title: Role of streptomycin-sensitive stretch-activated channel in chest wall impact induced sudden death (commotio cordis).
abstract: BACKGROUND
  Deaths secondary to low-energy impacts to the precordium in young individuals (commotio cordis) have been reported with increasing frequency. In a swine model, baseball impacts induce ventricular fibrillation when directed at the center of the left ventricle during the vulnerable portion of repolarization just prior to the T-wave peak. It has been hypothesized that activation of stretch-sensitive channels could be crucial for this electrophysiological phenomenon. In this study, a nonselective stretch-activated cation channel was pharmacologically blocked prior to chest blows to determine whether this channel represents a possible pathway by which commotio cordis events occur.
  
  
  METHODS
  In a randomized and blinded experiment, 12 swine (mean 17.1 +/- 2.5 kg) received either 2-g streptomycin intramuscularly (mean serum concentration 115 +/- 18 muM) or sterile water prior to chest impact. Each animal received six precordial impacts with a baseball propelled at 40 mph.
  
  
  RESULTS
  There was no significant difference in the frequency of induced VF in the animals administered streptomycin (10 of 19 impacts: 53%) compared to those control animals receiving only sterile water (10 of 31: 32%) (P = 0.15). However, the magnitude of ST segment elevation was less in the streptomycin-treated animals (19 +/- 19 mV) versus controls (61 +/- 46 mV) (P = 0.015).
  
  
  CONCLUSIONS
  Streptomycin did not alter the frequency of ventricular fibrillation in our commotio cordis model, indicating that the stretch-activated channel is not implicated in the genesis of chest blow-induced cardiac arrest. However, streptomycin did reduce ST elevation following impact suggesting that the stretch-activated channel may play a role in ST segment elevation following chest wall blows.
authors.affiliation: New England Cardiac Arrhythmia Center, Tufts-New England Medical Center, Boston, Massachusetts, USA.
authors.forename: Arthur R
authors.initials: AR
authors.lastname: Garan
authors.forename: Barry J
authors.initials: BJ
authors.lastname: Maron
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Wang
authors.forename: N A Mark
authors.initials: NA
authors.lastname: Estes
authors.forename: Mark S
authors.initials: MS
authors.lastname: Link
mesh_terms: D000818:Animals; D017920:Antiporters / Q000187:drug effects* / Q000378:metabolism; D016757:Death, Sudden, Cardiac / Q000209:etiology*; D004195:Disease Models, Animal; D004562:Electrocardiography; D006335:Heart Injuries / Q000150:complications*; D006352:Heart Ventricles / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology*; D011897:Random Allocation; D013307:Streptomycin / Q000494:pharmacology*; D013552:Swine; D013898:Thoracic Injuries / Q000150:complications*; D014693:Ventricular Fibrillation / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D017725:Ventricular Pressure / Q000502:physiology; D014949:Wounds, Nonpenetrating / Q000150:complications
chemical_list: D017920:Antiporters; D011500:Protein Synthesis Inhibitors; D013307:Streptomycin