Pulmonary Afferent Influences on Respiratory Modulation of Sympathetic Discharge

Gootman, Phyllis M.; Feldman, Jack L.; Cohen, Morton I.

doi:10.1007/978-3-642-67603-1_20

Cited by 20 publications

(12 citation statements)

References 10 publications

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“…It must be mentioned that when inflation pressures in excess of 10-2 cmH20 were used, inhibition, rather than excitation, of sympathetic activity in expiration occurred (Fig. 6), as previously shown by Gootman, Feldman & Cohen (1980). When the animal was ventilated with peak tracheal pressure of 7 cmH2O at various repetition rates,…”

Section: Sympathetic Activity In Expirationsupporting

confidence: 51%

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

Bachoo¹,

Polosa²

1986

The Journal of Physiology

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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.

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Section: Sympathetic Activity In Expirationsupporting

confidence: 51%

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

Bachoo¹,

Polosa²

1986

The Journal of Physiology

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“…In anaesthetized animals, inflation of the lungs causes reflex reductions of sympathetic nerve activity and vascular resistance in muscles (Gerber & Polosa, 1978; Gootman et al 1980; Citterio & Agostoni, 1983; Seals et al 1990). This is independent of changes in arterial blood pressure and cardiac filling pressure and is thus not mediated by cardiovascular reflexes (Gootman et al 1980; Citterio & Agostoni, 1983; Seals et al 1990; Guyenet, 2000). Others have shown that stimulation of pulmonary stretch receptors (evoked by hyperventilation) is strong enough to override the high sympathetic outflow, or vasoconstriction, evoked by chemoreceptor reflexes (for review see Marshall, 1994).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of augmented muscle vasoconstrictor drive following asphyxic apnoea in awake human subjects is not affected by relief of chemical drive

Seitz

Brown

Macefield

2012

Experimental Physiology

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New Findings r What is the central question of this study?Breath holding to the asphyxic break point causes a progressive increase in muscle sympathetic nerve activity, which is then immediately inhibited on the resumption of breathing, presumably due to relief of the elevated chemical drive. The purpose of this study was to determine whether lung inflation per se, rather than the relief from hypoxia and hypercapnia, is responsible for the inhibition of muscle sympathetic nerve activity after an end-expiratory apnoea. r What is the main finding and its importance?We show in human subjects that the duration of this inhibition is the same whether the apnoea is terminated by taking a single breath of room air or of 100% N 2 or 10% CO 2 + 90% N 2 . Given that there will be no inhibition of chemoreceptors in the latter two conditions, we conclude that lung inflation itself causes the inhibition of muscle vasoconstrictor drive.Progressive asphyxia, produced by a prolonged voluntary breath hold (end-expiratory apnoea), evokes large bursts of muscle sympathetic nerve activity (MSNA). These bursts increase in amplitude until the asphyxic break point is reached, at which point the bursts are inhibited. We tested the hypothesis that lung inflation, rather than relief from hypoxia and hypercapnia, is responsible for the inhibition of MSNA. Multiunit MSNA was recorded from motor fascicles of the common peroneal nerve in 11 subjects. Following a period of quiet breathing, subjects were instructed to behave as follows: (i) to hold their breath in expiration for as long as they could (mean duration 32.3 ± 1.9 s); (ii) to take a single breath of room air, 100% N 2 or 10% CO 2 + 90% N 2 at the asphyxic break point; (iii) to exhale and continue the apnoea until the next break point; and then (iv) to resume breathing. All subjects reported relief during inhalation of any gas, and could continue holding their breath for a further 30.7 ± 2.8 s with room air, 18.6 ± 1.7 s with N 2 and 11.8 ± 1.8 s with 10% CO 2 + 90% N 2 . Despite the exaggerated chemoreceptor drive in the latter two conditions (hence the significantly shorter latencies to the subsequent asphyxic break point), the inhibition still occurred; moreover, there was no significant difference in duration of the inhibition of MSNA following the single breath of room air (7.6 ± 0.7 s), N 2 (6.2 ± 0.6 s) or 10% CO 2 + 90% N 2 (5.5 ± 0.4 s). Following the resumption of breathing, however, the duration of MSNA inhibition (11.0 ± 1.0 s) was significantly longer than that following a single breath. To investigate the involvement of chemoreceptors in the respiratory modulation of MSNA

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

Seals

Suwarno

Joyner

et al. 1993

Circulation Research

155

142

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We determined the influences of breathing-induced changes in intrathoracic and intravascular pressures, central respiratory drive, and pulmonary vagal feedback on the within-breath variation in skeletal muscle sympathetic nerve activity (MSNA) in humans. MSNA (peroneal microneurography), arterial blood pressure (Finapres finger monitor), and tidal volume (VT) were recorded continuously in six normal subjects and four heart-lung transplant patients during: 1) spontaneous air breathing; 2) increased FiCO2; 3) voluntary augmentation of VT with and without inspiratory resistance; and 4) positive pressure, passive mechanical ventilation. During conditions 3 and 4, which were performed under isocapnic conditions with a high MSNA background (either high resting activity or nonhypotensive lower body suction), subjects breathed at control or elevated VT with normal or prolonged inspiratory time (TI); breathing frequency was 12 breaths per minute. During control breathing in normal subjects there was a distinct within-breath pattern of MSNA, with "701O of the activity occurring during low lung volumes (initial half of inspiration and latter half of expiration). This within-breath variation of MSNA was potentiated with increased VT breathing (>85% of activity occurring during low lung volumes; p

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Pulmonary Afferent Influences on Respiratory Modulation of Sympathetic Discharge

Cited by 20 publications

References 10 publications

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

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

Inhibition of augmented muscle vasoconstrictor drive following asphyxic apnoea in awake human subjects is not affected by relief of chemical drive

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

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