Effects of Ethanol on EEG and Cortical Blood Flow in the Cat

Aa, Hadji-Dimo; Ekberg, R; Dh, Ingvar

doi:10.15288/qjsa.1968.29.828

Cited by 36 publications

(4 citation statements)

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“…Ethanol is a CNS-suppressant, as defined by Kalant (1978), and the reduced CMRO 2 and CBF during acute severe ethanol intoxication reflects this fact. The results obtained during acute intoxication in rats are concordant with previous studies in other species (Battey et al 1953;Hadji-Dimo et al 1968). However, in a patient study, Battey et a1 (1953) reported a higher CBF during ethanol intoxication than after recovery although this was probably due to the hypercapnia prevailing during intoxication in these patients.…”

Section: Discussion: Physiological Conditions During Ethanol Intoxicasupporting

confidence: 92%

Cerebral Blood Flow and Cerebral Metablolicstate During Abstinence Folloowing Ethanol Intoxication in Rat

Hemmingsen

Barry

Chapman

1980

Acta Neurologica Scandinavica

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Section: Discussion: Physiological Conditions During Ethanol Intoxicasupporting

confidence: 92%

Cerebral Blood Flow and Cerebral Metablolicstate During Abstinence Folloowing Ethanol Intoxication in Rat

Hemmingsen

Barry

Chapman

1980

Acta Neurologica Scandinavica

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“…A low ethanol dose (55 mg/dL BAC) injected into the vena cava increased cortical blood flow in N 2 Oanesthetized but not pentobarbital-anesthetized cats. 9 In contrast, a higher ethanol dose (135 mg/dL) caused reduced cortical blood flow in both experimental groups. 9 Friedman, et al, 6 compared the response of rCBF to intravenous ethanol in awake dogs (0.231% BAC) versus pentobarbital-anesthestized dogs (0.219% BAC) and noted that the reduction in brain blood flow caused by ethanol was obscured by the reduction in rCBF caused by pentobarbital anesthesia.…”

Section: Discussionmentioning

confidence: 84%

“…1,6,7 Very few studies have addressed the issue regarding the interaction between anesthetic agents and ethanol on the response of the cerebral microcirculation, particularly in ventilated animals with comparable MABP and blood gas levels. Hadji-Dimo, et al, 9 have investigated the response of the cortical surface CBF to ethanol in cats using the Krypton-85 clearance technique and noted a complex response. A low ethanol dose (55 mg/dL BAC) injected into the vena cava increased cortical blood flow in N 2 Oanesthetized but not pentobarbital-anesthetized cats.…”

Section: Discussionmentioning

confidence: 99%

Anesthetic-dependent pial arteriolar response to ethanol

Gordon

Meno

Ngai

et al. 1995

Journal of Neurosurgery

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Anesthetic agents are often administered in the presence of ethyl alcohol, both in research and in the clinical setting. The authors tested the hypothesis that anesthetic agents may affect cerebrovascular responses to ethanol. A closed cranial window preparation in the rat was used to compare the response of pial arterioles to topically applied ethanol (0.01% to 1% vol/vol) in the presence of alpha-chloralose/urethane (50 and 600 mg/kg, respectively) or halothane (0.5% to 1%) anesthesia. Heart rate, mean arterial blood pressure, and blood gas levels were maintained stable and within the physiological range throughout each experiment. Ethanol induced significant vasoconstriction in alpha-chloralose/urethane-anesthetized animals (multivariate analysis of variance (MANOVA), p = 0.039); conversely, ethanol induced significant vasodilation of the pial arterioles in halothane-anesthetized animals (MANOVA, p = 0.017). These responses were significantly different from one another (MANOVA, p = 0.001). Thus, the choice of anesthetic agent alters the cerebrovascular response to ethanol, and care should be taken to ascertain the influence of anesthesia in both research and clinical settings.

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“…At low blood-alcohol concentrations (BAC) a transient increase in CBF is parallelled by ,changes in EEG suggestive of CNS activation. At higher BAC (1-2 g/l) CBF decreases in parallel to changes in EEG, this being due to suppression of neuronal activity by ethanol (Hadji-Dimo et al 1968). During severe clinical ethanol intoxication in man, cerebral oxygen consumption (CMR02) is suppressed by 30% (Battey et al 1953).…”

mentioning

confidence: 97%

Cerebral Blood Flow Autoregulation during Acute Ethanol Intoxication in the Rat

Barry

Hemmingsen

1984

Acta Pharmacologica et Toxicologica

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Autoregulation of cerebral blood flow (CBF) was studied in anaesthetized rats during acute ethanol intoxication (blood alcohol concentration 2.5 to 3 g/l). For each rat an autoregulation curve was determined: 8-10 CBF measurements were made over the mean arterial pressure range 129 mmHg to 20 mmHg. MAP was raised above the resting level by angiotension I1 infusion, then lowered by controlled haemorrhage. In control rats, CBF autoregulation was demonstrated within the MAP range 129 mmHg to 70 mmHg: at lower pressure autoregulation was inadequate and CBF fell. In ethanol intoxicated rats CBF autoregulation was demonstrated within the MAP range 129 mmHg to 50 mmHg: at lower pressure CBF fell. Although the lower limit of CBF autoregulation was thus at an MAP 20 mmHg less than in control rats, this probably reflects suppression of cerebral metabolism. rather than an effect of ethanol on CBF autoregulation per se.

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Effects of Ethanol on EEG and Cortical Blood Flow in the Cat

Cited by 36 publications

References 0 publications

Cerebral Blood Flow and Cerebral Metablolicstate During Abstinence Folloowing Ethanol Intoxication in Rat

Cerebral Blood Flow and Cerebral Metablolicstate During Abstinence Folloowing Ethanol Intoxication in Rat

Anesthetic-dependent pial arteriolar response to ethanol

Cerebral Blood Flow Autoregulation during Acute Ethanol Intoxication in the Rat

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