Studies on Phrenic Nerve Activity during Acute Non-Respiratory Acidosis in the Rabbit

In urethane anesthetized rabbits, arterial hydrogen ion concentration ([H^+]a) was altered by slow intravenous injection of 0.3 N HCl under the clamp of CO_2 concentration in end-expiratory air (F_ECO_2). Central respiratory activity of these preparations was monitored through phrenic nerve discharge. Under vagotomy and peripheral chemodenervation, [H^+]a increase above normal induced the fall of respiratory frequency. This fall was manifested by the prolongation in expiratory duration (T_E) but not by the prolongation in inspiratory duration (T_I). Contrary, the phrenic discharge height (A; correspond to tidal volume, V_T) increased gradually. These results seem to suggest that in acute non-respiratory acidosis the central chemoreceptors play respiratory compensation not through the control of respiratory frequency but through the control of V_T. Therefore, regulations of respiratory frequency and V_T may take place at different regions in the central nervous system. It may be speculated that respiratory frequency-related chemoreceptor is located deep in the brain which is affected by arterial blood, while V_T related-chemoreceptor is located on the surface of the brain which is affected by cerebro-spinal fluid (CSF) because response time lag was recognized in respiratory frequency and V_T. With vagotomy and intact peripheral chemoreceptors, respiratory frequencies remained at control value with constant T_I and T_E during the increase in [H^+]a. However, after starting acid injection, magnitude of phrenic discharge activity increased rapidly and reached the peak in about 20 min. Therfore, peripheral chemoreceptors, recovered respiratory frequency to the control level and incresed the V_T simultaneously. It is concluded that in acute non-respiratory acidosis the peripheral chemoreceptors play more urgent, important and essential role for respiratory compensation than the central chemoreceptors do