Key result
In an isolated rabbit heart model, streptomycin (80 microM) inhibited stretch-related shortening of repolarization, whereas verapamil had no effect.
Why the study?
Does streptomycin or verapamil prevent stretch-induced shortening of repolarization and arrhythmias in an isolated rabbit heart model?
Does streptomycin or verapamil prevent stretch-induced shortening of repolarization and arrhythmias in an isolated rabbit heart model?
Stretch-activated ion channels, but not specific calcium channels, appear to mediate stretch-related changes in repolarization and arrhythmias in isolated rabbit hearts, which can be blocked by streptomycin.
Answers are grounded in this paper and cite their sources.
May inform experimental models of stretch-induced repolarization changes; leaves open clinical relevance pending further study.
The exact mechanism of mechano-electrical feedback and stretch-induced arrhythmias is unknown, but the role of stretch-activated ion channels and specific calcium channels has been proposed. The aim of the present study was to test the hypothesis that stretch-activated ion channels and not calcium channels contribute to stretch-related alterations of repolarization and that these effects can be neutralized by stretch-activated channel block. We studied the interaction of acute ventricular dilatation and the stretch-activated channel blocker streptomycin and the specific calcium channel blocker verapamil in an isolated retrogradely perfused rabbit heart model in which the left ventricular size is modified by abruptly changing the volume of a fluid-filled balloon placed in the left ventricle. Acute ventricular dilatation led to a rate-dependent decrease in repolarization. The mean effective refractory period (ERP) and monophasic action potential duration (MAP90) for cycle lengths between 300 and 1,000 ms decreased from 174.2+/-9 ms and 178.9+/-7 ms to 161.6+/-11 ms and 169.7+/-5 ms, respectively. Streptomycin (80 microM) inhibited this stretch-related shortening of repolarization (ERP: 175.4+/-8 ms; MAP90: 179.7+/-8 ms, p < 0.05) but had almost no effect on already dilated ventricles. Counteraction of the observed electrophysiologic changes could only be achieved by increasing the streptomycin concentration to 200 microM. Streptomycin nearly completely suppressed stretch-related ectopic ventricular complexes. In contrast, verapamil (1 microM) had no effect on stretch-related changes in repolarization and stretch-induced arrhythmias. The present study indirectly implicates stretch-activated ion channels in the genesis of stretch-related changes in repolarization and arrhythmias. The electrophysiologic changes after ventricular dilatation to a degree that increases left ventricular pressure in a clinically relevant range can be influenced by the stretch-activated channel blocker streptomycin but not by specific calcium channel block. This may have clinically important implications for the development of new antiarrhythmic drugs.
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Eckardt et al. (2000) studied Stretch-induced arrhythmias and repolarization changes. Streptomycin vs. Untreated dilated ventricles and Verapamil (1 microM) was evaluated on Effective refractory period (ERP) and monophasic action potential duration (MAP90) (p=< 0.05). In an isolated rabbit heart model, streptomycin (80 microM) inhibited stretch-related shortening of repolarization, whereas verapamil had no effect.
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