Effect of inactivation of carotid sinus nerve by cold block on phrenic nerve activity in cats.

The effect of the elimination of input via the carotid chemoreceptor on respiratory output was examined quantitatively in anesthetized, vagotomized, and paralyzed cats. The integrated phrenic nerve activity (PNA) was recorded as an indication of output of the respiratory center. Also, the elimination of the carotid chemoreflex drive was repeatedly done by a cold block of the carotid sinus nerve at various PCO2 levels during hyperoxia, normoxia, and hypoxia. The blockade induced a reduction in PNA at each PCO2 level in every PO2 group. If the highest PNA value recorded at a high PCO2 in each PO2 condition was assigned a value of 100%, the reduction of the PNA by the blockade, i.e., the respiratory effect of the carotid chemoreflex drive, would be slightly larger during normoxia (16%) than during hyperoxia (8.7%), but would be independent of PCO2. During hypoxia, this chemoreflex effect was about 40% of a low PCO2, and decreased with increments of PCO2, finally reaching about 20% of a high PCO2 level. Furthermore, the relative contribution of the carotid chemoreceptor to respiratory output, expressed as the ratio of the PNA reduction during blockade to the PNA before blockade, was inversely proportional to both PO2 and PCO2. It is concluded that the interaction of the peripheral and central chemoreceptor drive is hypoadditive at moderate and high PCO2 levels in anesthetized cats, and this interaction is emphasized by central hypoxia.