Abstract
The ‘constant pH’ strategy of hibernators involves loading considerable amounts of CO2 during the entrance into hibernation, and hyperventilating to eliminate this CO2 during the arousal. Together with the decrease of blood alpha imidazole, this indicates that the blood pH and \({P_{c{o_2}}}\) observed in hibernation result from the combined effects of a respiratory acidosis and a change in temperature. The respiratory acidosis also affects most intracellular compartments of the body, except for the heart and liver, in which a metabolic compensation takes place, resulting in a nearly constant alpha imidazole. Respiratory acidosis exerts inhibitory influences on various nervous and metabolic processes, and probably contributes to the great amplitude of regulation of metabolic rate characteristic of hibernation. The inhibition would be at least partly removed early in the arousal by hyperventilation, while during deep hibernation heart and liver would be protected by the alphastat control of intracellular pH. Our ignorance of the mechanisms ensuring the selective inhibition or facilitation of pHi regulation according to tissues precludes the clinical application of the hibernation model.
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Malan, A. (1985). Acid-base regulation during hibernation. In: Rahn, H., Prakash, O. (eds) Acid-Base Regulation and Body Temperature. Developments in Critical Care Medicine and Anesthesiology, vol 10. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-5004-7_3
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DOI: https://doi.org/10.1007/978-94-009-5004-7_3
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