Abstract P21: Free Radicals Mediate Post-shock Contractile Impairment in Cardiomyocytes
Background Previous studies demonstrated myocardial dysfunction after electrical shock and indicated that it may be related to the generation of free radicals. Whether the free radicals are generated after electrical shock has not been documented at the cellular level and its effect on post-shock contractile function has not been clarified.
Hypothesis: Electrical shock generates intracellular free radicals inside cardiomyocytes. Reducing intracellular free radicals by pre-treatment of ascorbic acid (AA) would reduce the contractile dysfunction following electrical shock.
Methods: Cardiomyocytes isolated from adult male rats were divided into 4 groups, (1) electrical shock alone, (2) electrical shock pre-treated with AA, (3) pre-treated with AA alone and (4) control. AA was administered in an amount of 0.2 mM into the perfusate of the AA + electrical shock and AA groups. Electrical shock of 2 J was delivered in the electrical shock and AA+ electrical shock groups.
Results: DCFH-DA loaded cardiomyocytes showed increased intracellular free radicals after electrical shock. The length shortening and Ca2+ transients were recorded optically with fura-2 loading. Within 4 minutes following electrical shock in the electrical shock group, the length shortening decreased from 8.4±2.5% to 5.6±3.4% (P=0.000) and the Ca2+ transient decreased from 1.15±0.13 au to 1.08±0.1 au (P=0.038). Compared with control, a significant difference in length shortening (P=0.001) and Ca2+ transient (P=0.052) was observed. In the presence of AA, electrical shock did not affect length shortening and Ca2+ transient.
Conclusion: Electrical shock generates intracellular free radicals inside the cardiomyocyte. This is associated with contractile impairment and decrease of Ca2+ transient. Administering AA may decrease such damage by eliminating free radicals.