Abstract

The effect of an approximately 2 C rise in body temperature on arterial and cerebrospinal fluid (CSF) lactate concentration, pH, Pco2, and [HCO3–] was studied in eight artificially ventilated dogs maintained at constant end-tidal Pco2. The combined effect of hyperthermia and intravenous lactic acid infusion on CSF lactate concentration was also studied in three additional dogs. In normothermia the lactate concentration, Pco2, and [HCO3–] in the CSF were significantly higher than in arterial blood, whereas CSF pH was significantly lower than arterial pH. Rise in body temperature at constant end-tidal (and arterial) Pco2 resulted in no significant change in lactate concentration of blood or CSF, a parallel fall in arterial and CSF pH, a decrease in both arterial and CSF [HCO3–], and a rise in CSF PCO2. An intravenous lactic acid infusion had no measurable effect on CSF lactate concentration. A general entrance of lactate ion into the CSF from blood or brain does not appear to play a role in respiratory control during hyperthermia. The possibility remains that lactate enters CSF during exercise but from the brain rather than from the circulating blood. Limitations of the conventional pH scale preclude assessment of changes in hydrogen ion activity during hyperthermia.

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