Lack of Ventilatory Reaction to Endogenous and Exogenous Metabolic Brain-Stem Acidosis
It is generally assumed that metabolic acid-base disturbances in the extracellular body fluids are compensated by adjustment of the arterial Pco2 through pulmonary ventilation. Since the pH of the extracellular fluid (ECF) is one of the most accurately controlled variables, Winterstein1 postulated the H+-ions dissociated either from carbonic acid or from non-volatile acids as being the unique stimulus for the chemical control of breathing (Reaction Theory). Loeschcke2 adapted this theory to the central chemosensitive system and conducted a considerable amount of experiments supporting the ECF-pH at the ventral surface of the medulla oblongata to be the essential chemical signal to drive pulmonary ventilation. Indeed, ventilation in cats was highly sensitive against ECF-pH changes at the ventral medullary surface, if induced by CO2-inhalation2, 3. Unexpectedly, we did not observe any ventilatory reaction to even more pronounced ECF-pH changes if caused by post-hypoxic lactacidosis after carotid chemodenervation3. Endogenous accumulation of organic acid thus failed to drive ventilation, unlike exogenous infusion of strong anorganic acids4, 5, 6. Therefore, in the present study, the ventilatory reaction to equimolar plasma lactic acid concentrations was compared, either endogenously developed during a limited period of hypoxia or exogenously induced by intravenous infusion.
KeywordsLactic Acid Metabolic Acidosis Medulla Oblongata Pulmonary Ventilation Transient Release
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