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At least 19 recordsLinked to original sources
PubMed1975

Vagal modulation of respiratory control during exercise.

Vagal modulation of chemical control of ventilation during rest and exercise was studied in 15 anesthetized mongrel dogs. Arterial chemical stimuli--hypoxic, hypercapnic or a combination of both, increased ventilation by increasing both rate and depth of breathing during rest and exercise in the intact dogs. After bilateral vagotomy chemical drive increased ventilation mostly by depth and little by rate. The ventilatory response to the chemical drive, therefore, reached a plateau when tidal volume approached its maximal value ata relatively unchanged breath frequency. Muscular exercise, however, largely restored frequency response in the vagotomized animals. Since the rate response to chemical stimuli but not to exercise was impaired by vagotomy, we concluded that hyperpnea of exercise could occur through a mechanism not shared by the chemical control of ventilation. The relationship between tidal volume and breath cycle during chemical stimulation was modulated by the volume related vagal reflex. During exercise, another mechanism, presumably bulbo-pontine, is activated to influence the relationship independent of the lung volume.

Acidosis↗
PubMed1992

Vagal modulation of respiratory muscle activity in awake dogs during exercise and hypercapnia.

Using chronically instrumented awake tracheotomized dogs, we examined the contributions of vagal feedback to respiratory muscle activities, both electrical and mechanical, during normoxic hypercapnia (inspired CO2 fraction = 0.03, 0.04, 0.05, and 0.06) and during mild treadmill exercise (3, 4.3, and 6.4 km/h). Cooling exteriorized vagal loops eliminated both phasic and tonic mechanoreceptor input during either of these hyperpneas. At a given chemical or locomotor stimulus, vagal cooling caused a further increase in costal, crural, parasternal, and rib cage expiratory (triangularis sterni) muscles. No further change in abdominal expiratory muscle activity occurred secondary to vagal cooling during these hyperpneas. However, removal of mechanoreceptor input during hypercapnia was not associated with consistent changes in end-expiratory lung volume, as measured by the He-N2 rebreathe technique. We conclude that during these hyperpneas 1) vagal input is not essential for augmentation of expiratory muscle activity and 2) decrements in abdominal expiratory muscle activity may be offset by increments in rib cage expiratory muscle activity and contribute to the regulation of end-expiratory lung volume.

Afferent Pathways↗
PubMedDate not supplied

Vagal afferent modulation of nociception.

Chemical, electrical or physiological activation of cardiopulmonary vagal (cervical, thoracic or cardiac), diaphragmatic vagal (DVAG) or subdiaphragmatic vagal (SDVAG) afferents can result in either facilitation or inhibition of nociception in some species. In the rat, these effects depend upon vagal afferent input to the NTS and subsequent CNS relays, primarily in the NRM and ventral LC/SC, although specific relay nuclei vary as a function of the vagal challenge stimulus. Spinal pathways and neurotransmitters have been identified for vagally mediated effects on nociception and consistently implicate the involvement of descending 5-HT and noradrenergic systems, as well as intrinsic spinal opioid receptors. Species differences may exist with respect to both the effects of DVAG and SDVAG afferents on nociception and the efficacy of vagal afferents to modulate nociception. However, it is also possible that such differences reflect the modality of noxious input (e.g., visceral versus cutaneous), the type of neuronal activity investigated (e.g., resting versus noxious-evoked), spinal location of recording (e.g., thoracic versus lumbosacral) and/or parameters of stimulation. It is also possible that activation of some vagal afferents is aversive, but whether this contributes to changes in nociception produced by vagal activation has not clearly been established. Finally, the vagal-nociceptive networks described in this review provide a fertile area for future study. These networks can provide an understanding of physiological and pathophysiological peripheral events that affect nociception.

Afferent Pathways↗
PubMed1992

The effect of Ca2+ channel modulators on vagally induced bronchoconstriction in the guinea-pig.

The effects of N- and L-type voltage operated calcium channel (VOCC) antagonists were examined on the bronchoconstriction induced by vagal stimulation in artificially respired guinea-pigs. Vagal stimulation produced a reproducible and consistent bronchoconstrictor response which corresponded to an increase in pulmonary inflation pressure equivalent to (10.4 +/- 1.0%) of the maximum. This vagally induced rise in pulmonary inflation pressure was reduced (54% P less than 0.001) by pretreatment with atropine (1 mg/kg i.v.) and almost completely blocked by pretreatment with capsaicin (54.5 mg/kg s.c.) and atropine. omega-Conotoxin GVIA (CgTx) (5-20 micrograms/kg i.v.) caused a dose and time-related inhibition of the vagal response but did not affect either methacholine or substance P (SP)-induced bronchoconstriction. Combination studies with CgTx, atropine and capsaicin pretreatment revealed that CgTx effectively blocked both the atropine-sensitive cholinergic component and the capsaicin-sensitive non-adrenergic non-cholinergic (NANC) component of the vagal response. Selective L-type VOCC antagonists nicardipine, diltiazem and verapamil, at doses which had significant cardiovascular effects, did not reduce the rise in pulmonary inflation pressure to vagal stimulation. This study indicates that N-type VOCCs are important in controlling the release of neurotransmitters from both the cholinergic and NANC neurones within the airways of guinea-pigs.

Animals↗
PubMed1992

Respiratory-associated rhythmic firing of midbrain neurons is modulated by vagal input.

We recorded phrenic nerve activities and single unit firings of mesencephalic neurons in 19 decerebrate, paralyzed and ventilated cats, in which the spinal cord had been transected at C7-T1 and carotid sinus nerves cut but vagus nerves left intact. After we had found neurons with respiratory-associated rhythmic activity, we tested the effect of changing pulmonary vagal input by (1) stopping and restarting the ventilator; (2) changing the ventilator's tidal volume; (3) progressively cooling the vagus nerves to 6-7 degrees C; and (4) vagal section. All methods of testing yielded results that showed that vagal input, probably from pulmonary stretch receptors, tonically inhibits the respiratory-associated firing of the mesencephalic neurons by a direct mechanism that is independent of a vagal effect on medullary respiratory drive. We have suggested that these neurons are involved in the mechanism that conveys information about respiration to the cortex where it may be interpreted as the sensation of dyspnea. If so, movement and increased expansion of the lungs can be expected to lessen the sensation.

Animals↗
PubMed1992

[Somatostatin as a modulator of vagal effects on heart rhythm].

In 11 experiments on anesthetised cats burst stimulation of peripheral cut end of right vagus nerve leads to synchronization of cardiac and vagus rhythms. Alterations of burst sequence frequency within definite limits has been synchronously reproduced by heart thus creating managed bradycardia possibility. Somatostatin (10(-8)-10(-9) M intravenously) decreases heart rate and inhibits total vagus chronotropic effect. Vagolytic effect of somatostatin caused a decrease of tonic component of the vagus chronotropic effect. On the other hand, somatostatin augmented the extent of the vagal synchronizing influences and caused enlargement of the ranges of managed bradycardia. The observed results testify to participation of the peptidergic mechanisms in genesis of vagal managed bradycardia.

Animals↗
PubMed1992

[The role of mitral regurgitation in the neurovegetative regulation of mitral valve prolapse].

To define the role of mitral regurgitation (MR) on sympatho-vagal balance in mitral valve prolapse (MVP) patients, we analyzed 41 ambulatory MVP symptomatic patients. Twenty-seven patients (4 males, 23 females, aged 34 +/- 3 years) had significative MR assessed color Doppler, while 14 patients (5 males, 9 females, aged 29 +/- 3 years) had no MR; 36 age- and sex-matched subjects were studied as controls (C). Spectral analysis of heart rate variability (HRV) was performed at rest and during sympathetic activation (tilt). In the whole group of MVP patients spectral components did not differ significantly from C at rest and during tilt. When patients were subdivided in relation to the presence (+) or absence (-) of MR, HRV revealed in MR+ patients at rest an increased high frequency (HF) and a diminished low frequency (LF) component (47 +/- 5 and 41 +/- 5 normalized units, nu) with respect to C (34 +/- 3 and 54 +/- 3 nu, p < 0.05, respectively). Viceversa during tilt, in MR+ patients it was possible to observe a LF increase greater than in C (delta LF: 36 +/- 4 versus 25 +/- 3 nu, p < 0.05). As HF component is currently interpreted as a marker of vagal modulation of HRV, our results suggest an increased vagal tone associated with MR possibly due to stimulation of atrial vagal receptors; moreover, an increased sympathetic responsiveness to tilt seems to characterize MR+ patients.

Adult↗
PubMed1992

Cholecystokinin induces c-fos expression in hypothalamic oxytocinergic neurons projecting to the dorsal vagal complex.

Systemic administration of cholecystokinin (CCK) decreases gastric motility and stimulates pituitary secretion of oxytocin (OT). Although peripheral OT does not affect gastric function, increasing evidence suggests that central OT secretion acting within the dorsal vagal complex (DVC) can alter gastric motility. To evaluate whether systemically administered CCK is capable of activating oxytocinergic neurons projecting to the DVC, we utilized fluorogold retrograde labeling from the DVC in combination with c-fos and OT immunocytochemical staining to quantitatively analyze paraventricular nucleus (PVN) neurons of rats following injection of CCK at a dose known to cause maximal pituitary OT secretion (100 micrograms/kg i.p.). Our results showed that 2320 +/- 63 PVN neurons were retrogradely labeled from the DVC; 146 +/- 21 (6.3%) of these contained OT, and these cells were predominantly located in the medial parvocellular subdivision of the PVN. Of all retrogradely labeled cells, 671 +/- 112 (28.9%) expressed c-fos after CCK stimulation, and 68 +/- 14 of these (10.1%) contained OT. Approximately 50% of the OT-containing neurons retrogradely labeled from the DVC stained positively for c-fos. Many magnocellular OT neurons in the PVN that were not retrogradely labeled from the DVC also expressed c-fos after CCK stimulation. These results demonstrate that parvocellular OT neurons projecting to the DVC are co-activated along with magnocellular OT neurons projecting to the pituitary following administration of a large dose of CCK, and lend support to a possible functional role for OT as a central neurotransmitter that modulates vagal efferent traffic to the gastrointestinal tract.

Animals↗
PubMed1992

[Assessment of autonomic function by the spectral analysis of heart rate variability: an examination in a mirror drawing task].

The effect of an experimental task on autonomic function was investigated by spectral analysis of heart rate variability in 13 male college students. Power spectral density of heart rate variability has been said to contain two significant components: respiratory sinus arrhythmia (RSA) as an index of cardiac vagal activity, and Mayer wave related sinus arrhythmia (MWSA) as an index of sympathetic activity with vagal modulation. Those two components were examined during a task of mirror drawing on the CRT. In order to eliminate the effect of respiratory rate on RSA, the respiratory rate was controlled at 15 breaths/min. Furthermore, the coefficient of variance of R-R interval (CV-RR) and the fluctuation of plethysmograph (PTG) were calculated simultaneously. Results indicated that, while RSA decreased significantly, MWSA did not change during the task. On the other hand, neither CV-RR nor PTG showed any significant differences during the task. These findings indicated that cardiac parasympathetic activity was diminished in the mirror drawing task. The significance of spectral analysis of heart rate variability were discussed.

Adult↗
PubMed1978

Modulation of single vagal efferent fibre discharge by gastrointestinal afferents in the rat.

1. A single fibre dissection technique was used to record activity from efferent fibres in the left cervical vagus nerve of urethane anaesthetized rats. 2. The efferent discharge, in all units, was modulated by gastric inflation, gastric contractions or compression of the stomach wall. The receptors mediating these effects are the slowly adapting 'in-series' tension receptors in the gastric musculature with afferent fibres in the vagus nerves. 3. Efferent units were classified according to their response to passive gastric distension and active gastric contractions. 4. Four distinct types of efferent unit were isolated. Type I units were excited and Type II units were inhibited by gastric distension and contraction. Type III units were excited at low or moderate levels of inflation and inhibited at high levels of inflation or during gastric contractions. Type IV units were inhibited by low levels of inflation but excited at higher levels. 5. Since there is clearly a reciprocal organization at least of some neurones in the vagal nucleus the possibility of reciprocal control of antagonist, cholinergic and 'purinergic' vagal pathways is discussed.

Action Potentials↗
PubMed1979

The effects of PGF2 alpha on respiratory and cardiovascular variables in pig.

PGF2 alpha was injected into different parts of the circulatory system (intravenously by femoral and jugular veins, into the pulmonary artery, into the ascending or descending aorta and into the internal carotid artery at a level above the sinus and carotid body) of anaesthetized spontaneously breathing pigs. It caused changes in respiratory and cardiovascular variables. In vagosympathectomized animals the changes in pattern of breathing produced by PGF2 alpha were greatly reduced and total lung resistance was increased. This may indicates more than one site of action of PGF2 alpha, lung resistance being influenced by a direct action of PGF2 alpha and by an immediate reflex while the pattern of breathing being modulated by vagal efferents from the lungs.

Animals↗
PubMed1991

Effects of electrical stimulation of vagal afferents on spinothalamic tract cells in the rat.

The effects of electrical stimulation of cervical vagal afferents (VAS) on the background activity and on the responses of 25 spinothalamic tract (STT) neurons to noxious stimuli were studied in anesthetized rats. Background (spontaneous) activity of 9 (36%) STT neurons was inhibited by all intensities of VAS. 6 (24%) units were facilitated at lesser and inhibited at greater intensities of VAS, 5 (20%) units were only facilitated by all intensities of VAS, and 5 (20%) units were not affected by VAS. Responses of 8 (36%) STT neurons to noxious stimuli were only inhibited by VAS, 9 (41%) were facilitated at lesser and inhibited at greater intensities of VAS, and 5 units (23%) were only facilitated by VAS. There were no significant differences in VAS-produced modulatory effects between STT neurons and 16 unidentified lumbar spinal dorsal horn neurons studied under the same conditions. These results reveal that descending facilitatory and inhibitory pathways engaged by activation of vagal afferents modulate rostrally projecting nociceptive transmission neurons in the spinal cord, constituting an important regulatory network for nociception.

Anesthesia↗
PubMed1977

Effect of pentobarbital sodium on respiratory control in newborn rabbits.

Using the airway occlusion pressure technique, control of breathing was studied in unanesthetized and anesthetized newborn rabbits breathing various gas mixtures under steady-state conditions. Independent of the gas mixture breathed, barbiturate anesthesia resulted in a reduction of ventilation. This was not due to a change in inspiratory drive since for each gas mixture breathed the pressure generated by the inspiratory muscles 0.3 s after the onset of the occluded inspiration (P0.3) remained virtually unchanged, nor could this be attributed to changes in respiratory mechanics as indicated by the fact that the relation between P0.3 and V0.3 (the volume generated 0.3 s after onset of the immediately preceding unoccluded inspiration) did not change. On the other hand, during anesthesia inspiratory time was slightly shortened as a result of a change in both central (bulbopontine) and peripheral (volume-related vagal reflex) modulation, while expiratory duration was markedly prolonged. This disproportionate increase in expiratory duration with respect to inspiratory duration was responsible for most of the depression of ventilation found in the newborn rabbits during barbiturate anesthesia.

Animals↗
PubMed2026

Moderate alcohol intake and heart rate variability adaptations to high-intensity interval training in healthy young adults: the BEER-HIIT study.

BACKGROUND: It is unknown whether daily alcohol consumption influences training effects on heart rate variability (HRV). This study investigated: (i) the effects of a 10-week high-intensity interval training (HIIT) on HRV in healthy young adults; and (ii) the effects of daily alcohol consumption on HRV responses to exercise. METHODS: 71 healthy young adults (18-40 years old; 52.1% women) participated in the BEER-HIIT study. We conducted a 10-week (2 days/week) controlled trial (ClinicalTrials.gov ID: NCT03660579). Participants were allocated to 5 groups: a non-training group (N-T) and four HIIT groups. Participants in the training groups chose whether to consume alcohol. Those choosing alcohol were randomly allocated to receive beer (5.4%; T-Beer) or an equivalent amount of alcohol (vodka; T-Ethanol) in sparkling water. Those choosing no alcohol were randomly allocated to receive alcohol-free beer (0.0%; T-Zero) or sparkling water (T-Water). Training comprised eight weight-bearing exercises performed in circuit form. HRV was measured before and after the intervention. RESULTS: No statistically significant between-group differences in HRV outcomes were detected after the intervention (all p&#x2009;>&#x2009;0.05). CONCLUSIONS: Our findings indicate that: (i) no statistically significant differences in HRV responses were detected following a 10-week HIIT program using weight-bearing exercises performed twice per week; and (ii) no statistically significant differences in HRV responses were observed among the assigned beverage intervention groups. These findings should be interpreted cautiously because HRV was a secondary outcome and the study was not specifically powered to detect differences in these parameters.

alcohol↗