RELATIONSHIP BETWEEN INTRACELLULAR PH, EXTRACELLULAR PH, AND VENTILATION DURING DILUTION ACIDOSIS

Previous experiments showed that acute hyperosmolality results in an extracellular acidosis that does not stimulate respiratory compensation (C. E. Kasserra, D. R. Jones, and M. R. Hughes. Respir. Physiol. 85: 383-393, 1991). The data suggested that development of the extracellular dilution acidosis would also result in a concomitant intracellular contraction alkalosis. The effects of acute hyperosmolality and lactacidosis on systemic intracellular pH (pH(i)) were studied in the conscious Pekin duck in an effort to separate the effects of pH(e) and extracellular pH (pH(i)) on ventilatory control. Brain pH was also measured during systemic hyperosmolality to determine the relationship between blood and brain pH(i). Hyperosmolality caused a concurrent extracellular acidosis and intracellular alkalosis in pectoral muscle, whereas lactic acid infusion decreased both pH(e) and pH(i). Ventilation was stimulated only during lactacidosis and did not change during hyperosmolality. Brain pH(i) did not show a consistent significant increase in response to systemic hyperosmolality over I h but did show a trend toward an alkalosis. Measurement of high-energy phosphate metabolites (phosphocreatine, ATP, and P-i) indicated an increase of metabolic rate during hyperosmolality. With the assumption that similar pH(i) changes were occurring in chemoreceptive cells, the results suggest that ventilation was responding to pH(i) changes and that much of the depressive response to acute hyperosmotic disturbance was peripherally generated.