PMID- 15307897
OWN - NLM
STAT- MEDLINE
DCOM- 20040923
LR  - 20220310
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 21
IP  - 7
DP  - 2004 Jul
TI  - The effects of early post-traumatic hyperthermia in female and ovariectomized 
      rats.
PG  - 842-53
AB  - Episodes of post-traumatic hyperthermia commonly occur in the head-injured 
      patient population. Although post-traumatic hyperthermia has been shown to worsen 
      outcome in experimental studies using male rats, the consequences of secondary 
      hyperthermia following traumatic brain injury (TBI) have not been investigated in 
      female animals. Thus, the purpose of this study was to examine the effects of 
      post-traumatic hyperthermia after fluid-percussion (F-P) brain injury in intact 
      and ovariectomized female rats. Thirty-eight female Sprague-Dawley rats were used 
      in these experiments. Intact female rats underwent TBI followed 30 min later by a 
      4-h period of normothermia (37 degrees C) or brain hyperthermia (40 degrees C). 
      Female rats that had been ovariectomized 10 days prior to TBI were also 
      traumatized and followed by a period of normothermia or hyperthermia. At 72 h 
      after TBI, rats were perfusion-fixed for quantitative histopathological and 
      immunocytochemical evaluation. Following normothermic TBI, intact female rats 
      demonstrated significantly smaller contusion volumes, decreased frequency of 
      axonal beta-amyloid precursor protein (beta-APP) profiles, and greater numbers of 
      NeuN-positive cortical neurons compared to traumatized ovariectomized females. 
      Although post-traumatic hyperthermia increased contusion volume, cortical 
      neuronal cell death and axonal damage in both intact and ovariectomized female 
      groups, the effects of the induced hyperthermic period were more pronounced in 
      ovariectomized animals. These findings demonstrate for the first time that 
      post-traumatic hyperthermia worsens histopathological outcome in female rats, and 
      that neural hormones, including estrogen and progesterone, may protect against 
      secondary hyperthermic insults.
FAU - Suzuki, Takamoto
AU  - Suzuki T
AD  - The Miami Project to Cure Paralysis, Department of Neurological Surgery, 
      University of Miami School of Medicine, Miami, Florida 33101, USA.
FAU - Bramlett, Helen M
AU  - Bramlett HM
FAU - Ruenes, Gladys
AU  - Ruenes G
FAU - Dietrich, W Dalton
AU  - Dietrich WD
LA  - eng
GR  - NS30291/NS/NINDS NIH HHS/United States
GR  - NS42133/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Amyloid beta-Protein Precursor)
SB  - IM
MH  - Amyloid beta-Protein Precursor/metabolism
MH  - Animals
MH  - Brain Injuries/*complications/*pathology/physiopathology
MH  - Female
MH  - Fever/*etiology/pathology
MH  - Immunohistochemistry
MH  - Nerve Degeneration/*pathology
MH  - Ovariectomy
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sex Factors
EDAT- 2004/08/17 10:00
MHDA- 2004/09/24 05:00
CRDT- 2004/08/17 10:00
PHST- 2004/08/17 10:00 [pubmed]
PHST- 2004/09/24 05:00 [medline]
PHST- 2004/08/17 10:00 [entrez]
AID - 10.1089/0897715041526186 [doi]
PST - ppublish
SO  - J Neurotrauma. 2004 Jul;21(7):842-53. doi: 10.1089/0897715041526186.