Inspiratory inhibition of vagal responses to baroreceptor and chemoreceptor stimuli in the dog.

Abstract

SUMMARY1. Single and few-fibre cardiac efferent filaments were dissected from the cervical vagus nerve of dogs anaesthetized with chloralose and paralysed with pancuronium.2. Brief selective baroreceptor or chemoreceptor stimuli, given during the expiratory phase ofthe central respiratory cycle and while the lungs were motionless, evoked trains of action potentials in cardiac vagal efferent fibres. These vagal responses outlasted the duration of the stimuli by 1-3 s.3. Briefselective baroreceptororchemoreceptorstimuli given during the inspiratory phase of the central respiratory cycle (monitored as phrenic discharge) but while the lungs were motionless, failed to evoke reflex increases in discharge. Background vagal discharge was also inhibited during central inspiratory activity.4. Brief baroreceptor or chemoreceptor stimuli given during lung inflation but in the expiratory phase of the central respiratory cycle (phrenic silence), also failed to evoke any reflex increase in discharge, but left resting vagal tone relatively unaffected. Only when vagal tone was high was it markedly inhibited by lung inflation, in the absence of central inspiratory activity.5. A point of contrast between the inhibitory effects of lung inflation and of central inspiratory activity is that both tonic and reflexly evoked vagal discharge are inhibited during central inspiratory activity, but lung inflation more markedly inhibits reflexly evoked vagal discharge than tonic vagal discharge. 6. A model is suggested to explain the different mechanisms of inhibition by lung inflation and by central inspiratory activity.

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

“…Vagal inhibition is not seen following brief, selective stimulation of carotid baroreceptors using intracarotid pulses of pressure (Potter, 1981), although it was still apparent after the last pulse in a train of electrical stimuli applied to the carotid sinus nerve. Possibly the synchronous volley of action potentials produced in the carotid sinus nerve by electrical stimulation, but presumably not by functional stimulation of the baroreceptors, favoured the demonstration of vagal inhibition.…”

“…The prolonged responses of cardiac vagal motoneurones to brief trains of electrical stimuli (or pulses of intracarotid pressure: Potter, 1981) cannot be attributed solely to a temporal spread of arrival in the central nervous system of inputs along afferent fibres with different conduction velocities. Recording in the nucleus of the tractus solitarius from cells excited by electrical stimuli applied to the carotid sinus nerve, Trzebski et al (1975) found the spread of latencies to be from 3 to 21 ms.…”

“…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).…”

Some reflex cardioinhibitory responses in the cat and their modulation by central inspiratory neuronal activity.

“…On the premise that the cardiac vagal motoneurones are a homogenous group (Gilbey et al 1984), the differential modulation of reflex cardioinhibitory responses by inflation of the lungs (Daly & Kirkman, 1989) could be explained, as proposed by Potter (1981), by the fact that pulmonary stretch afferents have an independent effect earlier in each vagal excitatory pathway, although not directly on the afferent terminals (Jordan & Spyer, 1979). Such a hypothesis could explain the quantitative differences in the effects of central inspiratory activity on the four excitatory inputs to cardiac vagal motoneurones.…”

“…The effects of such stimuli are maximal during the expiratory phase of respiration; during the inspiratory phase, the cardiac vagal motoneurones are partly or wholly refractory to such excitatory stimuli. This inspiratory modulation of the cardiac vagal motoneurones is due to two components: an increase in central inspiratory neuronal activity and an increased activity of slowly adapting pulmonary stretch receptors (Anrep, Pascual & Rossler, 1936a, b;Davidson, Goldner & McCloskey, 1976;Gandevia, McCloskey & Potter, 1978;McAllen & Spyer, 1978a, b;Potter, 1981;Daly & Kirkman, 1989). It appears, however, that not all excitatory inputs to cardiac vagal motoneurones are affected in a similar way.…”