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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Neurotensin analog NT69L induces rapid and prolonged hypothermia after hypoxic ischemia.

OBJECTIVE: To determine whether the neurotensin analog NT69L, administered systemically, could induce mild brain hypothermia after asphyxial cardiac arrest (ACA) in rats. METHODS: The study design was experimental, blinded, randomized, and approved by the animal use committee. All rats had continuous monitoring of brain temperature and sustained 8 minutes of ACA, resuscitation, and either saline or NT69L intravenously after return of spontaneous circulation (ROSC). Rats surviving 14 days after ACA had a neurological deficit score (NDS) and a Morris Water Maze (MWM) test. RESULTS: Seven of eight rats in each group survived 14 days. Brain temperature was less than 35 degrees C 13.1 +/- 3 minutes (mean +/- standard deviation) after NT69L vs controls that remained 37.5 degrees C at the same ambient temperature (p < 0.05 ANOVA). The NT69L group remained below 35 degrees C for 300 +/- 100 minutes while the controls remained at 37.5 +/- 0.5 degrees C. The NDS in the NT69L rats was 3 +/- 3% vs controls 26 +/- 8% (p < 0.05, Kruskal-Wallis, 0% = normal, 100% = brain dead). The NT69L rats performed better on the MWM vs the controls (22 +/- 8 sec vs 45 +/- 26 sec, respectively, p < 0.05 ANOVA). CONCLUSIONS: NT69L induced rapid and prolonged mild brain hypothermia after ACA in this rat model and reduced neurological deficits.[1]

References

  1. Neurotensin analog NT69L induces rapid and prolonged hypothermia after hypoxic ischemia. Katz, L.M., Wang, Y., McMahon, B., Richelson, E. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. (2001) [Pubmed]
 
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