Effects of carbon dioxide, bicarbonate and pH on lactate and pyruvate in the brain of rats

Weyne, J; Demeester, G; Leusen, I

doi:10.1007/bf00592288

Cited by 35 publications

(8 citation statements)

References 40 publications

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“…Under these conditions there was an elevation of brain lactate comparabIe to the elevation we observed during sleep in Group A. One possible explanation for this effect is that anxious animals hyperventilate and reduce blood pCOz which in turn leads to cerebral vasoconstriction and tissue anoxia (WEYNE, DEMEESTER and LEUSEN, 1970), but our rats in Group A did not appear to hyperventilate. Furthermore, the data were not consistent with anoxia, as already mentioned, particularly since the ratios of lactate to pyruvate did not change.…”

Section: Discussionsupporting

confidence: 39%

Metabolism of Brain During Sleep and Wakefulness

Reich

Geyer

Karnovsky

1972

Journal of Neurochemistry

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Abstract— The levels in brain of lactate, pyruvate, creatine phosphate, ATP, ADP and AMP were examined in sleeping and waking adult rats. The animals were monitored electrophysiologically and the biochemical measurements were made after approx. 25 min of sleep or wakefulness. The previous treatment of the animals had a marked effect on the levels of brain metabolites during sleep. In animals not acclimatized to the observation chamber, brain levels of lactate and pyruvate rose during sleep above those in the waking state: creatine phosphate and ATP were depressed somewhat. When the animals were acclimatized by being placed in the observation chamber for at least 2 h on four or more consecutive days prior to the experiment, sleep was accompanied by a depression of brain levels of lactate and pyruvate and slight elevations of brain levels of creatine phosphate and ATP. No significant differences in the EEG recordings were noted between the sleeping rats of the acclimatized and non‐acclimatized groups. These observations on the effect of acclimatization on brain metabolism during sleep may have clinical relevance in man.

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Section: Discussionsupporting

confidence: 39%

Metabolism of Brain During Sleep and Wakefulness

Reich

Geyer

Karnovsky

1972

Journal of Neurochemistry

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“…Carbon dioxide administration was not associated with alterations in brain tissue ATP, ADP, or AMP concentrations in these studies. However, greatly elevated LPR levels did not appear until PaCO 2 reached extremely high levels [122][123][124][125][126] Hypothyroidism There appears to be an inverse relationship between thyroid function and LPR. Hypothyroid patients can have elevated blood LPR, and hyperthyroid patients can have abnormally low LPR [127,128].…”

Section: Hypercapniamentioning

confidence: 91%

Potential Non-Hypoxic/Ischemic Causes of Increased Cerebral Interstitial Fluid Lactate/Pyruvate Ratio: A Review of Available Literature

2011

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Microdialysis, an in vivo technique that permits collection and analysis of small molecular weight substances from the interstitial space, was developed more than 30 years ago and introduced into the clinical neurosciences in the 1990s. Today cerebral microdialysis is an established, commercially available clinical tool that is focused primarily on markers of cerebral energy metabolism (glucose, lactate, and pyruvate) and cell damage (glycerol), and neurotransmitters (glutamate). Although the brain comprises only 2% of body weight, it consumes 20% of total body energy. Consequently, the ability to monitor cerebral metabolism can provide significant insights during clinical care. Measurements of lactate, pyruvate, and glucose give information about the comparative contributions of aerobic and anaerobic metabolisms to brain energy. The lactate/pyruvate ratio reflects cytoplasmic redox state and thus provides information about tissue oxygenation. An elevated lactate pyruvate ratio (>40) frequently is interpreted as a sign of cerebral hypoxia or ischemia. However, several other factors may contribute to an elevated LPR. This article reviews potential non-hypoxic/ischemic causes of an increased LPR.

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“…Weyne et al (1970) have shown that decreasing blood pH reduces brain lactate concentration, so the observed change in plasma pH may have partly counteracted the ammonium-induced increases in lactate. Infusion of NaCl did not change plasma pH by more than 0.05 U.…”

Section: Blood Pressure and Vascular Resistancementioning

confidence: 99%

The Ammonium-Induced Increase in Rat Brain Lactate Concentration is Rapid and Reversible and is Compatible with Trafficking and Signaling Roles for Ammonium

Provent

Kickler

Barbier

et al. 2007

J Cereb Blood Flow Metab

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The glutamate-glutamine shuttle requires a flux of fixed N from neurons to astrocytes. The suggestion that some or all of this N is ammonium has received support from reports that ammonium (as NH 4 + ) rapidly enters astrocytes. Ammonium might also help control astrocyte energy metabolism by increasing lactate production. If ammonium has these functions, then its effect on brain metabolism must be rapid and reversible. To make a minimal test of this requirement, we have followed the time courses of the changes induced by a 4 min venous infusion of 1 mol/L NH 4 Cl, 2.5 mmol/kg body weight, in rat. Extracellular [NH 4 + ] in cortex, monitored with ion-selective microelectrodes, reached a peak of approximately 0.7 mmol/L 1.65 mins after the end of the infusion, then recovered. Brain metabolites were monitored non-invasively every 4 mins by 1 H magnetic resonance spectroscopy. Lactate peak area during the 3.2 min acquisition starting at the end of the infusion was 1.8460.24 times baseline (6s.e.m., P = 0.009, n = 9). Lactate increased until 13.262.1 mins after the end of the infusion and recovered halfway to baseline by 31.2 mins. Glutamate decreased by at least 7.1% (P = 0.0026). Infusion of NaCl caused no change in lactate signal. Cerebral blood flow, measured by arterial magnetization labeling, more than doubled, suggesting that the lactate increase was not caused by hypoxia. At least three consecutive ammonium-induced increases in lactate signal could be evoked. The results are compatible with an intercellular trafficking/signaling function for ammonium.

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Effects of carbon dioxide, bicarbonate and pH on lactate and pyruvate in the brain of rats

Cited by 35 publications

References 40 publications

Metabolism of Brain During Sleep and Wakefulness

Metabolism of Brain During Sleep and Wakefulness

Potential Non-Hypoxic/Ischemic Causes of Increased Cerebral Interstitial Fluid Lactate/Pyruvate Ratio: A Review of Available Literature

The Ammonium-Induced Increase in Rat Brain Lactate Concentration is Rapid and Reversible and is Compatible with Trafficking and Signaling Roles for Ammonium

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