PMID- 22595025
OWN - NLM
STAT- MEDLINE
DCOM- 20130522
LR  - 20120716
IS  - 1872-678X (Electronic)
IS  - 0165-0270 (Linking)
VI  - 208
IP  - 2
DP  - 2012 Jul 15
TI  - A new rabbit model for the study of early brain injury after subarachnoid 
      hemorrhage.
PG  - 138-45
LID - 10.1016/j.jneumeth.2012.05.010 [doi]
AB  - INTRODUCTION: Pathophysiological disturbances during subarachnoid hemorrhage 
      (SAH) and within the first few days thereafter are responsible for significant 
      brain damage. Early brain injury (EBI) after SAH has become the focus of current 
      research activities. The purpose of the present study was to evaluate whether a 
      novel rabbit SAH model provokes EBI by means of neuronal degeneration, brain 
      tissue death, and apoptosis in cerebral vascular endothelial cells. MATERIALS AND 
      METHODS: SAH was performed using an extra-intracranial blood shunt. Intracranial 
      pressure (ICP), cerebral perfusion pressure (CPP), and bilateral regional 
      cerebral blood flow (rCBF) were continuously measured. Apoptosis and 
      neurodegeneration were detected 24h post-SAH in basilar artery endothelial cells, 
      bilateral basal cortex, and hippocampus (CA1 and CA3) using terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and 
      Fluoro-jade B (FJB), respectively. RESULTS: ICP increase caused a CPP decrease to 
      almost zero (8+/-5mmHg) and decreases in left and right rCBF to 23+/-8% and 19+/-9% of 
      their baseline values. TUNEL- and FJB-stained sections revealed significant 
      apoptosis and neurodegeneration in both basal cortex and hippocampal regions 
      compared to sham-operated animals. The apoptotic index in basilar artery 
      endothelial cells was 74%+/-11%. CONCLUSIONS: The blood shunt rabbit SAH model 
      elicits acute physiological dearrangements and provokes marked and consistent 
      early damage to the hippocampus, basal cortex, and cerebral vasculature 24h 
      thereafter. These findings make the model a valid tool for investigation of 
      pre-vasospasm pathophysiological mechanisms and novel treatment modalities.
CI  - Copyright (c) 2012 Elsevier B.V. All rights reserved.
FAU - Marbacher, Serge
AU  - Marbacher S
AD  - Department of Intensive Care Medicine, Bern University Hospital and University of 
      Bern, Bern, Switzerland. serge.marbacher@ksa.ch
FAU - Andereggen, Lukas
AU  - Andereggen L
FAU - Neuschmelting, Volker
AU  - Neuschmelting V
FAU - Widmer, Hans Rudolf
AU  - Widmer HR
FAU - von Gunten, Michael
AU  - von Gunten M
FAU - Takala, Jukka
AU  - Takala J
FAU - Jakob, Stephan M
AU  - Jakob SM
FAU - Fandino, Javier
AU  - Fandino J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120514
PL  - Netherlands
TA  - J Neurosci Methods
JT  - Journal of neuroscience methods
JID - 7905558
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Brain Ischemia/etiology/pathology/physiopathology
MH  - Cerebral Cortex/blood supply/pathology/physiopathology
MH  - Cerebral Infarction/etiology/pathology/physiopathology
MH  - *Disease Models, Animal
MH  - Female
MH  - Hippocampus/blood supply/pathology/physiopathology
MH  - Nerve Degeneration/*etiology/pathology/*physiopathology
MH  - *Rabbits
MH  - Subarachnoid Hemorrhage/*complications/pathology/*physiopathology
MH  - Vasoconstriction/physiology
EDAT- 2012/05/19 06:00
MHDA- 2013/05/23 06:00
CRDT- 2012/05/19 06:00
PHST- 2012/03/25 00:00 [received]
PHST- 2012/05/07 00:00 [revised]
PHST- 2012/05/08 00:00 [accepted]
PHST- 2012/05/19 06:00 [entrez]
PHST- 2012/05/19 06:00 [pubmed]
PHST- 2013/05/23 06:00 [medline]
AID - S0165-0270(12)00163-X [pii]
AID - 10.1016/j.jneumeth.2012.05.010 [doi]
PST - ppublish
SO  - J Neurosci Methods. 2012 Jul 15;208(2):138-45. doi: 
      10.1016/j.jneumeth.2012.05.010. Epub 2012 May 14.