Abstract

Experiments were performed on decerebrate or urethane-anesthetized, gallamine-paralyzed cats with pneumothorax and intact vagi. Efferent splanchnic and cervical sympathetic nerve discharges were recorded monophasically (0.2–1000 HZ). Phrenic nerve discharge served as an indicator of respiratory center output. Lung inflation was applied co-incidentally with phrenic discharge during control cycles by means of a cycle-triggered pump. Changes in the timing of cycle-triggered pump inflations were used to evaluate effects of pulmonary afferent activity from lung stretch receptors on central respiratory modulation of sympathetic discharge. When inflation was not applied for one inspiratory phase, the Breuer-Hering inspiratory-inhibitory reflex did not occur: inspiratory prolongation with no change in slope of the integral of phrenic activity, as measured with an average-response computer. In contrast, this test produced an increase in slope of the integrated sympathetic discharge. This indicates that inflations during the control inspiratory phases inhibited sympathetic discharge. The striking difference in the slope of phrenic vs sympathetic activities implies that this inhibition of sympathetic activity was acting via circuits different from, but related to, those of the Breuer-Hering reflex. Lung inflation also inhibited sympathetic discharge during the expiratory phase, since inflations applied during the expiratory phase reduced sympathetic discharge, concomitantly with lengthening of the expiratory phase (Breuer-Hering expiratory-facilitatory reflex). The latency for sympathetic inhibition from the onset of inflation was of the order of 100–200 ms both for inspiratory and expiratory inflations. Vagotomy abolished these effects and resulted in an increased respiratory modulation of sympathetic discharge. These results indicate that pulmonary afferent activity exerts an important influence on the central respiratory modulation of sympathetic discharge.

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