Electrophysiological effects of ethmozin on canine myocardium.
The electrophysiological effects of ethmozin on canine myocardium were studied in anesthetised open-chest animals and in superfused Purkinje fibres. The drug did not change spontaneous sinus node cycle length and atrioventricular conduction time when selectively injected into the sinus nodal artery and into the posterior septal artery, respectively. Right and left ventricular diastolic excitability threshold and refractory period were increased following the intravenous administration of ethmozin, 4 mg/kg-1. Ethmozin (3 to 5 mg/kg-1 i.v.) markedly increased conduction delay in the ischaemic zone of the left ventricle during acute coronary artery occlusion. This change was associated with the development of ventricular fibrillation in 50% of the dogs. In vitro, ethmozin 1 X 10(-3) and 1 X 10(-2) g.litre-1 shortened Purkinje fibres' action potential duration. At 1 X 10(-2) g.litre-1, ethmozin decreased the rate of rise of phase 0, and slightly reduced action potential amplitude.[1]References
- Electrophysiological effects of ethmozin on canine myocardium. Ruffy, R., Rozenshtraukh, L.V., Elharrar, V., Zipes, D.P. Cardiovasc. Res. (1979) [Pubmed]
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