The pattern of sympathetic neurone activity during expiration in the cat.

Abstract

SUMMARY1. The properties of sympathetic preganglionic neurone activity during expiration were studied in pentobarbitone-anaesthetized (n = 26) and in non-anaesthetized, mid-collicular decerebrate (n = 5), paralysed, artificially ventilated cats in which the electrical activity of the phrenic nerve and of the cervical sympathetic trunk was recorded.2. In control conditions (end-tidal Pco, between 35 and 40 mmHg, zero endexpiratory pressure) sympathetic activity during expiration was either steady at a low level (n = 11) or showed a modest progressive increase from a low level in early expiration (n = 17). Very infrequently (n = 3), it showed a transient increase during the second half of expiration.3. Artificial ventilation with positive end-expiratory pressures in the range from 2-1 +0 4 (mean+ S.D.) to 6-7 +0-6 cmH2O caused, in cats with intact vagus nerves, an increase in sympathetic neurone activity during the second half of expiration. Within this range of pressures, the magnitude of the increase was related to the magnitude of the positive end-expiratory pressure. This effect reversed at higher positive end-expiratory pressures. Pressures in excess of 10-2 + 1-8 cmH2O caused inhibition of sympathetic activity.4. The sympatho-excitatory effect of positive end-expiratory pressure disappeared after bilateral cervical vagotomy. With intact vagus nerves, it also disappeared at levels of systemic hypocapnia (end-tidal PCO2 < 15 mmHg) which abolished phrenic nerve activity. In hypocapnia, artificial ventilation with peak tracheal pressures greater than 7-2 + I1 cmH2O caused inhibition of sympathetic activity, while ventilation with lower end-expiratory pressures had no effect on sympathetic activity. It may be concluded that the sympatho-excitatory effect of positive end-expiratory pressure is mediated by vagal afferents and requires a certain level of brain-stem respiratory neurone activity.5. Sympatho-excitation during expiration was also observed, in normocapnic conditions, during short-duration static lung inflation with tracheal pressures in the range from 2-5 + 0-3 to 7-0 + 0-8 cmH2O as well as during artificial ventilation with zero end-expiratory pressure when lung inflation occurred in expiration. These responses were abolished by bilateral cervical vagotomy and during systemic hypocapnia.6. Sympatho-excitation during expiration was also observed when systemic M. BACHOO AND C. POLOSA hypercapnia was produced in vagotomized cats by artificial ventilation with gas mixtures containing 5 or 10 % CO2.7. These results can be explained by the hypothesis that some brain-stem expiratory neurones are a source of facilitatory synaptic input to sympathetic neurones. The activity of brain-stem expiratory neurones is known to be enhanced by moderate degrees of lung inflation and by increased chemical drive. Under these conditions sympathetic neurone activity would be expected to increase during expiration.

Respiratory modulation of muscle sympathetic nerve activity in intact and lung denervated humans.

“…After vagotomy, however, most of the inspiratory-related inhibitory phase is removed and sympathetic activity actually rises throughout this phase, peaking at end inspiration. 8,9,27 To test the role of vagal feedback in humans, we used the heart-lung transplant patient as a model of pulmonary vagal denervation. Lung transplantation interrupts the pulmonary branch of the vagus nerve but retains a native tracheal remnant above the carina.…”

Medullary lateral tegmental field: control of respiratory rate and vagal lung inflation afferent influences on sympathetic nerve discharge

“…The extent to which each type of vagal inflation afferent participated in the synchronization of SND to ITP and the entrainment of PNA to lung inflation remains unclear. Nonetheless, whether the afferents are the same or different, our results provide new information on the question of whether vagal lung inflation afferent activity alters SND not only indirectly via their actions on respiratory networks but also via a more direct pathway to sympathetic neurons (4,59).…”

“…There are at least two sources of respiratory modulation of SND: input from vagal lung inflation afferents and an influence of the respiratory rhythm generator on central sympathetic neurons (4 -6, 21, 25, 33-35, 59). Although some investigators (38,49) have proposed that there is a common network controlling both respiratory and cardiovascular functions, others have suggested that cardiorespiratory synchronization reflects both the direct coupling of two distinct central networks and shared input from peripheral afferents (4,6,21,59).…”

“…In addition to controlling respiration, activation of pulmonary stretch receptors has been shown to inhibit or excite SND, depending on the volume of lung inflation (4,21,59). Anatomic and electrophysiological studies (25,27,58) show that pulmonary vagal afferents terminate in the nucleus of the tractus solitarius (NTS).…”

Central respiratory modulation of subretrofacial bulbospinal neurones in the cat.

“…4A). Whether this represented early inspiratory depression (Bainton et al 1985) or the end of a period of expiratory excitation (Bachoo & Polosa, 1986) was not determined.…”