Abstract 74: Worse Hemodynamics and Greater Oxidative Stress Response in Obese Rats Compared to Normal Rats Following Resuscitation From Cardiac Arrest
Introduction: Obesity is associated with cardiovascular fatal events, including cardiac arrest. Moreover, obesity is associated with greater oxidative stress response following an ischemic insult. In the setting of cardiac arrest, this may contribute to worse outcome following ROSC. We hypothesized greater oxidative stress following ROSC in obese rats compared to non obese rats and worse post resuscitation hemodynamics.
Methods: Ventricular fibrillation was induced in 5 SD rats, 470 ± 10 g, and 6 Zucker fat rats, 544 ± 19 g, and was untreated for 6 mins. CPR was then performed for 6 mins prior to defibrillations. Arterial and right atrial and coronary perfusion pressure (CPP) were continuously measured. Two hrs post ROSC, cardiac output was echocardiographically assessed. Animals were then sacrified and organs harvested for lipid hydroxides (LOOH) measurement, as marker of oxidative stress.
Results: No differences in CPP were observed between the two groups (Table) and each animal was successfully resuscitated. Two hrs post ROSC, obese rats had significantly lower arterial pressures and cardiac output compared to SD rats (Table). LOOH in heart and kidney increased after resuscitation (p<0.05) in each animal. However these increases were greater in the obese rats (p<0.01 vs SD, Fig). Oxidative stress in the brain was significantly greater in the SD rats, while LOOH increases in the kidney were observed only in the obese rats (p<0.01, Fig).
Conclusions: Obese rats achieved ROSC au pair than non obese rats, but showed worse post resuscitation hemodynamics. Greater oxidative stress was observed in heart, kidney and liver of obese animals, while brain was more protected.
- © 2010 by American Heart Association, Inc.