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Biomedical subjects

J H BURN

Publications and source records attributed to J H BURN.

At least 37 records · Page 2Linked to original sources
PubMed1961

Effect of noradrenaline on the action of nicotine and tyramine on isolated atria.

Both nicotine (in the presence of atropine) and tyramine cause a rise in the rate of isolated rabbit atria. When noradrenaline is allowed to act on the atria for 20 to 30 min and then removed from the bath by repeated changes of the bath fluid, the action of nicotine and of tyramine is greatly increased. The first addition of noradrenaline to the bath often has a much smaller effect on the response to nicotine or to tyramine than have later additions. Sometimes the greater effect after the addition of nicotine persists for 2 or 3 hr. When reserpine is added to the bath and left in contact with the atria for 1 to 2 hr, and is then removed from the bath, the effect of noradrenaline on the atrial rate is much reduced in size and duration. Bretylium abolishes the action of nicotine but increases the action of tyramine.

Animals↗
PubMed1961

Uptake of labelled noradrenaline by isolated atria.

The uptake of labelled noradrenaline by isolated rabbit atria has been studied, and the rate of outflow of radioactivity after a period of loading has been recorded. There is first a rapid outflow presumably from extracellular space, followed by a slow outflow presumably from intracellular space. Cocaine greatly diminished the intracellular uptake. Tyramine caused an increased outflow of radioactivity from intracellular sites which was not due to the increase in atrial rate, since noradrenaline which increased the rate more than tyramine had less effect on the outflow.

Animals↗
PubMed1960

The effect of precursors of noradrenalin on the response to tyramine and sympathetic stimulation.

Previous observations have shown that the effects of sympathetic stimulation and of tyramine were absent in the organs of animals treated with reserpine, but that they were restored by an infusion of noradrenaline. Observations are described showing that an infusion of adrenaline did not restore the pressor action of tyramine in the cat or in the rat, but that in the rat the pressor action was restored by an infusion of dopamine, or of (-)-dopa, or of m-tyrosine,or of phenylalanine. Observations are also described showing that the effect of postganglionic stimulation of the fibres to the nictitating membrane and to the iris was restored by an infusion of dopamine or of (-)-dopa; it was restored less well by an infusion of noradrenaline. An infusion of noradrenaline did not restore the action of tyramine on the denervated iris or on the denervated vessels of the cat's foreleg. An infusion of noradrenaline appeared to increase the effect of sympathetic stimulation of the hypogastric nerves to the uterus of the virgin cat about as much as an infusion of adrenaline. An infusion of noradrenaline restored the constrictor action of nicotine on the perfused vessels of the rabbit ear.

Animals↗
PubMed1960

Sympathetic postganglionic cholinergic fibres.

When the postganglionic fibres to the nictitating membrane are stimulated in a cat treated with reserpine, the membrane contracts. The contraction is increased after the injection of eserine and is abolished with atropine. Thus the fibres stimulated appear to be cholinergic. When the splenic nerve is stimulated in a cat treated with reserpine there is similar evidence of the presence of cholinergic fibres; the spleen dilates, the dilatation is greater in the presence of eserine and is abolished by atropine. The hypogastric nerves when stimulated cause inhibition of the uterus of the virgin cat. When the cat is treated with reserpine, stimulation then causes contraction which is increased in the presence of eserine and abolished by atropine. There is also evidence of cholinergic fibres in the postganglionic supply to the vessels of the rabbit's ear. From this and other evidence it is suggested that a form of adrenergic mechanism may exist such that cholinergic fibres in the postganglionic sympathetic supply liberate acetylcholine; this in turn liberates noradrenaline from a store around the sympathetic nerve ending.

Acetylcholine↗
PubMed1960

Anoxia and ventricular fibrillation; with a summary of evidence on the cause of fibrillation.

Experiments are described showing that ventricular fibrillation is more readily produced in isolated rabbit hearts by electrical stimulation when the oxygen supply to the heart is reduced. This evidence completes investigations which have been made into factors affecting the production of fibrillation. These investigations have shown that factors which shorten the duration of the action potential, particularly those which cause the "plateau" to disappear, facilitate fibrillation, and those which lengthen the duration of the action potential prevent fibrillation. The reason for the length of the cardiac action potential may therefore be to prevent fibrillation. When the action potential is of normal length the fact that two adjacent fibres are out of phase does not matter; the one which is first to contract is not re-excited by the one which is second to contract, because at that moment the first is inexcitable. If the action potential is short, then the first may be already repolarized and may be excited by spread of excitation from the second. Factors which inhibit metabolism shorten the action potential.

Action Potentials↗