The formation of an acetylcholine‐like substance by the isolated rabbit heart

Briscoe, Sheila; Burn, J. H.

doi:10.1113/jphysiol.1954.sp005202

Cited by 37 publications

(11 citation statements)

References 12 publications

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“…These substances inhibit the destruction of acetylcholine, and since in addition the fall in rate which they caused was abolished by a small amount of atropine, the conclusion was drawn that the effects observed were due to continuous liberation of small amounts of ACh. Briscoe & Burn (1954) demonstrated that the isolated heart of the rabbit formed ACh, and it was therefore reasonable to suppose that the ACh liberated in the heart-lung preparation came from the heart and not from the lungs.Burn, Vaughan Williams & Walker (1955a) showed that in the heart-lung preparation ACh, infused at constant rate, prolonged the P-R interval, reduced the systemic output of blood and produced A-V block. They also showed that the application of a few stimuli to the auricular appendage during the infusion of the appropriate amount of ACh caused auricular fibrillation.…”

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The formation of acetylcholine in the heart; its effect on the systemic output and its importance for auricular fibrillation caused by aconitine

Burn¹,

Williams²,

Walker³

1956

The Journal of Physiology

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Burn & Walker (1954) described experiments carried out in the heart-lung preparation of the dog which indicated that acetylcholine (ACh) was liberated in that preparation without stimulation of the vagus nerves. They observed that the addition of substances like eserine or neostigmine to the blood, even in low concentration, caused a large fall in the rate of the beat. These substances inhibit the destruction of acetylcholine, and since in addition the fall in rate which they caused was abolished by a small amount of atropine, the conclusion was drawn that the effects observed were due to continuous liberation of small amounts of ACh. Briscoe & Burn (1954) demonstrated that the isolated heart of the rabbit formed ACh, and it was therefore reasonable to suppose that the ACh liberated in the heart-lung preparation came from the heart and not from the lungs.Burn, Vaughan Williams & Walker (1955a) showed that in the heart-lung preparation ACh, infused at constant rate, prolonged the P-R interval, reduced the systemic output of blood and produced A-V block. They also showed that the application of a few stimuli to the auricular appendage during the infusion of the appropriate amount of ACh caused auricular fibrillation. In a later paper (1955b) they found that the addition of inhibitors of cholinesterase to the heart-lung preparation without ACh infusion had similar effects. The P-R interval was prolonged, the systemic outflow was reduced and, in sufficient concentration, there was A-V block. When stimulation was applied to the auricle, the rate at which A-V block began was much reduced. Finally, after stimulation at higher rates in the presence of eserine or paraoxon, auricular fibrillation occurred for a length of time which depended on the concentration of the inhibitor. All this evidence gave further support to the view that ACh was liberated by the heart.

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The formation of acetylcholine in the heart; its effect on the systemic output and its importance for auricular fibrillation caused by aconitine

Burn¹,

Williams²,

Walker³

1956

The Journal of Physiology

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“…Recordings of the transmembrane potentials from non-pacemaker and pacemaker areas were taken by the intracellular microelectrode. The recording electrode , less than 1 µ in diameter, drawn from special glass capillary tubing and filled with 3 M-KCI , having low resistance (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20), was selected and fixed on the arm of a micromanipulator . A chloride silver wire was pushed into the shaft of the electrode and was soldered onto flexible strand thereby connected to a d.c. amplifier with an input cathode follower of low grid current and reduced grid-earth capacity.…”

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Effect of Anticholinesterases on the Membrane Potential of the Rabbit Heart

Takaori

Inoki

Toda

et al. 1961

Japanese Journal of Pharmacology

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We have already reported on the action of drugs such as acetylcholine, epinephrine, reserpine, cardiac glycosides, antiarrhythmic agents, veratrine and chelating agents on the intracellular action potentials recorded from the ventricular muscle, sinoatrial node and the non-pacemaker atrial fibers of the isolated rabbit heart using the ultramicro electrode method (1-3).The present experiments were undertaken to determine the influences of anticholin esterases on the membrane potentials of the isolated rabbit atrial muscle exhibiting spon taneous beating. Observations on the antagonisms between the action of anticholinesterases and of cholinesterase reactivators on the membrane potentials were also designed . METHODSAs described previously (1-3), the experiments were carried out on the right incised atrium of rabbits. The endocardial surface of the dissected right incised atrium was pinned on a cork block mounted in a lucite chamber containing about 10 ml of oxygen saturated Tyrode solution at approximately 30°C. The drugs were added directly to Tyrode solution in the chamber and their concentrations were expressed in terms of w/v (g/ml). Recordings of the transmembrane potentials from non-pacemaker and pacemaker areas were taken by the intracellular microelectrode. The recording electrode , less than 1 µ in diameter, drawn from special glass capillary tubing and filled with 3 M-KCI , having low resistance (8-20 MQ), was selected and fixed on the arm of a micromanipulator . A chloride silver wire was pushed into the shaft of the electrode and was soldered onto flexible strand thereby connected to a d.c. amplifier with an input cathode follower of low grid current and reduced grid-earth capacity. The output of the amplifier was led to a cathode-ray oscilloscope and ink-writing recorder (Sanei's Type MPA-204) .

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“…In 1946 there were various sugge stions that ac etylcholine was synthe sized in the heart, and had a function which was in some way excitatory. We demonstrated the formation of acetylcholine (21 ) by perfusing the iso lated rabbit heart through the aorta with Locke's solution containing phy sostigmine, and recirculating the fluid through the heart for 40 minutes. At the end of this time the fluid was collected and fre eze-dried, and the residue was extracted with ethanol.…”

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confidence: 99%

Essential Pharmacology

Burn

1969

Annu. Rev. Pharmacol.

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The beginning.-When I went to Cambridge in 1909, I became a member of Emmanuel College, of which John Harvard had been a member some 300 years earlier. I had the good fortune to have as a tutor, whose duty it was to supervise my progress in a general way, a man called F. G. Hopkins! He was the pioneer biochemist who isolated tryptophan, who worked on what he called "accessory food factors," and discovered glutathione. He was one of the most modest, gracious and graceful men I have ever known.At Cambridge I expected to make Chemistry my principal subject, but I found that for the first two years, I had to read Physics and two other sub jects as well. With Hopkins' approval Physiology and Botany were chosen.I discovered that, compared with those who taught Physiology and Physics, the chemists were an unattractive lot, particularly those who demonstrated in the practical class. These seemed very undistinguished, had cheerless faces and wore rather shabby clothes. The physiologists and the physicists had far more personality. In Physics I heard lectures given by J. J. Thom son, who seemed to be not of this world, and one of the demonstrators was Aston who built the first mass spectrograph. In Physiology the Professor was Langley, always well-dressed, who rode to hounds (that is he hunted the fox) and spoke to no one so far as I could see. There was W. B. Hardy who, when not studying the behaviour of colloids, sailed a yacht in the rough seas of the English Channel. In the summer he pinned a notice on his door which said "Back tomorrow." Joseph Barcroft, an Ulsterman, also sailed boats, and Keith Lucas, who was in part an engineer, had a large motor vessd on the Cam. Hidden in his room was a young man called Adri an, who spent his spare time at one period painting pictures in the style of Marinetti for an exhibition. It is said that all the works were sold, mostly to eager, but unwary Faculty members.Then there was the striking athletic figure of A. V. Hill, the very distin guished-looking W. M. Fletcher, and finally, helping Barcroft and Hopkins to fill the place with humanity, was H. K. Anderson.To enter the Cambridge world after leaving the school world was like meeting sea breezes on the shore after being confined in a stuffy room, and for two years I was mainly interested in debates and discussions of politics, religion and literature, which at least taught me to form my own opinions. After my third year I began research with Barcroft on two small prob lems concerned with the oxygen capacity of haemoglobin. I learnt (to my surpr ise) that I could work accurately, but I was still only half-interested and was occupied with other things. I was secretary of a University Social Discussion Society, and of its Inner Ci rc le which invited di stingui shed public figures to address them. One of these figures I remember was Bea� trice Webb who had encyclopaedic knowledge .on the reform of the Poor Law. I may say that she stayed, unforgett ably, at the ho use of Mr. W. C. Dampier Whetham, and that he lived at Upwater Lodge...

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The formation of an acetylcholine‐like substance by the isolated rabbit heart

Cited by 37 publications

References 12 publications

The formation of acetylcholine in the heart; its effect on the systemic output and its importance for auricular fibrillation caused by aconitine

The formation of acetylcholine in the heart; its effect on the systemic output and its importance for auricular fibrillation caused by aconitine

Effect of Anticholinesterases on the Membrane Potential of the Rabbit Heart

Essential Pharmacology

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