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Mechanoelectric feedback after left ventricular infarction in rats.
I Kiseleva1, A Kamkin, K D Wagner
1Institute of Physiology, Humboldt-University (Charité), Berlin, Germany.
Cardiovascular Research
|March 23, 2000
Summary
Myocardial infarction (MI) increases cardiac myocyte sensitivity to mechanical stretch, causing abnormal electrical activity. This mechanoelectric feedback in the borderzone may explain post-infarction arrhythmias.
Area of Science:
- Cardiovascular Physiology
- Cardiac Electrophysiology
- Mechanoelectric Feedback
Background:
- Myocardial infarction (MI) can cause electrical abnormalities and rhythm disturbances.
- Limited data exists on the electrophysiological basis of post-MI arrhythmias.
- Regional contraction abnormalities are prominent after MI.
Purpose of the Study:
- Investigate if myocardial stretch at the infarction borderzone modulates cardiomyocyte electrophysiology.
- Determine if mechanoelectric feedback contributes to post-MI arrhythmia.
- Examine stretch-activated depolarizations (SADs) in infarcted hearts.
Main Methods:
- Experimental myocardial infarction (MI) induced in rats.
- Action potentials (AP) measured in left ventricular borderzone preparations.
- Sustained stretch applied via micrometer; SADs recorded.
Main Results:
- MI preparations showed spontaneous electrical and contractile activity.
- MI cardiomyocytes exhibited prolonged AP duration and more negative resting potential.
- Lower stretch levels elicited SADs in MI compared to sham operations (SO).
Conclusions:
- Spontaneous SADs occur at lower stretch degrees in the MI borderzone.
- Increased cardiac myocyte sensitivity to mechanical stimuli may drive post-MI arrhythmia.
- Stretch-activated channels likely mediate these observed SADs.