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Effects of Ethanol in an Experimental Model of Combined Traumatic Brain Injury and Hemorrhagic Shock
dc.contributor.authorZink, Brian J.en_US
dc.contributor.authorStern, Susan A.en_US
dc.contributor.authorWang, Xuen_US
dc.contributor.authorChudnofsky, Carl C.en_US
dc.date.accessioned2010-06-01T19:00:56Z
dc.date.available2010-06-01T19:00:56Z
dc.date.issued1998-01en_US
dc.identifier.citationZink, Brian J.; Stern, Susan A.; Wang, Xu; Chudnofsky, Carl C. (1998). "Effects of Ethanol in an Experimental Model of Combined Traumatic Brain Injury and Hemorrhagic Shock." Academic Emergency Medicine 5(1): 9-17. <http://hdl.handle.net/2027.42/72205>en_US
dc.identifier.issn1069-6563en_US
dc.identifier.issn1553-2712en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/72205
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=9444336&dopt=citationen_US
dc.description.abstractObjectives: Given that clinical and laboratory studies suggest that ethanol and hemorrhagic shock (HS) potentiate traumatic brain injury (TBI), the authors studied the effects of ethanol in a model of combined TBI and HS. Methods: A controlled porcine model of combined TBI and HS was evaluated for the effect of ethanol on survival time, hemodynamic function, and cerebral tissue perfusion. Anesthetized swine (17–24 kg) were instrumented, splenectomized, and subjected to fluid percussion TBI with concurrent 25-mL/kg graded hemorrhage over 30 minutes. Two groups were studied: control ( n = 11) and ethanol ( n = 11). Ethanol, 3.5 g/kg intragastric, was given 100 minutes prior to TBI/HS. Systemic and cerebral physiologic and metabolic parameters were monitored for 2 hours without resuscitation. Regional cerebral blood flow (rCBF) and renal blood flow were measured with dye-labeled microspheres. Data were analyzed with 2-sample t-test and repeated-measures ANOVA. Results: Ethanol levels at the time of injury were 162 ± 68 mg/dL. Average TBI was 2.65 ± 0.35 atm. Survival time was significantly shorter in the ethanol group (60 ± 27 min vs 94 ± 28 min, p = 0.011). The ethanol group had significantly lower mean arterial pressure, cerebral perfusion pressure, and cerebral venous O 2 saturation in the postinjury period. Cerebral O 2 extraction ratios and cerebral venous lactate levels were significantly higher in the ethanol group. A trend toward lower postinjury rCBF in all brain regions was observed in the ethanol group. Conclusion: In this TBI/HS model, ethanol administration decreased survival time, impaired the hemodynamic response, and worsened measures of cerebral tissue perfusion.en_US
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dc.format.extent3109 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherBlackwell Publishing Ltden_US
dc.rights1998 Society for Academic Emergency Medicineen_US
dc.subject.otherAlcoholen_US
dc.subject.otherEthanolen_US
dc.subject.otherInjuryen_US
dc.subject.otherShocken_US
dc.subject.otherHemorrhageen_US
dc.subject.otherBrainen_US
dc.subject.otherTraumaen_US
dc.titleEffects of Ethanol in an Experimental Model of Combined Traumatic Brain Injury and Hemorrhagic Shocken_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelMedicine (General)en_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumUniversity of Michigan, Ann Arbor, MI, Department of Surgery, Section of Emergency Medicineen_US
dc.identifier.pmid9444336en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/72205/1/j.1553-2712.1998.tb02568.x.pdf
dc.identifier.doi10.1111/j.1553-2712.1998.tb02568.xen_US
dc.identifier.sourceAcademic Emergency Medicineen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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