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.