Ventricular Fibrillation and Ion Transport

Armitage, A. K.; Burn, J. H.; Gunning, A. J.

doi:10.1161/01.res.5.1.98

Cited by 49 publications

(25 citation statements)

References 7 publications

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“…This method of arresting fibrillation was described by Dirken, Gevers, Heemstra and Huizing (1955). Effects of Chloroquine, Mepacrine and Pyrimethamine.- Armitage (1957) has observed that chloroquine, mepacrine and pyrimethamine have a quinidine-like action on the electrically-driven rabbit atria (Dawes, 1946). It therefore seemed likely that these substances would be effective in abolishing fibrillation, and their action was tested.…”

Section: Resultsmentioning

confidence: 99%

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Ventricular Fibrillation in the Isolated Rabbit Heart

Armitage

Burn

Gunning

1957

British Journal of Pharmacology and Chemotherapy

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Ventricular fibrillation has been produced in the isolated and perfused rabbit heart by stimulating electrically at a rate from 500 to 700/min. When the perfusion fluid contained normal amounts of sodium, potassium and calcium, the fibrillation persisted after the stimulation was stopped in about 40% of hearts. When the sodium was reduced to half, tonicity being maintained by sucrose or by choline chloride, persistent fibrillation was observed in 100% of hearts. The addition of eserine or of atropine or of carbachol did not alter the percentage of hearts in which fibrillation persisted. The antimalarial compounds chloroquine, mepacrine, and pyrimethamine arrested persistent fibrillation, restoring a normal rhythm.

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Section: Resultsmentioning

confidence: 99%

“…Armitage (1957) has shown that, when the isolated atria are exposed to the action of these substances, the contractions diminish in amplitude and frequency until they stop. They begin again when the external potassium concentration is lowered to one-half or one-quarter.…”

Section: Resultsmentioning

confidence: 99%

Ventricular Fibrillation in the Isolated Rabbit Heart

Armitage

Burn

Gunning

1957

British Journal of Pharmacology and Chemotherapy

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“…Use was then made of the observation (Armitage, Burn, and Gunning, 1957) that, when the potassium concentration was lowered, the proportion of hearts fibrillating was increased. The following experiment is an example.…”

Section: Resultsmentioning

confidence: 99%

“…Acetylcholine shortens the atrial action potential (Hoffman and Suckling, 1953) and facilitates atrial fibrillation in the dog (Burn, Vaughan Williams, and Walker, 1955). Acetylcholine has practically no effect on the ventricular action potential (Hoffman and Suckling, 1953) and has no effect on ventricular fibrillation (Armitage, Burn, and Gunning, 1957). Adrenaline lengthens the atrial action potential in the rat (Webb and Hollander, 1956), and prevents acetylcholine from causing atrial fibrillation (Burn, Gunning, and Walker, 1957).…”

Section: Discussionmentioning

confidence: 99%

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Anoxia and Ventricular Fibrillation; With a Summary of Evidence on the Cause of Fibrillation

Burn

Huković

1960

British Journal of Pharmacology and Chemotherapy

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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.When electrodes are attached to the ventricle of the isolated rabbit heart perfused through the aorta, a high rate of stimulation can then be applied for a given time. This causes the ventricles to fibrillate, as may be seen when the stimulation stops by using the electrodes as leads to an ECG. Ordinarily the fibrillation induced in this way continues only for 1 to 2 min. and a normal rhythm returns. However, under various conditions, such as in the presence of a low concentration of potassium or a high concentration of calcium, or in the presence of metabolic inhibitors, the fibrillation has been found to persist. The observations now to be described have been made to test the effect of a partial lack of oxygen. METHODS Rabbits were stunned and bled. The hearts were removed and attached to the apparatus for perfusion as already described (Armitage, Burn, and . The perfusion fluid contained (in mM.) NaCl 132, KCl 5.6, CaCI2 2.2, NaHCO3 2.5, NaH2PO4.2H20 0.92, dextrose 11.1, sucrose 13.1. The solution was saturated with 95 % oxygen+5% C02 for the control observations, and with 47.5% oxygen, 47.5% nitrogen and 5% CO2 for the rest. The temperature of the perfusing solution was 32°and was maintained within ±0.5°, using the device of Saxby (1956). Hearts were perfused at a pressure of 50 cm. water. Platinum fish-hook electrodes were inserted in the wall of the left ventricle, one at the apex and the other near the base. The stimuli were 1-2 mA. in strength, 2 msec. in duration and applied at a frequency of 20/sec. for 3 min. When stimulation was not being applied, the electrodes were used as leads to a Cossor electrocardiograph (model 1314); a record of the rhythm was obtained every 5 min. during fibrillation. The solutions saturated with the two gas mixtures were kept in separate flasks and perfused from separate Marriotte bottles.When perfusion with any solution was begun, it was continued for at least 15 min. b...

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The Effects of Induced Hypocalcemia on Myocardial Irritability and Conductivity

Kabakow¹

1958

AMA Arch Intern Med

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The role of calcium and potassium in myocardial irritability and contractility has been well studied. More recently the interrelationship between these ions and digitalis has been explored.The concept of synergism between, or additive effect of, calcium and digitalis has been debated for many years.1-4 The use of potassium salts orally and parenterally in the treatment of digitalis intoxication is well established.5,6 It is known, in addition, that low serum calcium levels potentiate the cardiac toxicity of hyperkalemia.7Digitalis is known to cause egress of potassium from the myocardial cell.8 It is this relative intracellular potassium depletion which may, in part, be responsible for the commonly observed electrocardiographic effects of digitalis.9 Calcium ions at the cell membrane exert a stabilizing influence, making more difficult the active reentry of potassium.10 This results in the same net effect. It seemed reasonable to expect that lowering the concentration of calcium ions at the cell membrane might facilitate entry of potassium back into the cell.The following study was undertaken pri¬ marily to ascertain whether the commonly observed electrocardiographic manifesta¬ tions of digitalis, varying from ST and changes to evidence of marked myocardial hyperirritability, could be influenced by an induced transient hypocalcémie state. Materials and MethodsThe chelating agent disodium ethylenediaminetetraacetate (Na· EDTA) was employed in this study to produce a transient hypocalcemia. This agent binds the available systemic calcium which is excreted in the urine as the calcium chelate. The duration and extent of the effective hypocalcemia is a function of the quantity and rapidity of ad¬ ministration of the Na2 EDTA, the route of ad¬ ministration, and the ability of the calcium stores of the subject to replace the chelated calcium.Twenty-six patients received a total of 27 intra¬ venous infusions of 4 gm. of Na2 EDTA in 250 cc.of 5% dextrose and water over a four-hour period. Electrocardiograms were taken prior to the infu¬ sions and after one, two, three, and four hours.In most cases, venous blood was drawn prior to and after the infusion and analyzed for calcium and potassium. The serum calcium was determined by the Kramer-Tisdall method,11 and the potas¬ sium, by the use of the Beckman Model 1400 Flame Photometer.The deviation of the ST segment is expressed in millimeters above or below the T-P segment (isoelectric line), where the latter is at the same horizontal level for two or more successive cycles and where no artifacts are present in the QRST complex. Amplitude of waves is expressed in millimeters measured from the top of the iso¬ electric line to the summit of an upright or from the bottom to the nadir of an inverted T.Twenty patients demonstrated cardiac arrythmias suggestive of altered myocardial excitability. Five patients, three of whom were taking main¬ tenance doses of a digitalis preparation, demon¬ strated marked ST depressions and T-wave inversions. One patient had no evidence of myo¬ card...

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Ventricular Fibrillation and Ion Transport

Cited by 49 publications

References 7 publications

Ventricular Fibrillation in the Isolated Rabbit Heart

Ventricular Fibrillation in the Isolated Rabbit Heart

Anoxia and Ventricular Fibrillation; With a Summary of Evidence on the Cause of Fibrillation

The Effects of Induced Hypocalcemia on Myocardial Irritability and Conductivity

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