Literature DB >> 10776911

Ethanol reduces metabolic uncoupling following experimental head injury.

D F Kelly1, D A Kozlowski, E Haddad, A Echiverri, D A Hovda, S M Lee.   

Abstract

Previous investigations have shown that ethanol is neuroprotective following experimental traumatic brain injury (TBI). This study sought to determine if the neuroprotective effects of ethanol in a controlled cortical impact (CCI) injury model are related to its effects on cerebral glucose metabolism and blood flow. Adult rats were given ethanol (1.0 g/kg) or saline by intraperitoneal injection followed 40 min later by injury. Regional cerebral blood flow (CBF) and cerebral metabolic rates of glucose (CMRglc) were determined immediately, and at 3, 6, 12, 24, and 72 h postinjury using quantitative autoradiography. Immediately after injury, CMRglc in the contusion core and penumbra was reduced in the ethanol group compared to the saline group: (core CMRglc: 52.2 +/- 16.0 versus 94.2 +/- 14.1 micromol/100 g/min, respectively,p < 0.001; penumbral CMRglc: 58.2 +/- 12.8 versus 82.8 +/-19.7 micromol/100 g/min, respectively; p < 0.05) However, at 24 and 72 h postinjury, penumbral CMRglc in the ethanol group was increased compared to the saline group (p < 0.05 and p < 0.001, respectively). Regarding CBF, contusion core values in the ethanol group were elevated compared to the saline group immediately postinjury, (70.4 +/- 17.1 versus 31.5 +/- 27.8 mL/100 g/min, respectively (p < .05), and at 6, 12, and 24 h postinjury (p < 0.05). Penumbral CBF was also higher at 6 and 72 h in the ethanol group compared to the saline group (p < 0.05). These results indicate that low-dose ethanol is associated with a marked attenuation of immediate postinjury hyperglycolysis and with more normal glucose metabolism in the injury penumbra over the ensuing 3 days. Simultaneously, the reduction in CBF typically seen within the contusion core and penumbra after CCI is less severe when ethanol is present. The net effect of these changes is a decreased degree of uncoupling between glucose metabolism and CBF that otherwise occurs in the absence of ethanol. These changes may likely explain the neuroprotective effect of ethanol.

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Year:  2000        PMID: 10776911     DOI: 10.1089/neu.2000.17.261

Source DB:  PubMed          Journal:  J Neurotrauma        ISSN: 0897-7151            Impact factor:   5.269


  16 in total

1.  Beneficial effects of sodium or ethyl pyruvate after traumatic brain injury in the rat.

Authors:  Nobuhiro Moro; Richard L Sutton
Journal:  Exp Neurol       Date:  2010-07-27       Impact factor: 5.330

2.  Alcohol use at time of injury and survival following traumatic brain injury: results from the National Trauma Data Bank.

Authors:  Chiung M Chen; Hsiao-Ye Yi; Young-Hee Yoon; Chuanhui Dong
Journal:  J Stud Alcohol Drugs       Date:  2012-07       Impact factor: 2.582

Review 3.  Influence of alcohol on mortality in traumatic brain injury.

Authors:  Razvan C Opreanu; Donald Kuhn; Marc D Basson
Journal:  J Am Coll Surg       Date:  2010-06       Impact factor: 6.113

4.  Association of Alcohol With Mortality After Traumatic Brain Injury.

Authors:  Jennifer S Albrecht; Majid Afshar; Deborah M Stein; Gordon S Smith
Journal:  Am J Epidemiol       Date:  2018-02-01       Impact factor: 4.897

5.  Use-dependent dendritic regrowth is limited after unilateral controlled cortical impact to the forelimb sensorimotor cortex.

Authors:  Theresa A Jones; Daniel J Liput; Erin L Maresh; Nicole Donlan; Toral J Parikh; Dana Marlowe; Dorothy A Kozlowski
Journal:  J Neurotrauma       Date:  2012-04-10       Impact factor: 5.269

6.  Neuroprotective effect of ethanol and Modafinil on focal cerebral ischemia in rats.

Authors:  Yusef Abbasi; Ronak Shabani; Kazem Mousavizadeh; Mansoureh Soleimani; Mehdi Mehdizadeh
Journal:  Metab Brain Dis       Date:  2019-01-15       Impact factor: 3.584

7.  Brain metabolism is significantly impaired at blood glucose below 6 mM and brain glucose below 1 mM in patients with severe traumatic brain injury.

Authors:  Roman Meierhans; Markus Béchir; Silke Ludwig; Jutta Sommerfeld; Giovanna Brandi; Christoph Haberthür; Reto Stocker; John F Stover
Journal:  Crit Care       Date:  2010-02-08       Impact factor: 9.097

8.  Controlled cortical impact results in an extensive loss of dendritic spines that is not mediated by injury-induced amyloid-beta accumulation.

Authors:  Charisse N Winston; Deepa Chellappa; Tiffany Wilkins; David J Barton; Patricia M Washington; David J Loane; David N Zapple; Mark P Burns
Journal:  J Neurotrauma       Date:  2013-10-12       Impact factor: 5.269

9.  Voluntary exercise or amphetamine treatment, but not the combination, increases hippocampal brain-derived neurotrophic factor and synapsin I following cortical contusion injury in rats.

Authors:  G S Griesbach; D A Hovda; F Gomez-Pinilla; R L Sutton
Journal:  Neuroscience       Date:  2008-04-09       Impact factor: 3.590

10.  Acute alcohol intoxication and long-term outcome in patients with traumatic brain injury.

Authors:  Rahul Raj; Markus B Skrifvars; Riku Kivisaari; Juha Hernesniemi; Jaakko Lappalainen; Jari Siironen
Journal:  J Neurotrauma       Date:  2014-11-13       Impact factor: 5.269

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