Cardiac vagal efferent activity and heart period in the carotid sinus reflex

Katona, P. G.; Poitras, JW; Go, Barnett; Terry, BS

doi:10.1152/ajplegacy.1970.218.4.1030

Cited by 319 publications

(141 citation statements)

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“…This is concordant with direct evidence of vagal deactivation before onset of phrenic nerve activity 36 and effectively rules out a primary role for direct or indirect mechanical effects of respiration on atrial size. By the same reasoning, a centrally mediated effect incorporating outflow from the respiratory control centers in the brain stem seems likely to play a role in mediating the observed changes.…”

Section: Autonomic Modulation Of Respiratory Sinus Arrhythmiasupporting

confidence: 72%

Mild hypovolemic stress alters autonomic modulation of heart rate.

1993

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In response to changes in central venous volume, changes in vagal efferent cardiac outflow have been demonstrated in animals but not in humans. In this study, frequency domain analysis was used to quantify modulation of heart rate by respiration and blood pressure in normal human adults undergoing mild central hypovolemic stress induced by blood donation and postural change. In supine subjects, blood donation caused no change in mean heart rate, pulse pressure, or in the variance of heart rate or blood pressure. There were small decreases in mean and systolic blood pressures. A significant decrease in vagal modulation of heart rate was seen in the 0.12-0.5-Hz frequency band, as measured by the change in the relation of lung volume to heart rate in this frequency band (-4.49 beats per minute [bpm] per liter [I], p<0.001). Comparison of supine and tilt positions revealed marked changes in heart rate and blood pressure means and variances consistent with more pronounced decreases in intracardiac filling pressures and unloading of the arterial baroreceptors. A further progressive decrease in the vagal modulation of heart rate by lung volume was observed in the 0.12-0.5-Hz band, with a near-linear response of magnitude of respiratory sinus arrhythmia over a range of estimated central venous volume. Transfer function analysis can detect changes in autonomic response to mild degrees of central hypovolemia, which are insufficient to cause changes in mean heart rate or heart rate variance. This represents evidence for modulation of heart rate control by cardiopulmonary baroreceptors. A near-linear relation between magnitude of respiratory sinus arrhythmia and central venous volume suggests that this may have clinical relevance in patient monitoring. (Hypertension 1993;21:236-247) KEY WORDS • autonomic nervous system • pressoreceptors • hemorrhage • heart rate

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Section: Autonomic Modulation Of Respiratory Sinus Arrhythmiasupporting

confidence: 72%

Mild hypovolemic stress alters autonomic modulation of heart rate.

1993

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“…These findings suggest that relative activity of parasympathetic nervous system was increased. However, the HF component of HR variability has been reported to be dependent on the respiration cycle and affected by respiration frequency and tidal volume [22][23][24][25]. Burst firing of the parasympathetic nerve (vagal nerve) disappears or decreases during inspiration, and the HR variability associated with the disappearance or decrease of the burst firing is observed as the HF component (i.e., respiratory sinus arrhythmia).…”

Section: Effect Of Pressure Application Over Tps On Autonomic Activitymentioning

confidence: 99%

Compression on trigger points in the leg muscle increases parasympathetic nervous activity based on heart rate variability

et al. 2009

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Massotherapy, the therapeutic use of massage, is used to treat various chronic pain syndromes. One type of massotherapy, pressure stimulus applied over trigger points (TPs), is reported to have excellent therapeutic effects. Its effect is possibly mediated through changes in the autonomic nervous system although little research has been conducted to assess autonomic activity during TP compression. We have investigated how compression applied over TPs affects the autonomic nervous system. Six healthy young adult females whose daily working routine was carried out predominantly in a standing position were enrolled in the study cohort. After a day's work, the subjects were asked to rest supine, and electrocardiograms (ECGs), instantaneous lung volume (ILV) and systolic and diastolic blood pressures (SBP, DBP) were measured before and after pressure application over the TPs in those lower limb muscles where the subjects felt muscle fatigue or discomfort. The subjects were also asked to coordinate breathing with the beeping sounds. The therapeutic effects of TP compression were assessed by a subjective fatigue scale. Parasympathetic nervous activity was also assessed by spectral analysis of heart rate (HR) variability. The transfer function from ILV to HR was evaluated using linear analysis. The results indicated that TP compression (1) decreased HR, SBP and DBP, (2) increased parasympathetic activity, (3) increased the gain from ILV to HR, and (4) improved the fatigue scores. These findings suggest that an increase in parasympathetic nervous activity after the TP compression induced a reduction of fatigue. The therapeutic mechanisms of TP compression to enhance parasympathetic nervous system are discussed.

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“…Excitation of efferent vagal axons or of their medullary cell bodies by such stimulation has become established as a means of their physiological identification as cardiac in destination (Iriuchijima & Kumada, 1963, 1964Jewett, 1964;Katona, Poitras, Barnett & Terry, 1970; Kunze, 1972; Davidson, Goldner & McCloskey, 1976; McAllen & Spyer, 1976& Spyer, , 1978 Spyer, 1979 Rijlant, 1936;Jewett, 1964). Also, it is now well established that cardiac vagal motoneurones are wholly or partially refractory during inspiration to electrical stimulation of the carotid sinus nerve and to selective functional stimulation of the carotid baroreceptors or chemoreceptors (Koepchen, Wagner & Lux, 1961 b; Katona et al 1970;Daly, 1972;Haymet & McCloskey, 1974Neil & Palmer, 1975; Melcher, 1976;Lopes & Palmer, 1976;Ekberg & Orshan, 1977;McAllen & Spyer, 1978;Spyer, 1979). This inhibition of the vagus during inspiration is caused by the activity of central 'inspiratory' neurones and by the excitation of intrapulmonary mechanoreceptors (Anrep, Pascual & Rossler, 1936a, b; Gandevia, McCloskey & Potter, 1978;Potter, 1981).…”

Section: Introductionmentioning

confidence: 99%

Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.

McCloskey¹,

Potter²

1981

The Journal of Physiology

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SUMMARY1. The carotid sinus nerve was electrically stimulated in dogs anaesthetized with chloralose. Stimuli (1 ms, 1-10 V, < 1 Hz) evoked responses in single cardiac efferent fibres dissected from the cervical part of the vagus nerve. The mean latencies of these responses varied, from fibre to fibre, between 30 and 120 ms.2. Stimuli given during the expiratory phase of the respiratory cycle evoked vagal responses with a shorter latency than similar stimuli given only during the inspiratory phase of the respiratory cycle.3. Following the vagal response to carotid sinus nerve stimulation a period of inhibition of vagal activity, lasting 100-150 ms, occurred. Refractoriness of the responding vagal motoneurone following an action potential could not account for this post-excitatory depression.4. The inhibitory effects of electrical stimulation of the carotid sinus nerve were further studied by applying pairs of similar electrical stimuli to the carotid sinus nerve. The second stimulus of a pair had to be given 80-100 ms after the first to evoke a second response.5. Trains of electrical stimuli (30-100 Hz) were also studied. At low frequencies the inhibitory effect of successive stimuli on vagal responses became less marked, but at higher frequencies only the first and last stimulus of the train reliably evoked responses. For trains of stimuli at both low and high frequencies, the last stimulus of the train evoked a vagal response, which was succeeded by a period of inhibition of vagal firing: this inhibition was then followed by further excitation before vagal discharge returned to resting levels.

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Cardiac vagal efferent activity and heart period in the carotid sinus reflex

Cited by 319 publications

References 0 publications

Mild hypovolemic stress alters autonomic modulation of heart rate.

Mild hypovolemic stress alters autonomic modulation of heart rate.

Compression on trigger points in the leg muscle increases parasympathetic nervous activity based on heart rate variability

Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.

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