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1. |
On the Relevance of Animal Models to Alcoholism in Humans |
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Alcoholism: Clinical and Experimental Research,
Volume 10,
Issue 4,
1986,
Page 361-363
Vincent P. Dole,
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ISSN:0145-6008
DOI:10.1111/j.1530-0277.1986.tb05107.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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2. |
Identification of Alcohol Abuse and Alcoholism with Biological Parameters |
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Alcoholism: Clinical and Experimental Research,
Volume 10,
Issue 4,
1986,
Page 364-385
Ronald R. Watson,
Mary E. Mohs,
Cteamond Eskelson,
Richard E. Samptiner,
Barbara Hartmann,
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摘要:
The prevalence and incidence of heavy alcohol consumption are major problems which have been increasing in many countries in recent years. It is crucial for physicians to consistently identify early drinking problems as well as the various end disease states in order to minimize suffering and maximize recovery. This paper reviews the evolutionary development of clinical tools for detection of alcohol abuse. The focus is primarily on dmical/biochemical indicators of alcohol abuse, emphasizing but not limited to changes in hematological characteristics, Hver enzyme activity, lipids, immune function factors, hormones, neurological factors, and some physicaty based tests. Use of test combinations and sophisticated statistical analysis of pattern changes in test batteries evidence increased diagnostic efficiency.
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1986.tb05108.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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3. |
Regression of Severe Alcoholic Cardiomyopathy after Abstinence of 10 Weeks |
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Alcoholism: Clinical and Experimental Research,
Volume 10,
Issue 4,
1986,
Page 386-387
Arthur S. Agatston,
Matthew E. Snow,
Philip Samet,
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摘要:
Alcohofc cardiomyopathy usuaRy has a poor prognosis, but the case i presented here documents a dramatic regression of left ventricular i dysfunction in a patient with alcoholic cardiomyopathy. Ejection fraction determined by echocardiography increased from 12% at the time of presentation to 45% 10 weeks later. This was associated I with clinical resolution of conjestive heart failure and a decrease in i cardiac and left ventricular size documented by chest x‐ray a
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1986.tb05109.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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4. |
Preferential Alcoholic Embryopathy among Contiguous Siblings of Long‐Evans Rats |
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Alcoholism: Clinical and Experimental Research,
Volume 10,
Issue 4,
1986,
Page 388-392
Russell F. Mankes,
Stanley D. Glick,
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摘要:
Ethanol exposure altars sex steroidogenesis and sexually dimorphic behaviors in rodent offspring. Contiguity to siblings of the same or opposite sex in utero also affects steroidogenesis and sexual dimorphism in rodents. The present study with Long‐Evans rats shows that maternal exposure to ethanol during the critical period of rodent organogenesis preferentially affects body weights and increases malformations in offspring dependent on their in utero contiguity to siblings of the opposite se
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1986.tb05110.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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5. |
The Effect of Ethanol Intake on Propoxyphene Absorption and Biotransformation in Dogs |
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Alcoholism: Clinical and Experimental Research,
Volume 10,
Issue 4,
1986,
Page 393-396
H. Olsen,
H. Aune,
P. Lilleaasen,
M. Gulliksen,
E. Bodd,
J. Mwland,
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摘要:
The effect of ethanol (0.5 and 1.0 g/kg) on gastrointestinal absorption and presystemic biotransformation of propoxyphene (4 mg/kg) was studied in dogs in a crossover design. Low ethanol doses (0.5 g/kg) had no effect on the bioavailability of propoxyphene. High ethanol doses (1.0 g/kg) enhanced the bioavailability of orally administered propoxyphene significantly (p<0.05). With this dose of ethanol, the area under the blood concentration versus time curve (AUC)0–5 hof propoxyphene was approximately 200% of the control value. The level of norpropoxyphene, a major metabolite of propoxyphene, was significantly decreased (p<0.05) after administration of high ethanol doses. In all blood samples, after propoxyphene administration, an unidentified metabolite of propoxyphene was found, which formation was dose dependentJy inhibited by ethano
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1986.tb05111.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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6. |
Pituitary‐Adrenal Responses to Morphine and Footshock Stress Are Enhanced following Prenatal Alcohol Exposure |
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Alcoholism: Clinical and Experimental Research,
Volume 10,
Issue 4,
1986,
Page 397-402
Linda R. Nelson,
Anna Newman Taylor,
James W. Lewis,
Russell E. Poland,
Eva Redei,
Berrilyn J. Branch,
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摘要:
The effect of prenatal ethanol exposure on pituitary‐adrenal function in adult offspring was assessed by measuring cortjcosterone (CS) levels in plasma following exposure to two forms of footshock stress, intermittent and continuous, and after administration of 20 mg/kg of morphine. The footshock experiments were conducted at two time points in the circadian pituitary‐adrenal cycle. Prenatally ethanol‐exposed (E) rats had higher levels of CS than pair‐fed and normal controls following intermittent footshock when tested at the crest of the CS circadian rhythm. However, this difference was not present when intermittent footshock was presented at the trough of the circadian cycle. At either time of day, there were no differences among the prenatal treatment groups in the basal condition or following continuous footshock. In addition, E rats had significantly higher levels of plasma CS than controls following morphine. Plasma adrenocorticotropin (ACTH) levels were measured after intermittent footshock at the crest of the circadian rhythm and were significantly higher in E rats than in controls. These results extend our previous reports of enhanced activation of the hypothalamo‐pituitary‐adrenal axis in response to other stressors as wed as to ethanol in adult rats exposed to ethanol in utero. They also confirm that E rats are differentially hyperresponsive only to intermittent footshock stress, not to continuous footshock, as we had found to be the case when the analgesia induced by these two stressors was the depend
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1986.tb05112.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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7. |
ANNOUNCEMENT |
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Alcoholism: Clinical and Experimental Research,
Volume 10,
Issue 4,
1986,
Page 402-402
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ISSN:0145-6008
DOI:10.1111/j.1530-0277.1986.tb05113.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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8. |
Effects of Dietary Fat on Alcohol‐Pyrazole Hepatitis in Rats: The Pathogenetic Role of the Nonalcohol Dehydrogenase Pathway in Alcohol‐Induced Hepatic Cell Injury |
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Alcoholism: Clinical and Experimental Research,
Volume 10,
Issue 4,
1986,
Page 403-411
Akira Takada,
Yoshiro Matsuda,
Shujiro Takase,
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摘要:
Rats were fed with two different alcohol‐containing (36% of total calories) liquid diets of high fat and low fat (35% and 15% of total calories) with or without 2 mm of pyrazole for 12 weeks. At the 12th week, the serum glutamic oxaloacetic transaminase level was significantly elevated in the alcohol‐pyrazole high fat group, but not in the low fat group. Ballooning and necrotic changes of the hepato‐cytes in the centrolobular area were more prominent in the alcohol‐pyrazole high fat group than in the low fat group and alcohol atone groups, indicating that high fat diet accelerates the development of alcohol‐pyrazole hepatitis. In the alcohol‐pyrazole high fat group, a decrease of hepatic microtubules content and an accumulation of hepatic export proteins in the hepatocytes were found. The protein accumulation was prominent only in the ballooned hepatocytes. Hepatic acetaldehyde levels were significantly higher in the alcohol‐pyrazole high fat group than in the alcohol‐pyrazole tow fat group. These results suggest that the accelerated ethanol metabolism in the nonalcohol dehydrogenase pathway by a high fat diet may play an important role in the development of hepatocybc injuries, by impairing the microtubular function of
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1986.tb05114.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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9. |
Binding, Uptake, and Metabolism of Chylomicron Remnants by Hepatocytes from Control and Chronic Ethanol‐Fed Rats |
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Alcoholism: Clinical and Experimental Research,
Volume 10,
Issue 4,
1986,
Page 412-418
M. R. Lakshmanan,
Mildred Ezekiel,
Barbara S. Campbell,
Richard A. Muesing,
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摘要:
Chylomicron remnants, but not lymph chylomicrons, showed a receptor‐dependent high affinity saturable binding to normal rat hepatocytes. The Scatchard analysis of the specific binding data showed a high affinity binding site for the remnants with a dissociation constant of 0.61 nut, assuming a molecular weight of 50 times 10sfor chylomicron remnants. Based on the heparin‐releasable bound radioactivity, approximately 80% of the bound remnants seemed to be internalized. The binding process was markedly inhibited by pronase as wen as by protein synthesis inhibitors. Competitive binding studies revealed that the order of competition for the binding of labeled remnants by homologous unlabeled lipoproteins was remnants>chylomicrons>very low density lipoproteins>high density lipoproteins. Human low density lipoproteins showed virtually no competition.Studies on the catabolism of triacylglycerol moiety of the remnants showed that 15.2% of the14C label in the triacylglycerol moiety of the remnants was catabolized by the hepatocytes to14CO2due to specific interaction. This amounted to 93% of the total14CO2evolution. This was in sharp contrast to the catabolism of the triacylglycerol moiety of very low density lipoproteins from human and rat, where most of the14CO2evolution was due to pathways associated with nonspecific binding.Chronic ethanol feeding caused a 29% (p<0.02) decrease in the dissociation constant of the high affinity binding site of the liver cell for the remnants, whereas the extent of internalization was decreased by 19% (p<0.01) as compared to the pair‐fed control animals. In contrast to these small decreases in binding affinity and internalization, the catabolism of both triacylglycerol and cholesterol ester moieties of remnants were markedly inhibited by 58% (p<0.001) and 44% (p<0.01), respectively, in hepatocytes from chronic ethanol‐fed animals. These results are compatible with the pathogenesis of fatty liver and defective regulation of hepatic cholesterol synthesis after chronic ethano
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1986.tb05115.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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10. |
Study of Dose‐Dependence and Urinary Folate Excretion Produced by Ethanol in Humans and Rats |
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Alcoholism: Clinical and Experimental Research,
Volume 10,
Issue 4,
1986,
Page 419-424
Kenneth E. McMartin,
Timothy D. Collins,
Cheng Quei Shiao,
Lori Vidrine,
Helmut M. Redetzki,
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摘要:
Acute ethanol ingestion by human alcoholic subjects produces a marked decrease in serum folate levels within 16 hr. A similar decrease occurs in rats and can be explained by a marked increase in urinary folate excretion following ethanol treatment To assess the effects of acute ethanol ingestion on urinary folate excretion in healthy human volunteers, two studies were carried out at initial ethanol dose levels of 0.8 g/kg and 1.0 g/kg, respectively. Blood ethanol levels peaked at 70 mg/dl in the first study, but in the second study were 100 ± 20 mg/dl through 6 hr. Only in the second study were urinary folate levels significantly increased by ethanol administration, and this 8 hr after ingestion. This increase was accompanied by a decrease in urine volume so that in neither study was the total amount of urinary folate excreted from 0–12 hr increased by ethanol ingestion. Studies with various dose levels of ethanol in rats showed that there was a linear dose‐response relationship between the total urinary folate excretion and the dose of ethanol. Peak urinary ethanol levels also correlated with urinary folate excretion. These results suggest that doses of ethanol larger than 1.0 g/ kg produce increases in urinary folate excretion and that the inability to observe large increases in studies in human subjects is probably related to the limited doses of ethanol ch
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1986.tb05116.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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