Abstract
Extract: Survival after 5 min of anoxia in 39 controls (8–12-day-old mice) was only 5% compared with 82% in 39 glucose-treated littermates. Even after decapitation there was a delay in the onset of terminal gasping in the isolated heads of glucose-treated animals (P = 0.03) and the last gasp occurred much later than in the heads of control animals (P < 0.001). To study the mechanism of this phenomenon mice were injected with 30 mmol/kg glucose subcutaneously. Control animals were given equiosmolal amounts of NaCl. One hour later the animals were exposed to nitrogen gas (O2 pressure < 5 mm Hg). In glucose-treated mice the initial glucose concentration in brain was 3 times the control value (P < 0.001). ATP, P-creatine, and glycogen levels were unchanged. Although the rate of use of these compounds during anoxia was similar in both groups of mice, the high level of glucose in brain in glucose-treated mice permitted considerable sparing of these energy-yielding metabolites. In terms of actual and potential molar equivalents of high energy phosphate (~P), the brain energy reserve after 4 min of anoxia in glucose-treated animals was twice that of controls, 10.70 ± 0.72 versus 4.75 ± 1.19 mmol/kg (P = 0.009).
Speculation: During acute anoxia, concentration of glucose in brains of young animals is critically reduced, although levels of glucose in plasma remain normal or may even become elevated. Pretreatment or concurrent administration of glucose increases anoxic survival. Because glucose has this dramatic life-saving effect in anoxic animals, the possibility that inadequate brain glucose supplies may occur in anoxic man in the face of normal or elevated levels of glucose in plasma should be considered.
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Holowach-Thurston, J., Hauhart, R. & Jones, E. Anoxia in Mice: Reduced Glucose in Brain with Normal or Elevated Glucose in Plasma and Increased Survival after Glucose Treatment. Pediatr Res 8, 238–243 (1974). https://doi.org/10.1203/00006450-197404000-00004
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DOI: https://doi.org/10.1203/00006450-197404000-00004
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