Abstract 18275: Exploratory Study of Emergency Cardiopulmonary Bypass for Resuscitation from Ventricular Fibrillation Cardiac Arrest in Rats
Background: Cardiopulmonary bypass (CPB) potentially provides immediate cerebral reperfusion, cardiovascular support, and temperature control for resuscitation from cardiac arrest (CA). A rodent model of ventricular fibrillation (VF) CA would help to optimize CPB use. We hypothesized that resuscitation with CPB would improve outcome after VF CA in rats vs. standard cardiopulmonary resuscitation (CPR).
Methods: Adult male Sprague-Dawley rats were intubated, and instrumented with catheters and CPB cannulae. Rats were randomized to a CPR, CPB or sham (surgery and anesthesia only) group. After 6 min of electrically induced VF, resuscitation was performed with drugs (epinephrine, sodium bicarbonate, heparin), mechanical ventilation and either manual chest compressions, 200/min in the CPR group, or CPB at a flow rate of 50 ml/min. After defibrillation at 2 min of resuscitation and 1 h of intensive care, rats were returned to their cages. Temperature was maintained at 37.0±0.5°C for 12 h after restoration of spontaneous circulation (ROSC). Outcome parameters included neurologic deficit scores (NDS; 0%=normal, 100%=dead), overall performance category (OPC; 1=normal, 5=dead), Morris watermaze (MWM) testing and counts of viable neurons in the CA1 region of the hippocampus at 14 d after the insult (% of sham).
Results: ROSC was not achieved in one rat in the CPR group. 7/10 rats in the CPB-group (6xOPC 1, 1 OPC 2), 5/10 in the CPR group (5xOPC 1) and 10/10 shams (10xOPC 1) survived to day 14. NDS (mean±SD) was 2±3; 1±1; and 0±0 in the three groups. There were no differences between groups in MWM performance. Viable neuron counts in the CA1 region of the hippocampus (median and interquartile range) were 100 (94; 109)% in the sham group, 20 (5; 71)% in the CPB-group, and 18 (7; 38)% in the CPR-group.
Conclusions: In a rat model of VF CA, either CPR or CPB lead to overall favorable functional outcome after 6 min of VF. However, marked neuronal death in CA1 was seen across CA groups. Although CPB may provide critical hemodynamic support clinically in the setting of myocardial infarction, it does not prevent delayed neuronal death in a rat model of VF CA. Future studies will determine benefit of CPB after longer CA durations, and test resuscitation adjuncts to prevent neuronal death.
- © 2010 by American Heart Association, Inc.