title: Cholecystokinin octapeptide induces hypothermia and improves outcomes in a rat model of cardiopulmonary resuscitation.
abstract: OBJECTIVE
  To investigate the effects of cholecystokinin octapeptide on thermoregulation, postresuscitation myocardial function, neurologic outcome, and duration of survival in a rat model of cardiopulmonary resuscitation.
  
  
  METHODS
  : Prospective, randomized, placebo-controlled experimental study.
  
  
  METHODS
  University-affiliated animal research laboratory.
  
  
  METHODS
  Ten male Sprague-Dawley rats.
  
  
  METHODS
  Ventricular fibrillation was induced and untreated for 6 mins. Defibrillation was attempted after 8 mins of cardiopulmonary resuscitation. Animal temperature was adjusted to 37.0 °C with the aid of a heating lamp. At 30 mins after resuscitation, animals were randomized to receive an intravenous injection of either cholecystokinin octapeptide (200 μg/kg in 0.3 mL saline) or vehicle placebo (0.3 mL saline). The ambient temperature settings and that of the distance of the heating lamp from the animal remained the same in both groups throughout the entire experiment.
  
  
  RESULTS
  Body temperature, hemodynamic measurements, and postresuscitation myocardial function, including cardiac output, left ventricular ejection fraction, and myocardial performance index, were measured together with neurologic deficit scores and duration of survival.
  
  
  RESULTS
  After injection of cholecystokinin octapeptide, blood temperature decreased progressively from 37.0 °C to 34.8 °C 5 hrs after resuscitation and returned to 37.0 °C at 9 hrs after injection. In the control group, blood temperature was sustained at 37.0 °C ± 0.2 °C during the same period of observation. Myocardial and neurologic function and duration of survival were significantly better in the cholecystokinin octapeptide-treated animals when compared to the control group.
  
  
  CONCLUSIONS
  : In a rat model of cardiopulmonary resuscitation, cholecystokinin octapeptide induced mild hypothermia, attenuated postresuscitation myocardial dysfunction, and improved neurologic outcome and duration of survival.
authors.affiliation: Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA.
authors.forename: Yinlun
authors.initials: Y
authors.lastname: Weng
authors.forename: Shijie
authors.initials: S
authors.lastname: Sun
authors.forename: Fengqing
authors.initials: F
authors.lastname: Song
authors.forename: Sung
authors.initials: S
authors.lastname: Phil Chung
authors.forename: Jeonghyun
authors.initials: J
authors.lastname: Park
authors.forename: Max
authors.initials: M
authors.lastname: Harry Weil
authors.forename: Wanchun
authors.initials: W
authors.lastname: Tang
mesh_terms: D000818:Animals; D001831:Body Temperature / Q000187:drug effects; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D004195:Disease Models, Animal; D006439:Hemodynamics / Q000187:drug effects; D007036:Hypothermia, Induced / Q000379:methods*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012844:Sincalide / Q000627:therapeutic use*
chemical_list: D012844:Sincalide