title: Individual effect of components of defibrillation waveform on the contractile function and intracellular calcium dynamics of cardiomyocytes.
abstract: OBJECTIVE
  Although electrical shock is a unique and effective treatment for fatal arrhythmia, it produces myocardial dysfunction closely related to the intensity of shock delivered. The isolated contribution of defibrillator components to postshock contractile impairment is not yet securely established. We sought to evaluate contractile function in cardiomyocytes following electrical shocks with different peak currents, energies, and durations. We hypothesized that peak current may play a more important role than energy in determining postshock dysfunction. Prolongation of the duration may reduce contractile impairment.
  
  
  METHODS
  Prospective, randomized, controlled study.
  
  
  METHODS
  University-affiliated research institute.
  
  
  METHODS
  Male albino Sprague-Dawley rats.
  
  
  METHODS
  We assigned 324 cardiomyocytes isolated from adult male rats to 11 groups having different waveforms (triangular and square), peak currents (derived from peak voltage gradients of 25 V/cm, 35.4 V/cm, 50 V/cm, 70.7 V/cm, and 100 V/cm), and durations (10 and 20 msecs) of shocks delivered. One single shock was given to each cardiomyocyte, and length shortening and Ca transients were recorded optically with fura-2 loading.
  
  
  RESULTS
  Increase of peak current and corresponding energy caused more cells to have irregular beating (p < .001) and reduced length shortening (p < .001). This was associated with increased Ca abnormality (p < .05). Increasing peak current independent of energy significantly impaired postshock contractile function (p < .05), whereas the change of energy alone did not. Prolongation of duration independent of energy and peak current reduced postshock contractile impairment (p < .05).
  
  
  CONCLUSIONS
  Peak current may play a more determinative role in producing postshock contractile dysfunction than does energy.
authors.affiliation: Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA. drsheart@aol.com
authors.forename: Min-Shan
authors.initials: MS
authors.lastname: Tsai
authors.forename: Wanchun
authors.initials: W
authors.lastname: Tang
authors.forename: Shijie
authors.initials: S
authors.lastname: Sun
authors.forename: Hao
authors.initials: H
authors.lastname: Wang
authors.forename: Gary
authors.initials: G
authors.lastname: Freeman
authors.forename: Wen-Jone
authors.initials: WJ
authors.lastname: Chen
authors.forename: Max Harry
authors.initials: MH
authors.lastname: Weil
mesh_terms: D000818:Animals; D015220:Calcium Channels / Q000378:metabolism*; D009202:Cardiomyopathies / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D002478:Cells, Cultured; D004554:Electric Countershock / Q000009:adverse effects / Q000379:methods*; D008297:Male; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000648:ultrastructure; D011446:Prospective Studies; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D015220:Calcium Channels