Abstract 77: Vitamin-C Compromises Cardiac Resuscitability in a Rat Model of Ventricular Fibrillation and Closed Chest Resuscitation
Introduction: Resuscitation from cardiac arrest is in part limited by progressive reduction in left ventricular distensibility, which compromises the ability of chest compression to generate blood flow. Interventions that maintain mitochondrial bioenergetic function during reperfusion injury help preserve left ventricular distensibility. A major pathogenic component of such injury is production of reactive oxygen species.
Hypothesis: We hypothesized that attenuating oxidative injury helps maintain left ventricular distensibility yielding higher return of spontaneous circulation (ROSC) and survival. Using vitamin-C as an antioxidant, we assessed effects on left ventricular distensibility — by determining the ratio between coronary perfusion pressure and depth of compression (CPP/Depth) -, ROSC, and survival.
Methods: VF was electrically induced in male rats and left untreated for 10 minutes before attempting resuscitation by 8 minutes of CPR and electrical shocks. Two series were conducted; one series to assess the effects of dehydroascorbate (DHA) — an oxidized form of vitamin-C that enters the cell via a GLUT4 transporter — and another series to assess the effects of ascorbate (AA) — the reduced form of vitamin-C that enters the cell via a specialized transporter. In each series, two groups of 8 rats each were randomized to receive a right atrial bolus (250 mg/kg) of DHA in series 1 and of AA in series 2 or their respective controls (Ctl) before starting chest compression with the investigators blind to the assignment.
Results: Contrary to our hypothesis, the CPP/Depth ratio was lower (NS) with DHA (1.63 ± 0.23 vs 1.87 ± 0.65 mmHg/mm) and with AA (1.81 ± 0.62 vs 1.92 ± 0.29 mmHg/mm) and resuscitability was compromised (Figure).
Conclusions: Vitamin-C failed to preserve left ventricular distensibility and had a detrimental effect on resuscitability, suggesting possible beneficial effects of oxidative stress disrupted by the antioxidant effect of vitamin-C.
- © 2010 by American Heart Association, Inc.