THE ROLE OF GLUCOSE IN THE INITIATION AND MAINTENANCE OF VENTRICULAR FIBRILLATION

Perfusion of isolated rabbit hearts with a glucose-free physiological solution facilitates the production of ventricular arrhythmias. On the other hand, glucose deprivation limits the duration of such arrhythmias. An hypothesis is proposed to explain the effect of glucose deprivation on the induction of fibrillation. </jats:p

HISTAMINE, MAGNESIUM DEFICIENCY, AND THYMIC TUMORS IN RATS

Histamine was measured in the plasma, liver, and thymus of male rats fed a magnesium-deficient diet for 65 days. Histological study of the thymus was also performed. Histamine levels in plasma and tissue increased rapidly and reached a maximum after 10 days of deficiency. Later on, the level of histamine in deficient animals decreased and fluctuated but was usually higher than in the controls. One rat killed after 60 days of deficiency showed a very large thymus, weighing 1.8 g, which extended into the thoracic cavity. Histological study revealed a complete replacement of the normal thymic cells by large basophilic lymphocytes invading the neighboring organs including the heart muscle. The tumor was transplanted successfully in normal rats receiving a well-balanced diet. Another smaller tumor was found in an animal killed at 65 days. Thymuses of control animals were all normal. The development of tumors of the thymus in magnesium-deficient rats is discussed in connection with the changes in tissue histamine.</jats:p

DIFFERENTIAL EFFECTS OF SOME PHENOTHIAZINE DERIVATIVES AGAINST CALCIUM-INDUCED VENTRICULAR ARRHYTHMIAS IN THE ISOLATED RABBIT HEART

This paper deals with the effects of five phenothiazine derivatives and quinidine against ventricular fibrillation induced in the isolated rabbit heart by small amounts of calcium chloride. Chlorpromazine and promethazine were more potent than quinidine in raising the calcium threshold for fibrillation. On the other hand, prochlorperazine and diethazine exerted biphasic effects: small concentrations increased the sensitivity of the heart to calcium chloride or induced fibrillation without calcium; higher concentrations had antifibrillatory effects and markedly depressed atrioventricular conduction. Thioproperazine was profibrillatory at all concentrations tested. </jats:p

ON THE MODE OF ACTION OF GLUCOSE IN THE MAINTENANCE OF VENTRICULAR FIBRILLATION

Glucose deprivation was previously shown to favor the induction of ventricular fibrillation in the isolated and perfused rabbit heart. On the other hand, glucose is required for the prolonged maintenance of the induced fibrillation.The mechanism of action of glucose in the maintenance of electrically induced fibrillation was studied in 54 hearts perfused with solutions containing either normal or decreased sources of available energy. Hearts perfused with a normal solution, a low-sucrose solution, or with a glucose-free solution containing lactate or adenosine-triphosphate develop long-lasting fibrillations.It is believed that glucose deprivation acts, initially, by inhibiting the active cardiac mechanism delaying repolarization and by reducing, therefore, the duration of the action potential and rendering the heart more vulnerable to fibrillatory factors. During a second phase, brought about by a decrease in the effectiveness of the sodium pump and by a shift in the sodium and potassium fluxes, glucose deprivation lengthens the duration of the action potential and refractory period and produces an antifibrillatory effect. Dinitrophenol is thought to act in a similar manner, but the fibrillatory action of adenosine triphosphate cannot be explained as satisfactorily. </jats:p

ON THE MODE OF ACTION OF GLUCOSE IN THE MAINTENANCE OF VENTRICULAR FIBRILLATION

Glucose deprivation was previously shown to favor the induction of ventricular fibrillation in the isolated and perfused rabbit heart. On the other hand, glucose is required for the prolonged maintenance of the induced fibrillation.The mechanism of action of glucose in the maintenance of electrically induced fibrillation was studied in 54 hearts perfused with solutions containing either normal or decreased sources of available energy. Hearts perfused with a normal solution, a low-sucrose solution, or with a glucose-free solution containing lactate or adenosine-triphosphate develop long-lasting fibrillations.It is believed that glucose deprivation acts, initially, by inhibiting the active cardiac mechanism delaying repolarization and by reducing, therefore, the duration of the action potential and rendering the heart more vulnerable to fibrillatory factors. During a second phase, brought about by a decrease in the effectiveness of the sodium pump and by a shift in the sodium and potassium fluxes, glucose deprivation lengthens the duration of the action potential and refractory period and produces an antifibrillatory effect. Dinitrophenol is thought to act in a similar manner, but the fibrillatory action of adenosine triphosphate cannot be explained as satisfactorily. </jats:p

THE ROLE OF GLUCOSE IN THE INITIATION AND MAINTENANCE OF VENTRICULAR FIBRILLATION

Perfusion of isolated rabbit hearts with a glucose-free physiological solution facilitates the production of ventricular arrhythmias. On the other hand, glucose deprivation limits the duration of such arrhythmias. An hypothesis is proposed to explain the effect of glucose deprivation on the induction of fibrillation. </jats:p

PHARMACOLOGICAL REACTIVITY OF DYSTROPHIC MUSCLE

The effects of curarizing drugs, anticholinesterases, and musculotropic substances were studied on the phrenic nerve – diaphragm preparation of the hereditarily dystrophic mouse and of the rat treated with N,N-dimethyl-p-phenylenediamine (PPD), a cytotoxic substance producing dystrophic-like lesions. Both species showed an increased resistance to the neuromuscular blocking activity of d-tubocurarine. Gallamine was also less potent in the dystrophic mouse than in its normal littermate. Both species showed an increased sensitivity to the initial stimulant effect of succinylcholine; on the other hand, the depressant effect of succinylcholine was less intense in PPD-treated rats but unaltered in the dystrophic mouse. The response to neostigmine and physostigmine was decreased in the PPD-treated rat but enhanced in the dystrophic mouse. Musculotropic drugs (chlorpromazine, tetrodotoxin, xanthine derivatives, and veratrine) produced similar effects in normal and dystrophic mice. Two hypotheses are suggested to explain these changes in sensitivity in the dystrophic mouse diaphragm: (a) an increased production of an acetylcholine-like material, and (b) an increase in the number of acetylcholine-sensitive sites on the cell membrane. The changes in drug reactivity of the PPD-treated rat are considered to be due to a functional denervation caused by the cytotoxic properties of PPD. </jats:p