Abstract 126: Cholecystokinin Octapeptide Induced Mild Hypothermia and Improved the Neurological Outcome After CPR
Systemic therapeutic hypothermia initiated after resuscitation has been shown to improve survival and long-term neurological outcome. In view of the limitations of physical cooling techniques, pharmacological hypothermia is now emerging as a new option for cardiac resuscitation. In the present study, we examined the effects of cholecystokinin octapeptide (CCK8) on thermoregulation and neurological outcome. We hypothesized that CCK8 could induce hypothermia and therefore improve neurological outcome after CPR. Ventricular fibrillation (VF) was induced and untreated in 10 male S-D rats weighing between 450–550g. CPR was initiated after 6 minutes of VF and coronary perfusion pressure was maintained at 24±2 mm Hg. Defibrillation was attempted after 8 minutes of CPR. Either CCK8 (200 μg/kg in 0.3 ml saline) or saline placebo (0.3 ml) was injected intravenously 30 minutes after ROSC. Blood temperature was monitored continuously and the neurological deficit scores (NDS) were measured 24, 48, 72 hours after resuscitation. Blood temperature decreased to 34.8°C in the CCK8 group 5 hours after injection and returned to 37°C 9 hours after injection (Figure 1). Blood temperature was unchanged at 37°C ±0.2 in control animals during the same period of observation. NDS in the CCK8 group were significantly better in comparison with the control group (52±19 vs 306±180, 24 hours, p<0.05; 25±13 vs 356±152, 48 hours, p<0.05; 4±2 vs 423±172, 72 hours, p<0.05) (Figure 2). In the rat model of CPR, CCK8 induced mild hypothermia and resulted in improved neurological outcome.
- © 2010 by American Heart Association, Inc.