Cardioprotective effects of lidoflazine during 1-hour normothermic global ischemia.

Abstract

NAYLERI suggested that lidoflazine exerts a protective effect on the ischemic and reperfused heart muscle. In the experiments on the isolated rabbit heart perfused by the Langendorff method, the drug was found to suppress the steep rise in end-diastolic conFrom the

Evaluation of protective effects of lidoflazine and mioflazine in cardiac ischemia

“…The cardioprotective characteristics of lidoflazine and its structural analogue mioflazine were documented in cardiopulmonary bypass-assisted experiments of global ischemia [Flameng et al, 1981Wood et al, 19851. As a relatively simple experimental approach that would produce global ischemia and permit the assessment of cardiac function and morphology during and after an ischemic insult, we employed the isolated working heart [Neely et al, 1967;Snoeckx, 1981;Ichihara and Yasushi, 19831.…”

Lidoflazine in the Early Stages of Acute Myocardial Ischaemia

“…The experimental studies with this compound have been reviewed by Parratt (1969) and, more recently, by Vanhoutte & Van Nueten (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, Xhon-neux, 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).…”

“…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.…”

Prevention of the “no reflow” phenomenon in the canine heart by mioflazine

“…These observations suggest that agents with cardioprotective properties rather .than pure vasodilators may influence the development of reduced reflow. Mioflazine and lidoflazine are potent cardioprotecting agents (14,15). Both drugs inhibit adenosine uptake in human erythrocytes (16,23).…”

“…This new drug is a chemical analogue of lidoflazine. Both drugs mioflazine and lidoflazine have significant cardioprotectire properties (14,15) probably related to an interaction with the sarcolemma (15,16). In the model presented in this study we pretreated dogs orally with mioflazine and measured hemodynamics, regional myocardial blood flow and infarct size during and after an interval of 90 minutes of coronary occlusion followed by reperfusion.…”