Abstract 76: Plasma Cytochrome c Level: A Marker of Post-Resuscitation Left Ventricular Dysfunction?
Background: We have previously reported that mitochondrial injury with cytosolic release of cytochrome c in left ventricular rat myocardium occurs after resuscitation from cardiac arrest. In the same study, cytochrome c was detected in plasma attaining levels inversely proportional to survival. Because failure to survive reflected progressive hemodynamic deterioration, we hypothesized that plasma cytochrome c could reflect myocardial injury and inversely correlate with indices of left ventricular function. In a study in which we compared the effects of two sodium hydrogen exchanger-1 inhibitors; i.e., AVE 4454B (AVE) and cariporide, we investigated the association between plasma cytochrome c and post-resuscitation left ventricular function.
Methods: VF was electrically induced in 20 Sprague-Dawley male rats and left untreated for 10 minutes before attempting resuscitation by 8 minutes of CPR and electrical shocks. Rats received a right atrial bolus dose of AVE (1 mg/kg, n = 10) or cariporide (1 mg/kg, n = 10) immediately before starting chest compression. Four AVE- and six cariporide-treated rats that survived 240 minutes post-resuscitation and were hemodynamically viable with a mean aortic pressure (MAP) > 40 mmHg were included in the analysis. Plasma cytochrome c was measured by HPLC.
Results: As expected, there was profound post-resuscitation myocardial dysfunction with only 50% of the rats surviving 240 minutes and with a left ventricular stroke work index (LVSWI) of only 30% baseline. As shown in Figure, plasma cytochrome c in these survivors was inversely correlated with MAP, cardiac index (CI), LVSWI, and the maximal rate of left ventricular pressure rise (+dP/dtmax).
Conclusions: Plasma cytochrome c correlated with post-resuscitation left ventricular dysfunction pointing to mitochondrial injury as a key pathogenic feature and suggesting that plasma cytochrome c levels could serve to assess the severity of such dysfunction.
- © 2010 by American Heart Association, Inc.