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Cardiovascular Research 2000 45(2):370-378; doi:10.1016/S0008-6363(99)00361-2
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Mechanoelectric feedback after left ventricular infarction in rats

Irina Kiselevaa,e, Andre Kamkina,e, Kay-Dietrich Wagnera,*, Heinz Theresb, Axel Ladhoffc, Holger Scholza, Joachim Günthera and Max J. Labd

aInstitute of Physiology, Humboldt-University (Charité), Tucholskystrasse 2, 10117 Berlin, Germany
bClinic Internal Medicine I, Humboldt-University (Charité), Schumannstrasse 20/21, 10117 Berlin Germany
cInstitute of Pathology, Humboldt-University (Charité), Schumannstrasse 20/21, 10117 Berlin, Germany
dNational Heart and Lung Institute, Imperial College School of Medicine, Charing Cross Hospital, London W6 8RF, UK
eDepartment of Physiology, Martin-Luther-University of Halle, Magdeburger Strasse 6, 0697 Halle/Saale, Germany

* Corresponding author. Tel.: +49-30-2802-6562; fax: 49-30-2802-6662 kay-dietrich.wagner{at}charite.de

Background: Myocardial infarction can lead to electrical abnormalities and rhythm disturbances. However, there is limited data on the electrophysiological basis for these events. Since regional contraction abnormalities feature prominently in infarction, we investigated whether stretch of myocardium from the infarction borderzone can modulate the electrophysiological properties of cardiomyocytes via mechanoelectric feedback providing a mechanism for post-infarction arrhythmia. Methods: Five weeks after experimental myocardial infarction (MI) in rats due to ligation of the left coronary artery (n=26) or after sham operation (SO, n=16), action potentials (AP) were measured in left ventricular preparations from the infarction borderzone. Sustained stretch was applied via a micrometer. Results: Preparations from MI generated spontaneous electrical and contractile activity. Cardiomyocytes from MI had a comparable AP amplitude, a more negative resting membrane potential, and a prolonged AP duration (APD) when compared to SO. In SO, stretch of 150 µm increased the APD90. This was associated with stretch activated depolarizations near APD90 (SAD-90). In MI, significantly lower stretch, of only 20 µm, elicited SAD-90s, or SADs near APD50 (SAD-50). Stretch-induced events were suppressed by gadolinium, at a concentration (40 µM) normally used to inhibit stretch-activated channels. Conclusion: After MI, SADs are generated in the infarction borderzone at lower degrees of stretch. Increased sensitivity of the membrane potential of cardiac myocytes to mechanical stimuli may contribute to the high risk of arrhythmia after infarction. These SADs may involve the opening of stretch-activated channels.

KEYWORDS Arrhythmia (mechanisms); Infarction; Ion channels; Membrane potential; Stretch/m-e coupling


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