Abstract 10467: Inflammation May Be Involved in Ischemic Preconditioning in Rat Model of CPR

Background: Ischemia preconditioning (IPC) is a potent strategy that minimizes post-resuscitation cardiac and neurological dysfunction via a K ATP channel-dependent mechanism. Inhibition of inflammation is also related to ischemic tolerance. In this study, we investigate the relation between the two intrinsic mechanisms in a rat model of cardiac arrest and CPR. Hypothesis: Activation of K ATP channels and anti-inflammatory response are two independent mechanisms of IPC to improve post-CPR myocardial and cerebral function. Methods: A total of 24 Sprague-Dawley rats (450-550g) were randomized into three groups (n=8 for each group): 1) control, 8 minutes of untreated ventricular fibrillation (VF) followed by 8 minutes of cardiopulmonary resuscitation and defibrillation; 2) IPC, remote IPC initiated 55 minutes before the induction of VF; 3) IPC+GLIB, glibenclamide (0.3 mg/kg, i.v.) was administered 45 minutes before remote IPC, and rest of protocol was the same as the IPC group. Doppler echocardiography, neurologic deficit score (NDS) scale, and the duration of survival were monitored in all animals. The level of NF-κB, IL-1β, IL-10 were evaluated using the enzyme-linked immunosorbent assay (ELISA). Results: Compared with the control groups, significantly greater CO and EF, lower MPI, improved NDS, and increased duration of survival were observed in both the IPC and IPC+GLIB group during post-resuscitation ( p < 0.05 or 0.01 versus control group). Glibenclamide partly reversed the improvement induced by ischemic preconditioning ( p < 0.05 or 0.01 versus IPC group) (Fig. 1). However, there were no significant differences in biomarkers between the IPC and IPC+GLIB group (Fig. 2). Conclusions: In a rat cardiac arrest model, anti-inflammatory response attenuated the myocardial and neurological dysfunction during the post-resuscitation via a non-K ATP channel-dependent mechanism.