• DOI:10.1097/01.CCM.0000114998.00860.FD
• Corpus ID: 41533372

Neurotensin-induced hypothermia improves neurologic outcome after hypoxic-ischemia*

@article{Katz2004NeurotensininducedHI,
  title={Neurotensin-induced hypothermia improves neurologic outcome after hypoxic-ischemia*},
  author={Laurence M. Katz and Amanda S Young and Jonathan E. Frank and Yuanfan Wang and Kyunam Park},
  journal={Critical Care Medicine},
  year={2004},
  volume={32},
  pages={806-810}
}

• L. Katz, Amanda S Young, +2 authors Kyunam Park
• Published 1 March 2004
• Medicine
• Critical Care Medicine

ObjectiveExternal cooling is commonly used to force induction of mild hypothermia but requires equipment, has a slow onset of action, and must be prolonged to provide permanent neurologic benefits after hypoxic-ischemia. It is unknown whether the method for inducing mild hypothermia affects neurologic outcome after near-drowning. The objective of the study was to induce mild hypothermia with neurotensin analog NT77 or external cooling in a rat model of near-drowning. We hypothesize that NT77 would be more effective for improving neurologic outcome than external cooling of the same duration. DesignRats were randomized to a normothermic control, neurotensin-induced hypothermia, brief external cooling, or prolonged external cooling group after asphyxial cardiac arrest. SettingLaboratory investigation. SubjectsForty-eight rats. InterventionsMild hypothermia was induced by external cooling for 4 hrs (brief external cooling) or 24 hrs (prolonged external cooling) or by neurotensin-induced hypothermia administration 30 mins after asphyxial cardiac arrest in rats. MeasurementsOutcome was assessed by a neurologic deficit score, the Morris water maze, and CA1 hippocampus histology 15 days after resuscitation. Main ResultsNeurologic deficit score at 72 hrs after asphyxial cardiac arrest was lower with neurotensin-induced hypothermia (score, 0) and prolonged external cooling (score, 0) vs. normothermic control (score, 20) and brief external cooling (score, 18; p < .05). Latency time in the Morris water maze 15 days after asphyxial cardiac arrest was decreased with neurotensin-induced hypothermia (14 ± 11 secs) and prolonged external cooling (18 ± 9 secs) vs. normothermic control (74 ± 17 secs) and brief external cooling (78 ± 18 secs, p < .05). There was less ischemic neuronal damage with neurotensin-induced hypothermia (28 ± 24%) and prolonged external cooling (21 ± 14%) vs. normothermic control (61 ± 32%) and brief external cooling (51 ± 32%). ConclusionsNeurotensin-induced hypothermia improved neurologic outcome after asphyxial cardiac arrest in rats vs. brief external cooling but was comparable to prolonged external cooling.