Mechanoelectric feedback after left ventricular infarction in rats

Citation
I. Kiseleva et al., Mechanoelectric feedback after left ventricular infarction in rats, CARDIO RES, 45(2), 2000, pp. 370-378
Citations number
46
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOVASCULAR RESEARCH
ISSN journal
0008-6363 → ACNP
Volume
45
Issue
2
Year of publication
2000
Pages
370 - 378
Database
ISI
SICI code
0008-6363(20000114)45:2<370:MFALVI>2.0.ZU;2-9
Abstract
Background: Myocardial infarction can lead to electrical abnormalities and rhythm disturbances. However, there is limited data on the electrophysiolog ical basis for these events. Since regional contraction abnormalities featu re prominently in infarction, we investigated whether stretch of myocardium from the infarction borderzone can modulate the electrophysiological prope rties of cardiomyocytes via mechanoelectric feedback providing a mechanism for post-infarction arrhythmia. Methods: Five weeks after experimental myoc ardial 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 meas ured in left ventricular preparations from the infarction borderzone. Susta ined stretch was applied via a micrometer. Results: Preparations from MI ge nerated spontaneous electrical and contractile activity. Cardiomyocytes fro m MI had a comparable AP amplitude, a more negative resting membrane potent ial, and a prolonged AP duration (APD) when compared to SO. In SO, stretch of 150 mu m increased the APD90, This was associated with stretch activated depolarizations near APD90 (SAD-90). In MI, significantly lower stretch, o f only 20 mu m, elicited SAD-90s, or SADs near APD50 (SAD-50). Stretch-indu ced events were suppressed by gadolinium, at a concentration (40 mu M) norm ally used to inhibit stretch-activated channels. Conclusion: After MI, SADs are generated in the infarction borderzone at lower degrees of stretch. In creased sensitivity of the membrane potential of cardiac myocytes to mechan ical stimuli may contribute to the high risk of arrhythmia after infarction . These SADs may involve the opening of stretch-activated channels. (C) 200 0 Elsevier Science B.V. All rights reserved.