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September 1, 1968The Journal of Physiology35 citationsOpen Access

Motor innervation of the coronary arteries of the cat

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ABArthur Brown

Structured PICO

P
Population
Cat model (feline heart)
I
Intervention
Selective stimulation of Adelta, B, and sC nerve fibers, and pharmacological interventions (noradrenaline, acetylcholine, propranolol, atropine, hypertensin)
O
Outcome
Coronary vascular resistance and coronary sinus oxygen saturationsurrogate

This preclinical study demonstrates that sympathetic post-ganglionic sC fibers mediate coronary vasodilatation via beta-adrenergic receptors.

Abstract

The effect on coronary vascular resistance of selective stimulation of the Adelta, B and sC fibre groups of the post-ganglionic cardiac sympathetic nerves was studied. The main left coronary artery was perfused at constant flow. The oxygen saturation of coronary sinus blood was measured continuously.2. Stimulation of the peripheral ends of the cut Adelta afferent fibres, normally excited by myocardial ischaemia, had no effect on coronary vascular resistance; these fibres do not evoke an axon reflex in the heart.3. Stimulation of the preganglionic B fibres that run without synapse through the stellate ganglion also had no measurable effect on coronary resistance.4. Stimulation of the post-ganglionic sC fibres of the cardiac sympathetic nerves caused coronary vasodilatation which occurred earlier than, and was initially independent of the decrease in coronary sinus oxygen saturation.5. The injection of noradrenaline into the perfusion system had the same effect as stimulation of the sC fibres. In the K(+)-arrested heart, both noradrenaline and stimulation of the post-ganglionic nerves elicited coronary vasodilatation without changing the oxygen saturation of coronary sinus blood.6. The intracoronary injection of acetylcholine caused coronary vasodilatation followed by an increase of coronary sinus oxygen saturation.7. Vagal stimulation caused brady cardia and a fall in coronary resistance.8. Propranolol blocked coronary vasodilatation elicited by sympathetic stimulation or noradrenaline without affecting the vasodilatation due to myocardial ischaemia or acetylcholine. Atropine blocked coronary vasodilatation evoked by acetylcholine without affecting that due to ischaemia or noradrenaline. Therefore smooth muscle of the coronary arteries has at least three different receptor sites from which vasodilatation can be elicited.9. Hypertensin caused coronary vasoconstriction.10. The presence of sympathetic cholinergic vasodilator fibres innervating the coronary arteries could not be demonstrated.

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Arthur Brown (1968) studied this question.

synapsesocial.com/papers/6a1e9a50edce398519af1276https://doi.org/10.1113/jphysiol.1968.sp008608
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Separation of cardioaccelerator and coronary vasomotor fibers in the dog1961 · 46 citations
  2. 2Effect of Epinephrine and Norepinephrine on Coronary Circulation1958 · 143 citations
  3. 3Sympathetic Control of Coronary Circulation1967 · 209 citations
  4. 4Excitation of afferent cardiac sympathetic nerve fibres during myocardial ischaemia1967 · 231 citations
  5. 5The depressor reflex arising from the left coronary artery of the cat1966 · 36 citations