A.

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“…It is well recognized that the brain cortex is het erogeneously perfused with oxygen (Davies and Bronk, 1957;Metzger and Heuber, 1977). At the penetration depth of 366 nm-exciting light (�500 /Lm), the oxygen tension of the brain cortex, mea sured with gold microelectrodes, varies from 0 to 60 mm Hg, with a mean value of �30 mm Hg (Metzger and Heuber, 1977).…”

Section: Resultsmentioning

confidence: 99%

“…At the penetration depth of 366 nm-exciting light (�500 /Lm), the oxygen tension of the brain cortex, mea sured with gold microelectrodes, varies from 0 to 60 mm Hg, with a mean value of �30 mm Hg (Metzger and Heuber, 1977). Davies and Bronk (1957), using surface oxygen electrodes, suggested that if oxygen tension decreased to <4-5 mm Hg, cortical oxygen consumption declines.…”

Section: Resultsmentioning

confidence: 99%

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Effect of Topically Administered Epinephrine, Norepinephrine, and Acetylcholine on Cerebrocortical Circulation and the NAD/NADH Redox State

Dóra

Kovách

1983

J Cereb Blood Flow Metab

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Summary:We investigated the effects of topically ad ministered catecholamines and acetylcholine (ACh) on the cerebrocortical microcirculation and NAD/NADH redox state in chloralose-anesthetized cats. NADH fluo rescence of the brain cortex and the volume of small in tracortical vessels were measured by fluororeflectometry, and in most of the experiments the pial vessels were photographed simultaneously through a cranial window. Cerebrocortical vascular volume (CVV) and the diameter of the pial vessels were decreased, and NADH was oxidized by concentrations of epinephrine and norepi nephrine as low as 3 x 10-8 M. Pial veins constricted approximately twice as much as pial arteries. ACh dila tated pial arteries, slightly constricted pial veins, and in creased CVV, but had no effect on the NAD/NADH redox state. Since pial and intracortical vessels were conThe dual sympathetic and parasympathetic in nervation of cerebral vessels is well recognized, and it has also been proved that cerebral vessels contain both adrenergic and cholinergic receptors (Ku schinsky and Wahl, 1975;Edvinsson and Owman, 1977; Auer et aI., 1981; Harik et ai., 1981; Ulrich et aI., 1982). In spite of this, the role of the autonomic nervous system and its humoral mediators in the regulation of cere bro vascular volume (CVV) and cerebral blood flow (CBF) is still a matter of controversy (Kuschinsky and Wahl, 1975;Kontos,

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“…However s measurement of nervous tissue o~gen tension from the surface J of the cerebral Cortex (Leniger-Fo1bert, 1975) as we1l as fram within the cerebral cortex with microelectrodes (Naïr et al, 1975;Metzger & Heuber, 1977) has shown that nervous tissue o~gen tension decreases rapidly cduring ventilation with hypoxic or anoxie gases. Recent wort / has a1so shawn a uni formi t y of o~gen consumption within different regions of the CNS (Buchweitz et al, 1980).…”

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confidence: 99%

Hypoxic responses of sympathetic preganglionic neurons in the acute spinal cat

Rohlicek¹,

Polosa²

1981

American Journal of Physiology-Heart and Circulatory Physiology

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The relation between arterial O2 tension (PaO2) and the firing rate of sympathetic preganglionic neurons (SPN) of the cervical sympathetic trunk was studied during graded isocapnic hypoxia and hyperoxia in unanesthetized acute C-1 spinal cats. In the PaO2 range between 40 and 400 Torr there was no relation between the two variables. Below 40 Torr firing rate increased as PaO2 decreased, reaching an average peak value of ten times control at a PaO2 of 20 Torr. Mean arterial blood pressure (MABP) was also independent of PaO2 between 40 and 400 Torr and increased by an average of 25% at PaO2 values below 40 Torr. Intravenous administration of hexamethonium or phentolamine abolished the MABP response but not the SPN response to hypoxia. Pentobarbital (5-60 mg/kg iv) did not modify the SPN response to hypoxia, although normoxic SPN background firing was considerably depressed. The excitatory effect of hypoxia seems independent of excitatory afferent input and appears to be a general property of SPN.

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Local oxygen tension and spike activity of the cerebral grey matter of the rat and its response to short intervals of O2 deficiency or CO2 excess

Cited by 46 publications

References 25 publications

Reversible uncoupling of oxidative phosphorylation at low oxygen tension.

Reversible uncoupling of oxidative phosphorylation at low oxygen tension.

Effect of Topically Administered Epinephrine, Norepinephrine, and Acetylcholine on Cerebrocortical Circulation and the NAD/NADH Redox State

Hypoxic responses of sympathetic preganglionic neurons in the acute spinal cat

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