摘要:

The cardiovascular effects of ethanol and acetaldehyde were investigated in five dogs chronically instrumented to record heart rate, left ventricular peak systolic pressure, dP/dt max, left circumflex coronary artery blood flow, coronary sinus oxygen saturation, and myocardial oxygen consumption during a regulated exercise treadmill test.

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1981.tb04865.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

摘要:

Studies utilizing diverse methaodologies in different populations have consistently demonstrated that alcoholism appears to be a genetically influenced disorder. One biological mechanism which could hypothetically influence the acute effects and metabolism of ethanol is the rate of alcohol absorption, a trait found to be relatively consistent for any one individual under similar conditions. This investigation tested the possibility that the magnitude of and time to peak blood alcohol level might be involved in a genetic propensity toward alcoholism with suitable controls. The study has revealed no differences in the time elapsed between oral intake and peak blood alcohol concentration and no differential in the height of the peak alcohol concentration for the two groups. The results are not consistent with the rate of absorption as an important mediator of a genetic propensity in alcoholism.

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1981.tb04866.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

摘要:

Comparison of the polydipsia and liquid diet procedures for ethanol exposure were used in female rats, either before and/or during gestation. Autopsy of the fetuses on day 20 of gestation found a significant weight reduction in the polydipsia‐exposed animals that could be attributed to ethanol. No such effect was found in the liquid diet‐exposed animals. The data are discussed in relation to the human fetal alcohol syndr

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1981.tb04867.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

摘要:

The rat model is used to verify disulfiram‐associated hypercholesterolemia and to determine a mechanism of action. Administration of disulfiram 15 mg/kg/day for 3 wk is associated with a 25% increase in serum cholesterol which is reversible with discontinuance of the drug. The hypercholesterolemia is due in part to a fourfold increase in activity of hepatic HMG‐CoA reductase, the rate‐limiting step in cholesterol biosynt

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1981.tb04868.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

摘要:

Human postmortem brain samples from temporal lobe of 23 alcoholics and 19 controls (13 with cancer and six without cancer) were used for determination of low Km (micromolar) and high Km (millimolar) aldehyde dehydrogenase activity. Despite histories of severe alcoholism leading to death through multiple complications, the mean values for either low or high Km activity did not differ significantly from that of controls similarly studied.

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1981.tb04869.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

摘要:

Treatment for 7 days with the thyreostatic drug propylthiouracil (5 mg/100 g of body weight) resulted in a hypothyroid hepatic state as shown by the marked decreased hepatic content of thyroxine and triiodothyronine. This regimen led to an enhanced activity of the microsomal ethanol‐oxidizing system, whereas the activities of alcohol dehydrogenase and catalase remained unchanged. Moreover, a hyperthyroid hepatic state achieved following the daily administration of L‐thyroxine (150 jig/100 g of body weight) or L‐3,3′, 5‐triiodothyronine (10 pg/100 g of body weight) for 7 days resulted in a similar increased activity of the microsomal ethanol‐oxidizing system. Under these conditions, a decrease of alcohol dehydrogenase activity and an unaffected catalase activity was observed. These findings, therefore, show that the administration of either propylthiouracil or thyroid hormones results in an increased activity of the microsomal ethanol‐oxidizing system, suggesting that the underlying mechanism for the induction of the microsomal ethanol‐oxidizing system by propylthiouracil is independent of the action of t

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1981.tb04870.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

摘要:

Ethanol has been demonstrated to cause aberrations in lipoprotein metabolism, cholesterol synthesis, biliary secretion, and bile acid synthesis. Although there is interdependency of cholesterol and bile acid metabolism, a role of ethanoMnduced lipid abnormalities in altering bile acid synthesis has not been found. The direct effects of ethanol administration on bile acid metabolism have been studied in animals and vary with the experimental design. Acutely, ethanol causes decreased bile acid secretion and synthesis, but other effects are less well defined. Chronic ethanol use in man may result in cirrhosis, a condition in which abnormalities of bile acid metabolism have been described in detail. Cholic acid synthesis and pool size are markedly depressed In advanced cirrhosis. Che‐nodeoxycholic acid synthesis is effected less than cholic acid synthesis, probably because 12a‐hydrox‐ylase activity is markedly depressed in cirrhosis, although other steps may also be influenced such as 7a‐hydroxylation of cholesterol or availability of cholesterol precursor. The deoxycholic acid pool is depressed probably because of changes in fecal flora. Despite the decrease in total bile acid pool, lithogenicity of bile is not increased in cirrhotic patients because of a concomitant decline in cholesterol and phospholipid secretion. Changes in hepatic blood flow and hepatic extraction cause an increase in plasma bile acid levels which may have clinical re

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1981.tb04871.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

摘要:

A major effect of ethanol on lipoprotein metabolism is the development of hypertriglyceridemia. Triglyceride‐rich lipoproteins are secreted by the liver and intestine and undergo a two‐stage sequential catabolism–first in peripheral tissues, and second in the liver–mediated in part by the associated apolipoproteins. The argments for increased very low density lipoprotein production as an explanation for the hypertriglyceridemia are reviewed and found to be unconvincing. Experiments investigating the catabolism of chylomicrons are conflicting but appear on balance to suggest a catabolic defect. A potential relationship between plasma triglyceride‐rich lipoprotein metabolism and hepatic steatosis is considered. The lack of knowledge of the status of apolipoproteins in the setting of ethanol precludes definite conclusions, but defects in the incorporation or dissociation of the apolipoproteins on the triglyceride‐rich lipoproteins could explain some of the ethanol‐induced metabolic

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1981.tb04872.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1981.tb04873.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

摘要:

The effects of ethanol on bile formation have been studied in the rat, dog, and man, in both acute and chronic models. The acute and chronic effects differ. Given acutely, ethanol suppresses bile flow and bile acid secretion rate. Chronic administration appears to increase both components of canalicular flow and bile acid secretion rate. Intestinal and hepatic actions are probably involved in the latter effect. Secretion of other biliary lipids and diagnostic anions are also reduced by ethanol.

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1981.tb04874.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY