Influence of lidoflazine on cardiac transmembrane potentials and experimental arrhythmias

Carmeliet, Edward; Xhonneux, R.

doi:10.1007/bf01020076

Cited by 20 publications

(12 citation statements)

References 18 publications

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“…The incidence of early (within 1 h) ventricular fibrillation was 16 out of 20 in the controls but only 2 out of 10 in the lidoflazine-treated group. This striking result was not discussed by the authors but one explanation, suggested by Carmeliet & Xhonneux (1971) (1982) has clearly demonstrated, would reduce the incidence and severity of ventricular arrhythmias resulting from subsequent coronary artery ligation. The present studies demonstrate, both in the rat and the greyhound, that acute pretreatment with lidoflazine reduces the severity of these arrhythmias.…”

Section: Discussionmentioning

confidence: 74%

“…Schaper, Xhonneux, Jageneau & Janssen (1966) showed in dogs that prolonged oral treatment with the drug reduced the incidence of ventricular fibrillation following abrupt coronary artery occlusion whereas Carmeliet & Xhonneux (1971) found that lidoflazine was ineffective in reversing ventricular arrhythmias 24 h after coronary artery ligation. The aim of the present studies was three fold.…”

Section: Introductionmentioning

confidence: 99%

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Lidoflazine in the Early Stages of Acute Myocardial Ischaemia

Coker

Fagbemi

Parratt

1982

British J Pharmacology

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Gl 1XW1 Pretreatment of anaesthetized rats with intravenously administered lidoflazine (an antianginal agent) reduced the incidence and severity of ventricular arrhythmias which resulted from acute coronary artery ligation. Ventricular fibrillation was completely prevented by doses of 50 pg/kg and 2 mg/kg and no animal so treated died (contrast 50% incidence of fibrillation in the controls and 30% mortality). 2 In anaesthetized greyhound dogs, lidoflazine (2 mg/kg) administration resulted in transient reductions in systemic arterial pressure, LV dP/dt max and cardiac output. Coronary sinus P02 was markedly increased, indicating pronounced coronary vasodilatation. 3 Lidoflazine pretreatment inhibited the increase in epicardial ST-segment elevation which resulted, in dogs, from short (3 min) occlusions of the left anterior descending coronary artery. This effect was especially marked at sites where, in control occlusions, ST-segment elevation was most pronounced. 4 Lidoflazine greatly reduced the number of ventricular ectopic beats which usually resulted from more prolonged (30 min) periods of acute coronary artery occlusion. There was no ventricular fibrillation in these dogs (contrast 25% incidence in the controls). (1980). There has been renewed interest in lidoflazine because of the evidence that it protects cardiac muscle against the deleterious effects of ischaemia and subsequent reperfusion (Nayler, 1980; Flameng, Daenen, Xhonneux, Van de Water & Van Belle, 1980;Flameng, Daenen, Borgers, Thone, Xhonneux, Van de Water & Van Belle, 1981). The mechanism of this protection is unclear but lidoflazine interferes with the slow channel transport of Ca2+, at least in smooth muscle, and it is possible that lidoflazine alleviates myocardial damage, at least in part, by preventing mitochondrial calcium overload (Flameng et al., 1981).Despite some evidence (de Geest, Kesteloot & Piessens, 1979) that prolonged treatment with lidoflazine is of some benefit in the long term management of patients following myocardial infarction, little is known about the effects of the drug on the 0007-1188/82/060347-08 $01.00 early life-threatening ventricular arrhythmias which are a consequence of acute myocardial ischaemia. Schaper, Xhonneux, Jageneau & Janssen (1966) showed in dogs that prolonged oral treatment with the drug reduced the incidence of ventricular fibrillation following abrupt coronary artery occlusion whereas Carmeliet & Xhonneux (1971) found that lidoflazine was ineffective in reversing ventricular arrhythmias 24 h after coronary artery ligation. The aim of the present studies was three fold. Firstly to determine whether lidoflazine is effective against the early life-threatening arrhythmias that occur soon after coronary artery occlusion. Secondly, to determine if it reduces the incidence of arrhythmias following reperfusion and thirdly to examine, using epicardial mapping techniques, whether lidoflazine reduces the severity of myocardial ischaemic damage. Methods Studies in anaesthetized ratsThe effect of lidoflazine...

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Section: Discussionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Lidoflazine in the Early Stages of Acute Myocardial Ischaemia

Coker

Fagbemi

Parratt

1982

British J Pharmacology

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“…The exigencies of cost enforced the choice of onc to represent the effect of blocking the second inward current (24,37,44). The second type of calcium antagonist, exemplified by lidoflazine, mioflazine and flunarizine do not block the second inward current (7,8) but are potent in blocking the nonelectrogenic calcium entry of prolonged depolarisation (17) and reperfusion after ischaemia (19). All of these prevent myocardial damage in a global model of one hour ischaemia followed by half an hour of reperfusion (15,53).…”

Section: Interpretation Of Results On Reduction~limitation Of Infarctmentioning

confidence: 99%

Effects on infarct size of reperfusion and pretreatment with β-blockade and calcium antagonists

et al. 1989

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The "mass of tissue at risk" and the myocardial infarct developed was studied in dogs subjected to either 24-h occlusion of the left anterior descending coronary artery or 2-h occlusion followed by 22-h reperfusion. The "mass of tissue at risk" was defined under anaesthesia at the time of occlusion using the microsphere technique. Twenty-four hours later the hearts were removed, sliced transversely and stained with 2,3,5-triphenyltetrazolium chloride to define the infarcted tissue. All myocardial tissue was mapped and cut into small pieces for weighing and radioactive counting. Radioactivity was present in all tissue, including the infarct. In the centre of the infarct, counts remained low and then increased very rapidly with distance just beyond the edge. Tissue at risk from infarction was taken as that with less than 15% of the peak left ventricular (non-ischaemic) counts. A linear relationship was found between the mass of the left ventricular infarct and the left ventricular "mass of tissue at risk". The effect of 22 hours reperfusion was examined by this method and expressed by a regression equation. There was a significant decrease in slope for the regression line of the reperfusion data, (p less than 0.05, analysis of covariance), indicating less infarcted tissue for each gram of underperfused tissue. None of the drug pretreatments explored had any effect on infarct size in the 24-h occlusion model. With reperfusion, propranolol and flunarizine diminished infarct size compared with reperfusion only (p less than 0.05 for reduced slope, the new slope being not significantly different from zero). The effect of diltiazem was not so marked. Thus infarct size can be reduced with pretreatment, as long as the myocardium is reperfused.

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“…Lidoflazine has definite effects on the cell membrane of guinea-pig and sheep atrial, Purkinje and ventricular fibers [6]. Chronic atrial fibrillation and flutter have been effectively converted by oral lidoflazine therapy [21,22], Serious arrhythmias before, during or after exercise were never observed in any of the patients of the present group.…”

Section: Discussionmentioning

confidence: 75%

Long-Term Evaluation of Lidoflazine in Angina Pectoris Based on Exercise Tolerance

Piessens¹,

Geest²

1972

Cardiology

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32 patients with angina pectoris were treated with lidoflazine for 4.1-12.8 months. During this open study 24 of them showed definite alleviation of angina and a higher exercise tolerance. These 24 patients then entered a placebo- controlled double-blind study for up to 14.5 months, and t hereafter 22 were returned to lidoflazine therapy for up to 9.3 months. Exercise tolerance increased progressively during lidoflazine therapy, receded to pretrial levels during placebo treatment and, after re-institution of lidoflazine, returned to the levels previously attained under lidoflazine. Resting and exercising heart rate decreased on lidoflazine and increased when placebo was administered. These effects paralleled the subjective improvement and deterioration.

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Influence of lidoflazine on cardiac transmembrane potentials and experimental arrhythmias

Cited by 20 publications

References 18 publications

Lidoflazine in the Early Stages of Acute Myocardial Ischaemia

Lidoflazine in the Early Stages of Acute Myocardial Ischaemia

Effects on infarct size of reperfusion and pretreatment with β-blockade and calcium antagonists

Long-Term Evaluation of Lidoflazine in Angina Pectoris Based on Exercise Tolerance

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