Abstract 32: Pharmacological Postconditioning With Sevoflurane After Cardiopulmonary Resuscitation Reduces Myocardial Dysfunction but Not Neurological Deficits
Background: Both myocardial and neurological dysfunctions are critical issues after successful cardiopulmonary resuscitation (CPR). Volatile anesthetics have been suggested to be both cardio- and neuroprotective in ischemia/reperfusion injury.
Methods: Twenty anesthetized (4 mg/kg/h propofol) pigs were subjected to electrically-induced cardiac arrest. After 8 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started according to the current AHA guidelines. After successful return of spontaneous circulation (ROSC; n=16), animals were randomized either to i) continuing 4 mg/kg/h propofol anesthesia (Control) or to ii) the volatile anesthetic sevoflurane (2.0 Vol% SEVO). Animals were weaned from the ventilator 4h after ROSC. 24h after ROSC, first neurological performance was evaluated using a neurological deficit score (CCM 1994; 22: 282–90). Then, pigs were again anesthetized with propofol in order to obtain left ventricular ejection fraction (LVEF) by transesophageal echocardiography and to take cardiac and cerebral cortex tissue samples. Serum troponin T levels were determined. The effects on cardiac and cerebral tissue interleukin (IL)-1β protein expression were studied using ELISA technique.
Results: Animals treated with SEVO showed increased LVEF, lower troponin T peak levels (Fig. 1a,b; p<0.05) and reduced cardiac IL-1β protein expression levels (0.12±0.01 vs. 0.15±0.02 pg/ total protein in μg; p<0.05) compared to the Control group. Neurological deficit scores (Fig. 1c) and cerebral IL-1β protein expression levels did not differ between groups.
Conclusions: After cardiopulmonary resuscitation, the application of the volatile anesthetic sevoflurane showed postconditioning effects by reducing myocardial damage and dysfunction possible via a reduced rate of pro-inflammatory cytokine expression, but did not improve neurological deficits.
- © 2010 by American Heart Association, Inc.