Acute ethanol intoxication in a model of traumatic brain injury with hemorrhagic shock: effects on early physiological response

Zink, Brian J.; Sheinberg, Michael; Wang, Xu; Mertz, M.; Stern, Susan A.; Betz, A. Lorris

doi:10.3171/jns.1998.89.6.0983

Cited by 36 publications

(29 citation statements)

References 62 publications

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“…Another possibility is that alcohol may impact hemodynamic and respiratory brainstem control centers accentuating acidosis through longer posttraumatic apnea periods, decreased ventilation, and impaired ventilatory responses, subsequently leading to decreased cerebral perfusion pressure and lower post-injury regional cerebral blood flow for hours post-injury (McQueen and Posey, 1975;Zink et al, 1993Zink et al, , 1995Zink et al, , 1998Zink et al, , 1999. A third mechanism implicates alcohol as a factor in facilitating WILDE ET AL.…”

Section: Interactive Effects Of Alcohol and Tbi Hypothesismentioning

confidence: 97%

Alcohol Abuse and Traumatic Brain Injury: Quantitative Magnetic Resonance Imaging and Neuropsychological Outcome

Wilde

Bigler

Gandhi

et al. 2004

Journal of Neurotrauma

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Prior or concurrent alcohol use at the time of traumatic brain injury (TBI) was examined in terms of post-injury atrophic changes measured by quantitative analysis of magnetic resonance imaging (MRI) and neuropsychological outcome. Two groups of TBI subjects were examined: those with a clinically significant blood alcohol level (BAL) present at the time of injury (TBI + BAL) and those without a significant BAL (TBI-only). To explore the potential impact of both acute and chronic alcohol use, subjects in both groups were further clustered into one of four subgroups (NONE, MILD, MODERATE or HEAVY) based upon available information regarding their pre-injury alcohol use. One-way analysis of covariance (ANCOVA) and multiple analysis of covariance (MANCOVA) were used with subject grouping as the main factor. Age, injury severity as measured by Glasgow Coma Scale (GCS) score, years of education, total intracranial volume (TICV), and the number of days post-injury were included as covariates where appropriate. Increased general atrophy was observed in patients with (a) a positive BAL and/or (b) a history of moderate to heavy pre-injury alcohol use. In addition, performance on neuropsychological outcome variables (WAIS-R and WMS-R Index scores) was generally worse in the subgroups of patients with positive BAL and a history of preinjury alcohol use, as compared to the other TBI groups though not statistically significant. Implications of alcohol use, at the time of brain injury, are discussed.

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Section: Interactive Effects Of Alcohol and Tbi Hypothesismentioning

confidence: 97%

Alcohol Abuse and Traumatic Brain Injury: Quantitative Magnetic Resonance Imaging and Neuropsychological Outcome

Wilde

Bigler

Gandhi

et al. 2004

Journal of Neurotrauma

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“…Instead, significant hypotension, prolonged apnea, and increased mortality have been reported (Shapira et al, 1997;Yamakami et al, 1995;Zink and Feustel, 1995;Zink et al, 1993Zink et al, , 1998. Similarly, in a rat spinal cord 24, and 72 h).…”

mentioning

confidence: 89%

Ethanol Reduces Metabolic Uncoupling Following Experimental Head Injury

Kelly

Kozlowski²,

Haddad³

et al. 2000

Journal of Neurotrauma

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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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“…The instrumentation procedure has been previously described in detail (Zink et al, 1998(Zink et al, , 1999. Immature swine (20 kg) were sedated with ketamine, intubated, and anesthetized with isoflurane (1.15%) at an F I O 2 of 0.28.…”

Section: Instrumentationmentioning

confidence: 99%

“…In previous studies from our laboratory, which utilized a porcine fluid percussion model, we found early respiratory depression, decreased cerebral perfusion pressure (CPP), and decreased cerebral blood flow (CBF) in ethanol-treated animals (Zink and Feustel, 1995;Zink et al, 1993). When TBI is accompanied by hemorrhage, the deleterious effects of ethanol are magnified (Zink et al, 1998(Zink et al, , 1999.…”

mentioning

confidence: 92%

Effects of Ethanol and Naltrexone in a Model of Traumatic Brain Injury With Hemorrhagic Shock

Zink

Schultz

Stern

et al. 2001

Alcoholism Clin & Exp Res

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Acute ethanol intoxication in a model of traumatic brain injury with hemorrhagic shock: effects on early physiological response

Abstract: In this model of TBI, acute EtOH intoxication in the presence of HS potentiates the physiological and metabolic alterations that may contribute to secondary brain injury.

Cited by 36 publications

References 62 publications

Alcohol Abuse and Traumatic Brain Injury: Quantitative Magnetic Resonance Imaging and Neuropsychological Outcome

Alcohol Abuse and Traumatic Brain Injury: Quantitative Magnetic Resonance Imaging and Neuropsychological Outcome

Ethanol Reduces Metabolic Uncoupling Following Experimental Head Injury

Effects of Ethanol and Naltrexone in a Model of Traumatic Brain Injury With Hemorrhagic Shock

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