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      Role of streptomycin-sensitive stretch-activated channel in chest wall impact induced sudden death (commotio cordis).

      Journal of Cardiovascular Electrophysiology
      Animals, Antiporters, drug effects, metabolism, Death, Sudden, Cardiac, etiology, Disease Models, Animal, Electrocardiography, Heart Injuries, complications, Heart Ventricles, physiopathology, Male, Protein Synthesis Inhibitors, pharmacology, Random Allocation, Streptomycin, Swine, Thoracic Injuries, Ventricular Fibrillation, Ventricular Pressure, physiology, Wounds, Nonpenetrating

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          Abstract

          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. 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. 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). 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.

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