Vagus cardioinhibitory fibers in rats

1. The contribution of cardiac vagal C fibres to vagal chronotropic control in anaesthetized cats, rats and rabbits was analysed using electrical stimulation of the vagus nerve with a selective anodal block technique. 2. After bilateral vagotomy and pretreatment with atenolol, 10 Hz continuous selective stimulation of unmyelinated fibres in the cut peripheral end of the cervical vagus evoked a bradyeardia in anaesthetized rats, cats and rabbits. With this stimulation protocol the three species exhibited a similar lengthening of the heart period (R-R interval) when expressed as a percentage of their basal cardiac interval. 3. The mechanism of action of the selective blocking technique was analysed by recording eighty-nine single A-(n = 12), B-(n = 22) and C-fibre (n = 55) vagal-projecting neurones in the medulla of the rat. This demonstrated that the technique can selectively block conduction in myelinated fibres and that 'break excitation' is seen mainly in unmyelinated fibres. Although thirty C fibres showed break excitation sixteen did not and this difference could not be correlated with their axonal conduction velocity, chronaxie or initial segment frequency following. 4. Using the anodal block technique the vagal effects on heart rate were reanalysed in the cat by incorporating a collision technique. B fibres were activated orthodromically to evoke cardioinhibition and simultaneously antidromically to collide with errant B-fibre spikes activated at the electrode producing anodal block. With this protocol it was noted that the B-and C-fibre bradycardias were not additive. Using a double anodal block and collision technique, it was demonstrated that this phenomenon was likely to be due to occlusion of the effects of B and C fibres. 5. In conclusion, in addition to the well-defined effects of vagal B fibres on heart rate, selective stimulation of vagal C fibres also had a cardioinhibitory effect in all three species studied. However, since the effects of cardiac C fibres on heart rate was small, these neurones alone cannot account for the cardioinhibition of the pulmonary chemoreflex. It is likely that activation of both B-and C-fibre cardiac vagal preganglionic neurones accounts for this reflex cardioinhibition.

Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 93%

mentioning

confidence: 99%

See 1 more Smart Citation

Heart rate responses to selective stimulation of cardiac vagal C fibres in anaesthetized cats, rats and rabbits.

Jones

Wang

Jordan

1995

“…In the dog non-myelinated fibres are reported to have no action on the heart (Donald, Samueloff & Ferguson, 1967), but in the rat both myelinated and non-myelinated fibres are reported to produce a bradyeardia (Nosaka, Yasunaga & Kawano, 1979). The cardioinhibitory actions of non-myelinated fibres in the rat were blocked by hexamethonium and thus the mechanism underlying their action appears to be different to that in the rabbit.…”

Section: Discussionmentioning

confidence: 76%

The effects of electrical stimulation of myelinated and non‐myelinated vagal fibres on heart rate in the rabbit.

Ford¹,

McWilliam²

1986

SUMMARY1. The bradyeardia evoked by electrical stimulation of the peripheral end of the rabbit vagus nerve is mediated by both myelinated and non-myelinated fibres.2. Stimulation of myelinated fibres at 5 Hz for 20 s resulted in a fall in heart rate from a control value of 204 + 1-3 to 182 + 1-2 beats min-1 (means + S.E. of means). On stimulation of both myelinated and non-myelinated fibres, heart rate fell to 169 + 2 1 beats min-1. Heart rate returned rapidly to control value following stimulation of myelinated fibres but only slowly after stimulation of both myelinated and non-myelinated fibres. Thus recruitment of non-myelinated fibres increased both the magnitude and duration of the bradyeardia.3. Atropine abolished all effects ofvagal stimulation on heart rate. Hexamethonium abolished the effect of myelinated fibres on heart rate; however, recruitment of non-myelinated fibres still produced a bradyeardia.4. It is suggested that the prolonged effect following stimulation of non-myelinated fibres may reflect the persistent action of a non-cholinergic excitatory transmitter at the ganglion.

“…Department of Cardiovascular Studies, The University, Leeds LS2 9JT The bradycardia on electrical stimulation of the vagus in the cat has been attributed solely to myelinated efferent fibres (Middleton, Middleton & Grundfest, 1950). Recruitment of non-myelinated fibres enhances the bradyeardia in the rat (Nosaka, Yasunaga & Kawano, 1979), but in the rabbit is reported to attenuate the bradyeardia (Neef, Jansen & Versprille, 1983). The present study re-examines the effects of vagal stimulation in the rabbit.…”

mentioning

confidence: 87%

Proceedings of the Physiological Society, 28‐29 March 1985, University College London Meeting: Communications

1985

We have previously shown that the Lambert-Eaton myasthenic syndrome (L.E.M.S.) is an autoimmune disorder (Lang, Newsom-Davis, Prior & Wray, 1983). IgG autoantibodies interfere with release of acetylcholine from presynaptic nerve terminals of the skeletal neuromuscular junction. The experiments reported here were designed to investigate the mechanism of action of these antibodies at depolarized nerve terminals.Mice were injected with control or L.E.M.S. IgG (30 mg/day, i.P.) for 2 days, and the diaphragm muscle removed on the third day, as previously described (Lang et al. 1983). Miniature end-plate potentials (m.e.p.p.s) were recorded using microelectrodes in Krebs solution (23-26 'C) containing high K+ concentration (15-9 mM) and a range of Ca2+ concentrations (0-25-2-5 mm).In controls, m.e.p.p. frequency increased with Ca2+ concentration from a value of 5 03 + 0 69 s-1 (n = 19 end-plates) at 0-25 mM-Ca2+ concentration to a plateau value of 79-3 + 6-8 s-1 (n = 18) at 1-5 mM-Ca2+ concentration. Further increase in Ca2+ concentration produced no further increase in this plateau value. The curve of m.e.p.p. frequency versus Ca2+ concentration for L.E.M.S. IgG-treated animals was similar in shape to that for controls, but with significantly reduced (P < 0-002) m.e.p.p. frequency values at all Ca2+ concentrations. The extent of these reductions was to 34 46 % of control values. Thus the curve was shifted to the right with a reduced plateau. The plateau value of m.e.p.p. frequency was reached at similar Ca2+ concentrations as for controls but was reduced to 36-4 + 4-9 s51 (n = 19, Ca2+ concentration = 1-5 mM).These reductions in m.e.p.p. frequency at potassium-depolarized nerve terminals by L.E.M.S. IgG indicate that it is unlikely that this antibody acts solely (if at all) on action potential mechanisms, since no action potentials were involved in the present experiments. On the other hand, voltage-dependent Ca2+ channels would be expected to be opened by the depolarization produced under the above experimental conditions. L.E.M.S. IgG may act on these latter channels to cause their loss of function as suggested previously (Lang, Newsom-Davis, Prior & Wray, 1984). The present results are consistent with such an action, and the reduced plateau value of the above curve produced by the L.E.M.S. IgG shows further that the mechanism is not one of competitive antagonism.