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Ventricular fibrillation in the isolated rabbit heart.

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.

Animals↗

Metabolic factors and ventricular fibrillation.

Ventricular fibrillation has been studied in the isolated rabbit heart to determine the effect of factors modifying the metabolism. Sodium azide, sodium monoiodoacetate and sodium fluoride were found to cause fibrillation, the effect of sodium fluoride being neutralized by magnesium chloride. Fibrillation was also caused by lack of glucose and could be arrested by adding glucose; the effect of glucose in arresting fibrillation was facilitated by insulin. In other experiments mannose and pyruvate could arrest fibrillation due to lack of glucose, but L(-)lactate could not. The effect of temperature changes, of adrenaline and of cyanide were also studied. When all oxygen was removed from the perfusing solution fibrillation was arrested.

Arrhythmias, Cardiac↗

The relation between temperature and changes in ion concentration on ventricular fibrillation induced electrically.

Further observations have been made on ventricular fibrillation induced by electrical stimulation in the isolated rabbit heart, in extension of the finding that fibrillation was arrested by cooling from 37 degrees to 32 degrees . The observations now made suggest that at 37 degrees the isolated rabbit heart perfused with Locke solution is on the edge of anoxia, but that at 32 degrees the oxygen supply is adequate. At the lower temperature the proportion of hearts fibrillating at any given potassium concentration was reduced, so, although the proportion of hearts fibrillating rose as the potassium concentration fell, even when the latter was one-quarter of the normal the proportion was not higher than 67%. The relation of the concentration of calcium ions to the proportion of hearts fibrillating changed from biphasic at 37 degrees to almost rectilinear at 32 degrees , the proportion increasing as the concentration of calcium ions rose. It was confirmed that a reduction in sodium concentration also raises the proportion of hearts fibrillating.

Animals↗

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↗