Ethanol potentiation of central nervous system trauma

Flamm, Eugene S.; Demopoulos, Harry B.; Seligman, Myron L.; Tomasula, John J.; Crescito, V. De; Ransohoff, Joseph

doi:10.3171/jns.1977.46.3.0328

Cited by 131 publications

(37 citation statements)

References 19 publications

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“…22 Ethanol is well known for its free radical potentiating effects in the CNS. 14 In our studies, the decrease in the ascorbyl radical is indicative of a consumption of this antioxidant in an attempt to quench the free radical peroxidation of membrane lipids. The reduction in the ascorbyl radical one hour after MCA occlusion, and the continued decrease up to 24 hours, indicates that this change begins at a time when histologic, biochemical, and clinical changes are all reversible and continues through the period of infarction.…”

Section: Discussionmentioning

confidence: 55%

Free radicals in cerebral ischemia.

Flamm¹,

Demopoulos²,

Seligman³

et al. 1978

Stroke

565

190

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SUMMARYThe possibility that cerebral ischemia may initiate a series of pathological free radical reactions within the membrane components of the CNS was investigated in the cat. The normally occurring electron transport radicals require adequate molecular oxygen for orderly transport of electrons and protons. A decrease in tissue oxygen removes the controls over the electron transport radicals, and allows them to initiate pathologic radical reactions among cell membranes such as mitochondria. Pathologic radical reactions result in multiple products, each of which may be present in too small a concentration to permit their detection at early time periods. It is possible to follow the time course, however, by the decrease of a major antioxidant as it is consumed by the pathologic radical reactions. For this reason, ascorbic acid was measured in ischemic and control brain following middle cerebral artery occlusion. There was a progressive decrease in the amount of detectable ascorbic acid ranging from 25% at 1 hour to 65% at 24 hours after occlusion. The reduction of this normally occurring antioxidant and free radical scavenger may indicate consumption of ascorbic acid in an attempt to quench pathologic free radical reactions occurring within the components of cytomembranes.

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Section: Discussionmentioning

confidence: 55%

Free radicals in cerebral ischemia.

Flamm¹,

Demopoulos²,

Seligman³

et al. 1978

Stroke

565

190

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“…Under conditions of head or spinal cord injury the use of ethanol or related alcohols to protect from hypoxic injury may be contraindicated in that more extensive damage has been reported in animals pretreated with these compounds. 33 Our results might therefore be more relevant to hypoxia uncomplicated by central nervous system trauma.…”

Section: Dose Response Of Ethanolmentioning

confidence: 91%

The role of ethanol in diluents of drugs that protect mice from hypoxia.

Moursi¹,

Luyckx²,

DʼAlecy³

1983

Stroke

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SUMMARY This study evaluates the hypothesis that ethanol alone, or in diluents for drugs used to protect hypoxic mice, is responsible in part for an increased tolerance to hypoxia (4-5% oxygen). The change in hypoxic tolerance following i.v. or i.p. administration of ethanol, diazepam, nimodipine and various diluent components was measured. Diazepam (50 mg/kg i.v.) increased hypoxic tolerance to 700 ± 47% (n = 11) of saline control, its diluent increased hypoxic tolerance to 468 ± 60% (n = 10) of saline control but the ethanol component of the diluent accounted for almost half of this diluent effect. Nimodipine (2 mg/kg i.p.), a calcium antagonist, increased tolerance to 180 ±18% of control (n = 19) and nimodipine diluent showed an even greater increase to 226 ±25% of control (n = 15). In this case essentially all of the protective effect of nimodipine diluent (81.3%) is accounted for by ethanol. Dose response curves indicate the maximum ethanol induced increase in hypoxic tolerance was approximately 335% of control at a dose of 2.4 g/kg. Buffers, etc. in the diluents evidently add to the protective effect of ethanol. Our data clearly indicate ethanol is the important component of some treatments which protect mice from hypoxia. The pharmacological activity of ethanol, even when used in a diluent, should not be ignored in evaluating therapeutic intervention for protection from hypoxia. Stroke Vol 14, No 5, 1983THE INCREASED SURVIVAL TIME in mice sub jected to hypoxia has been investigated in several labo ratories to identify procedures which may be of thera peutic value in cerebral hypoxia. The importance of these experiments stems from the high morbidity and mortality associated with cerebral hypoxia. The brain appears to be particularly sensitive to hypoxia presum ably because of its high metabolic rate, relatively small stores of high energy phosphates and glucose as well as a relatively low capillary density.1 Although the cause of death or sequence of events leading to death in the hypoxic mouse model have not been established there is evidence to suggest that during hypoxia the cessation of spontaneous ventilation results from reduced brain activity. Recent work in our laboratory using a Levine rat preparation, which includes on-line monitoring of blood pressure, heart rate, respiratory rate, central ve nous pressure and electroencephalogram, indicates that loss of cerebral electrical activity invariably pre cedes loss of spontaneous respiration and ultimate loss of cardiac activity 2 when an animal is exposed to hy poxia. In contrast it has been shown that cardiac func tion is maintained during hypoxia because coronary blood flow is increased by local mechanisms in order to maintain a relatively constant myocardial oxygen tension. 3Clinically, hypoxia may be encountered at high altitudes, 4 during childbirth, deep-sea diving, as a complication during surgery, with a sedative over dose, or because of carbon monoxide poisoning. Fur thermore, hypoxia has been identified as an avoidable extracranial factor as...

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“…As blood alcohol levels rise, psychomotor skills and reaction time Borgialli et al • CHARACTERISTICS OF MVC DEATHS diminish, attention and judgment are impaired, and the risk of crash involvement increases. In addition, alcohol has been shown to negatively affect injury outcome in human 16,17 and animal [18][19][20][21] studies. That is, all other factors being equal, the same physical impact tends to produce more severe injury when alcohol use is present.…”

mentioning

confidence: 99%

Effects of Alcohol on the Geographic Variation of Driver Fatalities in Motor Vehicle Crashes

Borgialli

Hill

Maio

et al. 2000

Academic Emergency Medicine

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Abstract. Objective: To determine whether the increased risk of dying in a rural vs nonrural motor vehicle crash (MVC) can be attributed to driver demographics, crash characteristics, or police-reported alcohol use. Methods: A retrospective cohort study was conducted, comparing all rural (116,242) and a 20% random sample of nonrural (104,197) Michigan drivers involved in an MVC during [1994][1995][1996]. Data consisted of all police-reported traffic crashes on public roadways. A logistic regression model was created, using survival as the dependent variable and gender, age, crash characteristics, and rural or nonrural county as independent variables. Driver alcohol use, as reported by the investigating officer, was introduced into the model, and the effect was analyzed. Results: Nonsurvivors represented 0.2% of the total; 99.8% were survivors. Police-reported alcohol use was reported for 3.9% of drivers. Drivers in rural MVCs were more likely to be male, to be more than 50 years of age, to have been drinking alcohol, and to have more severe vehicle deformation as a result of the MVC. The relative risk (RR) for MVC nonsurvivors was 1.69 [95% confidence interval (CI) = 1.3 to 2.1] times higher for drivers in rural than nonrural counties. After adjusting for demographic and crash characteristics, the RR was 1.56 (95% CI = 1.2 to 1.9). Controlling for alcohol and its interactions decreased the RR to 1.26 (95% CI = 0.6 to 2.4), a nonsignificant difference between rural and nonrural MVC mortalities. Conclusions: Alcohol use by drivers in Michigan was a significant contributor for nonsurvivors of rural crashes. Efforts to decrease rural MVC mortality must address alcohol use.

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Ethanol potentiation of central nervous system trauma

Cited by 131 publications

References 19 publications

Free radicals in cerebral ischemia.

Free radicals in cerebral ischemia.

The role of ethanol in diluents of drugs that protect mice from hypoxia.

Effects of Alcohol on the Geographic Variation of Driver Fatalities in Motor Vehicle Crashes

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