Document Detail


Severe hemodilutional anemia increases cerebral tissue injury following acute neurotrauma.
MedLine Citation:
PMID:  17556499     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Anemia may worsen neurological outcomes following traumatic brain injury (TBI) by undefined mechanisms. We hypothesized that hemodilutional anemia accentuates hypoxic cerebral injury following TBI. Anesthetized rats underwent unilateral TBI or sham injury (n > or = 7). Target hemoglobin concentrations between 50 and 70 g/l were achieved by exchanging 40-50% of the blood volume (1:1) with pentastarch. The effect of TBI, anemia, and TBI-anemia was assessed by measuring brain tissue oxygen tension (Pbr(O(2))), regional cerebral blood flow (rCBF), jugular venous oxygen saturation (Sjv(O(2))), cerebral contusion area, and nuclear staining for programmed cell death. Baseline postinjury Pbr(O(2)) values in the TBI and TBI-anemia groups (9.3 +/- 1.3 and 11.3 +/- 4.1 Torr, respectively) were lower than the uninjured controls (18.2 +/- 5.2 Torr, P < 0.05 for both). Hemodilution caused a further reduction in Pbr(O(2)) in the TBI-anemia group relative to the TBI group without anemia (7.8 +/- 2.7 vs. 14.8 +/- 3.9 Torr, P < 0.05). The rCBF remained stable after TBI and increased comparably after hemodilution in both anemia and TBI-anemia groups. The Sjv(O(2)) was elevated after TBI (87.4 +/- 8.9%, P < 0.05) and increased further following hemodilution (95.0 +/- 1.6%, P < 0.05). Cerebral contusion area and nuclear counts for programmed cell death were increased following TBI-anemia (4.1 +/- 3.0 mm(2) and 686 +/- 192, respectively) relative to TBI alone (1.3 +/- 0.3 mm(2) and 404 +/- 133, respectively, P < 0.05 for both). Hemodilutional anemia reduced cerebral Pbr(O(2)) and oxygen extraction and increased cell death following TBI. These results support our hypothesis that acute anemia accentuated hypoxic cerebral injury after neurotrauma.
Authors:
Gregory M T Hare; C David Mazer; James S Hutchison; Anya T McLaren; Elaine Liu; Alipasha Rassouli; Jinglu Ai; Rachel E Shaye; Julia A Lockwood; Cynthia E Hawkins; Nancy Sikich; Kevin To; Andrew J Baker
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-06-07
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  103     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-08-28     Completed Date:  2007-12-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1021-9     Citation Subset:  IM    
Affiliation:
Department of Anesthesia, University of Toronto, St. Michael's Hospital, 30 Bond St., Toronto, Ontario M5B 1W8, Canada. hareg@smh.toronto.on.ca
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MeSH Terms
Descriptor/Qualifier:
Anemia / complications,  physiopathology*
Animals
Blood Gas Analysis
Brain / pathology,  physiopathology*
Brain Injuries / complications,  pathology,  physiopathology*
Cerebrovascular Circulation / physiology
Hemoglobins / metabolism
In Situ Nick-End Labeling
Male
Oxygen / physiology*
Rats
Rats, Sprague-Dawley
Chemical
Reg. No./Substance:
0/Hemoglobins; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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