Relationship Between Microflow, Local Tissue Po2 and Extracellular Activities of Potassium and Hydrogen Ions in the Cat Brain During Intraarterial Infusion of Ammonium Acetate

Gronczewski, J.; Leniger-Follert, E.

doi:10.1007/978-1-4684-1188-1_23

Cited by 4 publications

(3 citation statements)

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“…Some microelectrode studies in skeletal muscle show low P%'s (e.g., Heinrich et al, 1985). Mean P%'s in the range of 15-25 mmHg have also been found in the cerebrum of guinea pig (e.g., LUbbers, 1977) and rat (Feng et al, 1988), but only rarely in cat (Gronczewski and Leniger-Follert, 1984), where the mean is instead generally >30 mmHg (Leniger-Follert, 1985) and there are few values < 10 mmHg. Most of the recordings in cat brain have been made with surface electrodes, however, and the Po 2 distribution might be different deeper in the tissue.…”

Section: Inner Retinal Pomentioning

confidence: 97%

Oxygen distribution and consumption in the cat retina during normoxia and hypoxemia.

Linsenmeier

Braun

1992

The Journal of General Physiology

221

230

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Oxygen tension (Po2) was measured with microelectrodes within the retina of anesthetized cats during normoxia and hypoxemia (i.e., systemic hypoxia), and photoreceptor oxygen consumption was determined by fitting Po~ measurements to a model of steady-state oxygen diffusion and consumption. Choroidal Po 2 fell linearly during hypoxemia, about 0.64 mmHg/mmHg decrease in arterial Po~ (Pao~). The choroidal circulation provided ~91% of the photoreceptors" oxygen supply under dark-adapted conditions during both normoxia and hypoxemia. In light adaptation the choroid supplied all of the oxygen during normoxia, but at Pao~'s <60 mmHg the retinal circulation supplied ~ 10% of the oxygen. In the dark-adapted retina the decrease in choroidal Po2 caused a large decrease in photoreceptor oxygen consumption, from ~ 5.1 ml OJ 100 g.min during normoxia to 2.6 ml Off 100 g'min at a P,o 2 of 50 mmHg. When the retina was adapted to a rod saturating background, normoxic oxygen consumption was ~ 33% of the darkadapted value, and hypoxemia caused almost no change in oxygen consumption. This difference in metabolic effects ofhypoxemia in light and dark explains why the standing potential of the eye and retinal extracellular potassium concentration were previously found to be more affected by hypoxemia in darkness. Frequency histograms of intraretinal Po~ were used to characterize the oxygenation of the vascularized inner half of the retina, where the oxygen distribution is heterogeneous and simple diffusion models cannot be used. Inner retinal Po~ during normoxia was relatively low: 18 -12 mmHg (mean and SD; n = 8,328 values from 36 profiles) in dark adaptation, and significantly lower, 13 -+ 6 mmHg (n --4,349 values from 19 profiles) in light adaptation. Even in the dark-adapted retina, 30% of the values were < 10 mmHg. The mean Po~ in the inner (i.e., proximal) half of the retina was well regulated during hypoxemia. In dark adaptation it was significantly reduced only at Pao2's < 45 mmHg, and it was reduced less at these P~o~'s in light adaptation.

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Section: Inner Retinal Pomentioning

confidence: 97%

Oxygen distribution and consumption in the cat retina during normoxia and hypoxemia.

Linsenmeier

Braun

1992

The Journal of General Physiology

221

230

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“…Under pathological conditions such as spreading depression, transient glial alkalinization caused by elevated [K + Iãnd membrane depolarization are accompanied by concomitant acidification of extracellular fluid and of neuronal pH (Somjen et al, 1992). In acutely hyperammonemic cat, elevation of [K + Iwas accompanied by acidification of interstitial fluid by 0.15 pH unit in vivo, although glial pH was not measured (Gronczewski and Leniger-Follert, 1984). Acidification of extracellular fluid is known to depress neuronal excitability through proton-induced inhibition of N-methyl-D-aspartate-gated glutamate receptor channel and activation of GABAA-gated chloride channel (Deitmer and Rose, 1996).…”

Section: T)mentioning

confidence: 99%

Glial Alkalinization Detected In Vivo by ¹H‐¹⁵N Heteronuclear Multiple‐Quantum Coherence‐Transfer NMR in Severely Hyperammonemic Rat

Kanamori

Ross

1997

Journal of Neurochemistry

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glutamine amide protons were selectively observed in vivo by 1H-15N heteronuclear multiple-quantum coherence-transfer NMR in spontaneously breathing, severely hyperammonemic rats during intravenous [15N]ammonium acetate infusion and the subsequent recovery period. The Iinewidth of brain [5-15N]glutamine amide proton H~increased from 36 ± 2 Hz at 3.4 h to 58 ±6 Hz after 5.7 h of infusion, a net increase of 22 ± 6 Hz. Concomitantly, brain ammonia concentration increased from 1.7 to 3.5 ± 0.2~tmol/gand the rat progressed from grade Ill to grade IV encephalopathy. On recovery to grade Ill and decrease of brain ammonia concentration to 1.3~mol/g, the Iinewidth returned to 37 ± 2 Hz. In aqueous solution, [5-15N]glutamine amide proton H~underwent a 17-Hz linebroadening when pH was raised from 7.1 to 7.5 at 37°C,due to the increased rate of base-catalyzed exchange with water proton. Hence, linebroadening is a sensitive measure of changing intracellular pH. The 22-Hz linebroadening observed in vivo in severely hyperammonemic grade IV rats strongly suggests that the intracellular pH increases from 7.1 to about 7.4-7.5 in astrocytes where glutamine is synthesized and mainly stored. Probable mechanisms for the ammoniainduced alkalinization and decreased intraglial buffering capacity, as well as implications of the result for pathogenesis of hepatic encephalopathy, are discussed.

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“…In hippocampal slices exposed to ammonia, in creases in extracellular K+ activity ([K+le) were observed that may have passively contributed to alterations in postsynaptic potentials (Alger and Nicoll, 1983). Injec tion of ammonium acetate directly into the carotid artery of a cat was shown to increase [K+]e (Gronczewski and Leniger-Follert, 1984). However, [K+]e has not been well studied in vivo during hyperammonemia.…”

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confidence: 99%

Methionine Sulfoximine, a Glutamine Synthetase Inhibitor, Attenuates Increased Extracellular Potassium Activity during Acute Hyperammonemia

Sugimoto

Koehler

Wilson

et al. 1997

J Cereb Blood Flow Metab

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Summary: Hyperammonemia causes glutamine accumulation and astrocyte swelling. Inhibition of glutamine synthesis re duces ammonia-induced edema formation and watery swelling in astrocyte processes. Ordinarily, astrocytes tightly control ex tracellular K+ activity [K+le. We tested the hypothesis that acute hyperammonemia interferes with this tight regulation such that [K+le increases and that inhibition of glutamine syn thetase reduces this increase in [K+le. Ion-sensitive microelec trodes were used to measure [K+le in parietal cortex continu ously over a 6-h period in anesthetized rats. After i.v. sodium acetate infusion in eight control rats, plasma ammonia concen tration was 33 ± 26 fLmollL (± SD) and [K+le remained stable at 4.3 ± 1.6 mmollL. During ammonium acetate infusion in nine rats, plasma ammonia increased to 594 ± 124 fLmollL at 2 h and to 628 ± 135 fLmollL at 6 h. There was a gradual increase Various forms of liver disease and congenital urea cycle disorders cause selective swelling of astrocytes (Bruton et aI., 1970; Martinez, 1968; Zimmerman et aI., 1981). Experimental hyperammonemia also causes se lective astrocyte swelling (Diemer, 1978; Gibson et aI., 1974; Voorhies et aI., 1983). Plasma-labelled ammonia is rapidly taken up by brain (Cooper et aI., 1979(Cooper et aI., , 1985 and used in the amidation of glutamate by glutamine synthe tase, an enzyme enriched in astrocytes (Norenberg and Martinez-Hernandez, 1979). With acute hyperammone mia, tissue glutamine concentration increases over a pe riod of several hours (Bosman et aI., 1990; Fitzpatrick et Received April I, 1996; final revision received June 10, 1996; ac cepted June 10, 1996. 44in [K+le from 3.9 ± 0.7 to 6.8 ± 2.7 mmollL at 2 h and 11.8 ± 6.7 mmollL at 6 h. In eight rats, L-methionine-D,L-sulfoximine (150 mg/kg) was infused 3 h before ammonium acetate infu sion to inhibit glutamine synthetase. At 2 and 6 h of ammonium acetate infusion, plasma ammonia concentration was 727 ± 228 and 845 ± 326 fLmollL, and [K+le was 4.5 ± 1.9 and 6.1 ± 3.8 mmollL, respectively. The [K+Je value at 6 h was significantly less than that obtained with ammonium acetate infusion alone but was not different from that obtained with sodium acetate infusion. We conclude that acute hyperammonemia impairs astrocytic control of [K+lc and that this impairment is linked to glutamine accumulation rather than ammonium ions per se. Key Words: Ammonia-Astrocytes-Glutamine-Hepatic encephalopathy-Potassium-Rats.aI., 1989), and watery astrocyte processes are observed at 6 h (Willard-Mack et aI., 1996). We found that inhibition of glutamine synthetase with L-methionine-D,L sulfoximine (MSO) pretreatment prevented increased cortical glutamine concentration and tissue water content (Takahashi et aI., 1991), increased intracranial pressure (Takahashi et aI., 1992), watery swelling of astrocyte processes (Willard-Mack et aI., 1996), and loss of cere brovascular CO2 reactivity (Hirata et aI., 1996; Takaha shi et aI., 1992) associated with acute hyperammonemia. Thus, some of the ...

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Relationship Between Microflow, Local Tissue Po2 and Extracellular Activities of Potassium and Hydrogen Ions in the Cat Brain During Intraarterial Infusion of Ammonium Acetate

Cited by 4 publications

References 10 publications

Oxygen distribution and consumption in the cat retina during normoxia and hypoxemia.

Oxygen distribution and consumption in the cat retina during normoxia and hypoxemia.

Glial Alkalinization Detected In Vivo by ¹H‐¹⁵N Heteronuclear Multiple‐Quantum Coherence‐Transfer NMR in Severely Hyperammonemic Rat

Methionine Sulfoximine, a Glutamine Synthetase Inhibitor, Attenuates Increased Extracellular Potassium Activity during Acute Hyperammonemia

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Relationship Between Microflow, Local Tissue Po2 and Extracellular Activities of Potassium and Hydrogen Ions in the Cat Brain During Intraarterial Infusion of Ammonium Acetate

Cited by 4 publications

References 10 publications

Oxygen distribution and consumption in the cat retina during normoxia and hypoxemia.

Oxygen distribution and consumption in the cat retina during normoxia and hypoxemia.

Glial Alkalinization Detected In Vivo by 1H‐15N Heteronuclear Multiple‐Quantum Coherence‐Transfer NMR in Severely Hyperammonemic Rat

Methionine Sulfoximine, a Glutamine Synthetase Inhibitor, Attenuates Increased Extracellular Potassium Activity during Acute Hyperammonemia

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Glial Alkalinization Detected In Vivo by ¹H‐¹⁵N Heteronuclear Multiple‐Quantum Coherence‐Transfer NMR in Severely Hyperammonemic Rat