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

Abstract

Phillips, Shaun W., Gerard L. Gebber, and Susan M. Barman. Medullary lateral tegmental field: control of respiratory rate and vagal lung inflation afferent influences on sympathetic nerve discharge. Am J Physiol Regul Integr Comp Physiol 288: R1396 -R1410, 2005. First published December 16, 2004; doi:10.1152/ajpregu.00632.2004.-We used spectral analysis and event-triggered averaging to determine the effects of chemical inactivation of the medullary lateral tegmental field (LTF) on 1) the relationship of intratracheal pressure (ITP, an index of vagal lung inflation afferent activity) to sympathetic nerve discharge (SND) and phrenic nerve activity (PNA) and 2) central respiratory rate in paralyzed, artificially ventilated dial-urethane-anesthetized cats. ITP-SND coherence value at the frequency of artificial ventilation was significantly (P Ͻ 0.05; n ϭ 18) reduced from 0.73 Ϯ 0.04 (mean Ϯ SE) to 0.24 Ϯ 0.04 after bilateral microinjection of muscimol into the LTF. Central respiratory rate was unexpectedly increased in 12 of these experiments (0.28 Ϯ 0.03 vs. 0.95 Ϯ 0.25 Hz). The ITP-PNA coherence value was variably affected by chemical inactivation of the LTF. It was unchanged when central respiratory rate was also not altered, decreased when respiratory rate was increased above the rate of artificial ventilation, and increased when respiratory rate was raised from a value below the rate of artificial ventilation to the same frequency as the ventilator. Chemical inactivation of the LTF increased central respiratory rate in four of six vagotomized cats but did not significantly affect the PNA-SND coherence value. These data demonstrate that the LTF 1) plays a critical role in mediating the effects of vagal lung inflation afferents on SND but not PNA, 2) helps maintain central respiratory rate in the physiological range, but 3) is not involved in the coupling of central respiratory and sympathetic circuits. cardiorespiratory synchronization; dorsal respiratory group; HeringBreuer reflex; phrenic nerve activity; respiratory-related rhythm; ventral respiratory group IT HAS LONG BEEN RECOGNIZED that neural mechanisms controlling the respiratory and cardiovascular systems are tightly linked (25,34,38,49,55). This interaction facilitates the complementary functions of the two systems: respiration maintains appropriate levels of arterial blood gases, while the cardiovascular system transports these gases to and from tissues. One indication of this cardiorespiratory coordination was noted by Adrian et al. (1) in 1932 when they made the first recordings of sympathetic nerve discharge (SND). They found that the amplitude of the cardiac-related bursts of SND waxed and waned on the time scale of the respiratory cycle. 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 bo...

Medullary lateral tegmental field mediates the cardiovascular but not respiratory component of the Bezold-Jarisch reflex in the cat

“…Specifically, blockade of N-methyl-Daspartate (NMDA) receptors in the LTF significantly reduced baroreceptor-mediated inhibition of SND and the cardiacrelated rhythm in SND (26), whereas blockade of non-NMDA EAA receptors reduced the increases in SND produced by activation of arterial chemoreceptors and electrical stimulation of afferents in the cervical vagus nerve (27). Also, we showed that chemical inactivation of the LTF with microinjection of muscimol eliminated the component of SND time-locked to intratracheal pressure (ITP, an index of vagal lung inflation afferent activity) without disrupting the entrainment of phrenic nerve activity (PNA) to ITP (29). These data led us to postulate that the LTF was involved in mediating changes in SND elicited by activation of all afferents whose primary site of termination is in the NTS.…”

“…As was the case in earlier studies (26,29), we maintained mean arterial pressure (MAP) at approximately the same level throughout the experiment by adjusting the rate of an intravenous infusion of a mixture of dextran and saline. This was done to maintain a reasonably stable level of baroreceptor afferent nerve activity.…”

“…The inferior cardiac postganglionic branch of the left stellate ganglia was exposed retropleurally by removing the head of the first rib (13), and the right phrenic nerve was isolated in the neck (29). The nerves were covered with silicone release agent (Dow Corning 7 compound).…”

“…We considered this possibility in light of recent work from our laboratory (26,27,29) and a study by Vayssettes-Courchay et al (37). Vayssettes-Courchay et al (37) suggested that the cat LTF was involved in mediating this reflex because some LTF neurons with activity correlated to SND responded to right atrial administration of PBG.…”

“…However, they did not determine whether chemical inactivation of the LTF blocked the cardiovascular and respiratory components of the Bezold-Jarisch reflex. Investigations from our laboratory (26,27,29) have shown that LTF neurons in the cat are elements of the medullary pathways that mediate baroreceptor, chemoreceptor, and vagal afferent influences on SND. Specifically, blockade of N-methyl-Daspartate (NMDA) receptors in the LTF significantly reduced baroreceptor-mediated inhibition of SND and the cardiacrelated rhythm in SND (26), whereas blockade of non-NMDA EAA receptors reduced the increases in SND produced by activation of arterial chemoreceptors and electrical stimulation of afferents in the cervical vagus nerve (27).…”