Document Detail


Effects of hypothermia on cerebral autoregulatory vascular responses in two rodent models of traumatic brain injury.
MedLine Citation:
PMID:  22364620     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Traumatic brain injury (TBI) can trigger disturbances of cerebral pressure autoregulation that can translate into the generation of secondary insults and increased morbidity/mortality. Few therapies have been developed to attenuate the damaging consequences of disturbed autoregulatory control, although some suggest that hypothermia may exert such protection. Here we reexamine this issue of traumatically induced autoregulatory disturbances and their modulation by hypothermic intervention, examining these phenomena in two different models of TBI. Adult rats were subjected to either impact acceleration injury (IAI) or lateral fluid percussion injury (LFPI) followed by the insertion of cranial windows to assess the pial arteriolar cerebral autoregulatory vascular response to the post-traumatic induction of sequential reductions of arterial blood pressure. The potential for continued pial vasodilation in response to declining blood pressure was directly measured post-injury and compared with that in injured groups subjected to 33° C of hypothermia of 1-2 h duration initiated 1 h post-injury. We observed that the TBI resulted in either impaired or abolished cerebral vascular dilation in response to the sequential declines in blood pressure. Following IAI there was a 50% reduction in the vasculature's ability to dilate in response to the induced hypotension. In contrast, following LFPI, the vascular response to hypotension was abolished both ipsilateral and contralateral to the LFPI. In animals sustaining IAI, the use of 1 h post-traumatic hypothermia preserved vascular dilation in response to declines in blood pressure in contrast to the LFPI in which the use of the same strategy afforded no improvement. However, with LFPI, the use of 2 h of hypothermia provided partial vascular protection. These results clearly illustrate that TBI can alter the cerebral autoregulatory vascular response to sequentially induced hypotensive insult, whereas the use of post-traumatic hypothermia provides benefit. Collectively, these studies also demonstrate that different animal models of TBI can evoke different biological responses to injury.
Authors:
Motoki Fujita; Enoch P Wei; John T Povlishock
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2012-04-16
Journal Detail:
Title:  Journal of neurotrauma     Volume:  29     ISSN:  1557-9042     ISO Abbreviation:  J. Neurotrauma     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-04-26     Completed Date:  2013-02-05     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  8811626     Medline TA:  J Neurotrauma     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1491-8     Citation Subset:  IM    
Affiliation:
Department of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, Virginia 23298, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain Injuries / physiopathology*,  therapy*
Cerebrovascular Circulation / physiology*
Disease Models, Animal
Homeostasis / physiology*
Hypothermia, Induced / methods*
Male
Rats
Rats, Sprague-Dawley
Grant Support
ID/Acronym/Agency:
HD055813/HD/NICHD NIH HHS; NS047463/NS/NINDS NIH HHS
Comments/Corrections

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