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The role of hypercapnia in terminating trigeminal (Vth) nerve inhibition of respiration is not clear. Phrenic nerve responses to Vth nerve stimulation were examined during eucapnia and hypercapnia. We hypothesized that hypercapnic stimulation might not be sufficient to overcome the inhibitory effects of the Vth nerve, and thus would fail to restore respiratory center output to baseline values. Isolated rat brainstem-spinal cord preparations from newborn rats were placed in a tissue bath and superfused with modified Krebs solution at 27 degrees C. Respiratory related activity was recorded from cut C1 or C5 ventral roots. Tonic stimulation of the Vth nerve (1 Hz for 15 min) under eucapnic conditions initially inhibited the frequency of respiratory activity over the first 1-2 min, followed by partial recovery after 4 min to 50-60% of the control level. Stimulation of the Vth nerve at 0.5 Hz initially decreased the respiratory frequency to about 40% of baseline over the first 3 min, which then increased to control levels within 6 min despite continued Vth nerve stimulation. Exposure to hypercapnia (15 KPa PCO2) increased the baseline respiratory frequency. However, hypercapnic stimulation only partially reduced the degree of the Vth nerve inhibitory effect. We conclude that 15 KPa PCO2 only partially reverses the inhibitory effect of the Vth nerve stimulation at the level of the central respiratory controller.

EFFECT OF CO2 ON Vth NERVE INHIBITION OF RESPIRATION IN ISOLATED RAT NERVOUS SYSTEM