Abstract 11379: Intravenous Ascorbic Acid Administration During Cardiopulmonary Resuscitation Reduces Mitochondrial Damage After Ventricular Fibrillation and Electrical Shock in a Rat Model
Background: Electrical shock (ES) generates free radicals inside the cardiomyocyte, causing contractile impairment, and administering ascorbic acid (AA) reduces the damage. Intravenous administration of AA during CPR facilitates resuscitation and improves outcomes in a rat model of VF. However, the effect of AA on the intracellular damage after VF and ES has not been clarified.
Hypothesis: Intravenous administration of AA during CPR reduces mitochondrial damage after VF and ES.
Methods: The animals were equally randomized to AA, control and sham groups. In rats of AA group and control group, VF was induced and untreated for 5 minutes, followed by 1 minutes of CPR, and then one electrical shock of 5 J. The AA group received intravenous administration of AA (100 mg/kg) simultaneously at the start of CPR, and the control group received saline as placebo. After ES, animals were sacrificed immediately. The sham group received the same treatments except VF induction, resuscitation, drugs and ES. The mitochondria were isolated from left ventricles for measurement of mitochondrial permeability transition pore (mPTP) opening and complex activity.
Results: The Glomori stain showed that subsarcolemmal aggregation of mitochondria in the control group, suggesting VF and ES resulted in mitochondrial damage. The application of AA alleviated the mitochondrial aggregation. MPTP opening caused mitochondrial swelling. After adding CaCl2, the mitochondria of the control group showed accelerated mitochondrial swelling. AA prevented the acceleration of mitochondrial swelling (Fig 1a). Compared with the sham group, the activity of NADH cytochrome c reductase (NCCR) and cytochrome c oxidase (CCO) but succinate cytochrome c reductase (SCCR) decreased in the control group (Fig 1b-d) . AA prevented the decreased activity of NCCR and CCO after VF and ES.
Conclusion: Intravenous administration of AA during CPR reduces mitochondrial damage after VF and ES.
- Cardiac arrest
- Free radicals/Free-radical scavengers
- Ventricular fibrillation
- Electric countershock
- © 2010 by American Heart Association, Inc.