No abstract

Antiarrhythmic effects of phosphorylated glycolysis intermediates glucose-l-phosphate, fructose-l,6-diphosphate, and phosphoenolpyruvate in early postocclusion arrhythmias are shown in rat experiments; in contrast to these, D-glucose, sodium pyruvate, and monoiodacetate, a glycolysis inhibitor, exert no appreciable antiarrhythmic effect. Key Words: occlusion arrhythmias; glycolysis; glycolysis intermediatesThere is no doubt that prolongation of glycolytic energy production during administration of glycolysis intermediates and electron acceptors has a favorable impact on the course of acute myocardial ischemia, improving the hemodynamic parameters and decreasing the size of the necrosis zone [1,5,6,8]. The contribution of glycolysis to the development of early postocclusion arrhythmias and ventricular fibrillation is still being debated [2,3].We investigated the effects of monoiodacetate glycolysis intermediates on the course of postocclusion arrhythmias and the incidence of ventricular fibrillation in acute myocardial ischemia. MATERIALS AND METHODSExperiments were carried out with Wistar rats weighing 160 to 240 g narcotized with sodium thiopental in a dose of 50 mg/kg intraperitoneaUy. The descending branch of the left coronary artery was occluded in a single step during artificial ventilation of the lungs. The ECG was continuously recorded in the II standard lead. The following characteristics of arrhythmia were assessed: latent period before the development of occlusion arrhythmias, mean number of ventricular extrasystoles, frequency and duration of paroxysms of ventricular tachycardia, and incidence of ventricular fibrillation. The tested compounds: monoiodacetate (MIA), Dglucose (DGL), glucose-l-phosphate (G-I-P), fructose-l,6-diphosphate (FDP), phosphoenolpyruvate (PEP), and pyruvate (PV) were intravenously injected as a sodium salt solution in 0.5 ml normal saline with a microdosing device according to the following scheme: 25% of the dose in a jet before coronary artery occlusion and 75% by drip infusion for 10 min after the occlusion. MIA was jet-injected 2 min before occlusion. Doses of the compounds are presented in Table 1. The data were statistically processed using Student's t test and Z 2 methods. RESULTSIn the control the development of early postocclusion arrhythmias lasting for 70+16 sec was observed as soon as 218+39 sec after coronary artery occlusion in 100% of experiments. In 5 of the 13 experiments the animals developed ventricular fibrillation (Table 1).