Neural respiratory and circulatory interaction during chemoreceptor stimulation and cooling of ventral medulla in cats.

The effects on respiratory and sympathetic neural activity, measured as integrated phrenic and cervical nerve activities respectively, during changing input from the central chemoreceptors was studied in anaesthetized, paralysed cats whose carotid sinus nerves and vagus nerves had been cut. Central respiratory drive was altered either by graded cold block of the intermediate areas, located bilaterally near the ventral surface of the medulla oblongata, or by step increases in end-tidal PCO2. Cervical nerve activity showed both a tonic (or mean) level of activity and a prominent cyclic discharge that was in phase with phrenic nerve activity. Graded focal cooling of the intermediate areas to 20 degrees C when end-tidal PCO2 was kept constant caused progressive decreases in phrenic activity, the amplitude of the inspiratory related discharge and mean arterial pressure, but only a small decrease in mean cervical nerve activity. Cooling the intermediate areas in the absence of the inspiratory related discharge (i.e. when phrenic activity was below the apnoeic threshold) led to a much smaller decrease in arterial pressure. Step increases of end-tidal PCO2 caused progressive increases of both cervical and phrenic nerve activities. The increase in cervical activity was due primarily, if not wholly, to a progressive increase in the amplitude of the inspiratory related discharge. These findings show that the predominant effect on sympathetic activity during stimulation of the central chemoreceptor and graded cold block of the intermediate areas is a change in the amplitude of the inspiratory related discharge and suggest that the change in arterial pressure that accompanies central chemoreceptor stimulation and graded cold block of the intermediate areas is mediated by the inspiratory related discharge rather than by an increase in the mean level of sympathetic activity. When phrenic activity was lowered to below apnoeic threshold by cooling the intermediate areas, step increases in end-tidal PCO2 caused inhibition rather than stimulation of cervical nerve activity. This finding indicates that sympathetic neurones are not activated by central chemoreceptor input directly, but rather indirectly via intracranial connexions with neuronal networks involved in regulation of respiration.