title: Mechanoelectric feedback after left ventricular infarction in rats.
abstract: 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 microns increased the APD90. This was associated with stretch activated depolarizations near APD90 (SAD-90). In MI, significantly lower stretch, of only 20 microns, elicited SAD-90s, or SADs near APD50 (SAD-50). Stretch-induced events were suppressed by gadolinium, at a concentration (40 microM) normally used to inhibit stretch-activated channels.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institute of Physiology, Humboldt-University (Charité), Berlin, Germany.
authors.forename: I
authors.initials: I
authors.lastname: Kiseleva
authors.forename: A
authors.initials: A
authors.lastname: Kamkin
authors.forename: K D
authors.initials: KD
authors.lastname: Wagner
authors.forename: H
authors.initials: H
authors.lastname: Theres
authors.forename: A
authors.initials: A
authors.lastname: Ladhoff
authors.forename: H
authors.initials: H
authors.lastname: Scholz
authors.forename: J
authors.initials: J
authors.lastname: Günther
authors.forename: M J
authors.initials: MJ
authors.lastname: Lab
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D005246:Feedback; D005682:Gadolinium / Q000494:pharmacology; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D008297:Male; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013314:Stress, Mechanical; D020257:Ventricular Remodeling
chemical_list: D007473:Ion Channels; D005682:Gadolinium