A modified model of global ischaemia: application to the study of syncytial mechanisms of arrhythmogenesis

Abstract

These findings strongly support the theory that current of injury between ischaemia and adjacent non-ischaemic zones is necessary for initiation of ischaemia induced VF, since susceptibility was maximal when ischaemic and uninvolved regions were equivalent in size (and the scope for injury current was maximal) whereas susceptibility was negligible when scope was minimal. In contrast, reperfusion induced VF appears to depend only on the presence and amount of reperfused tissue, indicating that flow of injury current between involved and uninvolved tissue is unnecessary for its initiation. Discrimination of the mechanism of action of antiarrhythmic interventions may be possible since drugs effective solely via amelioration of flow of injury current (or incrementation of collateral flow) will not influence arrhythmias in this model. Modification of injury current and collateral flow do not appear to contribute to the antiarrhythmic action of substitution of extracellular chloride by nitrate.