ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1989.tb00273.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Previous studies have clearly demonstrated a reduction in plasma levels of IGF‐1 in rats chronically fed an ethanol diet. The purpose of this study was to determine whether the reduction in IGF‐1 was associated with alterations in growth hormone secretory dynamics. Male Sprague‐Dawley rats were fed either a liquid diet containing 5% ethanol or an identical volume of diet made isocaloric with maltose‐dextrin (pair‐fed controls). After 4 months of continuous feeding, another group of animals of the same age was introduced into the colony and fed the maltose‐dextrin diet ad libitum. All animals were atrial cannulated 4.5 months after the initiation of the experiment and serial samples of blood removed at 20‐min intervals for periods up to 6 hr. Plasma was separated and growth hormone and IGF‐1 concentrations determined by radioimmunoassay. Growth hormone secretory dynamics were analyzed by Cluster Analysis. Our results demonstrated that (a) chronic ethanol administration decreases plasma IGF‐1 concentrations compared to either ad libitum or pair‐fed control animals, (b) a reduction in dietary intake of approximately 33% reduces both the number of detectable growth hormone pulses and nadir concentrations of this hormone but has no effect on peak height, peak width, or area under the peak, and (c) ethanol feeding increases the amplitude of growth hormone pulses compared to pair‐fed rats. We conclude that the decrease in plasma IGF‐1 levels in ethanol as compared to pair‐fed control animals is not caused by a further reduction in growth hormone secretory dynamics. Our results support the hypothesis that ethanol directly inhibits IGF

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1989.tb00274.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

This study investigated the effects of ethanol withdrawal on sensory responses of single neurons recorded in the somatosensory (SI) cortex of awake, behaving, ethanol‐dependent rats. Eleven rats were fed an ethanol‐containing liquid diet for 90‐120 days, while 11 weight‐matched controls were pair‐fed an equivalent sucrose containing diet to equalize caloric intake. Single SI cortical neurons in the chronically treated rats were recorded continuously over several hours after withdrawal from ethanol, and after reintoxication induced by intraperitoneal injection of 10% (v/v) ethanol solution. Intoxication and withdrawal related changes in sensory responsiveness of these neurons were quantitatively measured by stimulating through electrodes chronically implanted under the skin of the forepaw. Sensory response histograms constructed from these stimuli showed a characteristic pattern, typically consisting of two early excitatory peaks (Ela and Elb), followed by an inhibition (11), and in some neurons, a late excitatory response (E2). As withdrawal advanced, the sensory response histograms exhibited marked increases in the magnitudes of the Ela, 11, and E2 responses, coupled with a reduced spontaneous discharge rate. These changes are similar to, but quantitatively greater than, those which have previously been observed in normal and control rats during “immobile arousal” behaviors, which can be evoked when an experimenter holds the animals still, producing an immobile “aversive arousal.” In withdrawing animals this same “holding” manipulation tended to markedly exacerbate and accelerate behavioral and neurophysiological signs of withdrawal. By contrast, the same manipulations had little effect when carried out during light intoxication or early stages of withdrawal. Thus, the physiological effects produced during withdrawal were similar to, and synergited with those normally associated with aversive arousal, producing effects far in excess of those s

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1989.tb00275.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

The amount and type of dietary fat is thought to be important in the pathogenesis of alcoholic liver disease (ALD). We investigated the role of different dietary fats in our rat model for ALD. Liver pathology was evaluated in rats fed ethanol and lard or tallow or corn oil over a period of 2 to 6 months. All experimental animals were pair‐fed the same diet as controls except that glucose was isocalorically replaced by ethanol. Rats fed tallow and ethanol developed none of the features of ALD, those fed lard and ethanol developed minimal to moderate disease, rats fed corn oil and ethanol developed the most severe pathology. The degree of histopathological abnormality correlated with the linoleic acid content of fat in the diet (tallow 0.7%, lard 2.5%, corn oil 56.6%). We postulate that linoleic acid facilitates development of ALD and provides an explanation for our previous epidemiological observation

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1989.tb00276.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

To determine whether acute ethanol administration affects the function of the adrenergic system the concentrations of plasma catecholamines and cyclic AMP (CAMP), the level of lymphocytic β‐receptors, the concentration of basal and isoproterenol‐stimulated lymphocytic cAMP and the excretion of urinary catecholamine metabolites were studied in six healthy men. These parameters were also measured during the hangover, both under resting condition and during an anaerobic ergometer exercise. Acute intake of ethanol (1.5 g/kg body weight) had no statistically significant effect either on plasma adrenaline and noradrenaline concentrations or β‐adrenergic receptor levels. Ethanol consumption did neither change the urinary excretion of catecholamine metabolites (homovanillic acid, normetanephrine, metanephrine, and 3‐methoxyhydroxymandelic acid). Exercise was associated with a 6‐10‐fold elevation in plasma adrenaline and noradrenaline concentrations and with a two‐ to threefold elevation on β‐adrenergic receptor levels. This effect of exercise was not modified by preceding alcohol intake and resulting hangover. These preliminary findings suggest that acute alcohol intake does not significantly alter the concentration and functioning of human β

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1989.tb00277.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Conditions for maintaining the activity of alcohol dehydrogenase in cultures of hepatocytes isolated from female rats were studied. The activity of alcohol dehydrogenase in freshly isolated cells was 1.7 U/mg DNA. When cultured, the activity declined 20% after one day of culture, irrespective of the culture conditions. In a conventional medium with 5mmglucose the activity after one week of culture was only 30% of that initially measured in culture. Addition of 25 mmglucose or a high concentration of amino acids delayed the decrease. When these compounds were added together it was possible to maintain the initial activity for one week, but the activity declined during the following week. Addition of growth hormone had no effect during the first week of culture but abolished the fall during the second week. The initial metabolism of ethanol was 0.65 μmol/min × mg DNA and declined to two‐thirds during the 2 weeks of cult

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1989.tb00278.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Male and female rat pups were administered ethanol (3 g/kg/dose) twice daily by intragastric intubation between postnatal Day (PN) 4 and 8. Pups were maternally reared throughout the exposure period and until sacrifice on PN20. The consequences of this growth spurt exposure to ethanol were measured by an impact upon body growth, as well as upon specific growth parameters and cholinergic neurochemical factors within the cerebral cortex and corpus striatum. Specific endpoints included muscarinic receptor binding dynamics, acetylcholinesterase (AChE) and choline acetyltransferase (CAT) activities, regional wet weights, and subcellular protein content. In male pups, ethanol resulted in a significant enhancement of body weight gain and an increase in striatal but not cortical mass. Additionally, ethanol exposure resulted in a significant increase in striatal muscarinic receptor affinity, regardless of gender. This was accompanied by evidence of a significantly greater density of striatal muscarinic receptors in males versus females, regardless of treatment. Overall, the ethanol‐associated effects are suggestive of a drug‐induced developmental delay. Gender‐specific, treatment‐independent differences were also detected in the developing brain regions. Thus, regardless of treatment, cerebral cortical S1‐level protein content was found to be significantly greater in males than in females. Furthermore, there were gender‐based, significant differences in AChE activity within the striatum of control pups (males>females). Ethanol exposure resulted in a loss of this gender‐based difference. We conclude that the cholinergic neurochemical development occurring in the striatum of the female rat brain between PN4 and 8 is exquisitely sensitive to ethanol‐induced developmental delays which are not remediable by 12 subsequent days of maternal rearing in the absence of e

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1989.tb00279.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Pavlovian conditioning studies with alcohol in humans have been performed exclusively with men subjects. Men demonstrate a placebo response opposite in direction to alcohol, which Newlin (Alcohol Clin Exp Res 9411‐416, 1985) termed an antagonistic placebo response. The current study used normal women subjects given alcohol, placebo, or a soft drink control. Placebo significantly (p<0.05) increased heart rate compared to the control condition, and this placebo response was in the same direction as the effect of alcohol. The correlation of heart rate change with reported intoxication was +0.44 in women, when it was negative in men (Newlin DB Alcohol Clin Exp Rer 9:411‐416, 1985). These results, when considered in relation to other data concerning individual differences in antagonistic placebo responding, suggest a pattern in which risk for alcoholism is negatively related to placebo respond

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1989.tb00280.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Beginning at very low concentrations (0.001 g/100 ml), alcohol elicited dose‐dependent contractions of the human umbilical artery in vitro. Additionally, 16 of the 108 arteries tested had a 5‐10‐min spasm in response to alcohol. Alcohol (0.2 91100 ml) also increased tension developed in response to all angiotensin II doses, but had no effect on serotonin‐induced contractions. These results suggest that alcohol may increase umbilicoplacental resistance in vivo, thus decreasing fetal‐placental b

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1989.tb00281.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

The role of verbal intelligence (VI) as an antecedent and moderator of alcohol‐related problems was investigated for a national sample of young adults. A measure of VI was used to predict alcohol related behavior 5 years later. Results indicated that lower VI was associated with lower risk for drinking per se. Lower VI was also associated with higher risk for alcohol‐related problems among those who drink. These findings were robust across gender, age, and to a large extent across different areas of alcohol related problems. Cognitive‐behavioral functions associated with intelligence, such as social judgement, social inference, and social skills, are proposed as possible moderators of the relationship between intelligence and alcohol‐related p

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1989.tb00282.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY