Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The (+)-cyanidanol-3 is used as an antihepatotoxic and hepatoprotective drug in both men and animals against alcoholic and experimental liver injury. Histologic staining techniques give mostly qualitative or semiquantitative description of liver damages. Experiments have been carried out to determine the hepatoprotective effects of (+)-cyanidanol-3 on alcoholic liver damage (i.e., fatty liver and hepatomegaly) by morphometric measurement of the liver tissue sections. Ethanol was administered ad lib to CFY rats to cause mild alcoholic liver damage together with 200 mg/kg/day (+)-cyanidanol-3 to prevent the tissue deterioration. The changes of hepatic lobule and hepatocytes were measured morphometrically. The chronic ethanol consumption results in hepatocellular hypertrophy, a significant increase in size of the hepatocytes and a mild increase of the intralobular extrahepatocytic space as well when compared with controls. The volume of cytoplasm was increased while the parameters of nuclei were unchanged. The (+)-cyanidanol-3 prevents changes and the morphometric parameters in the treated group were almost the same as in the controls. The treatment with (+)-cyanidanol-3 alone does not affect the hepatic tissue parameters. The results show the hepatoprotective effect of (+)-cyanidanol-3 and the suitability of the morphometric method for quantitative comparison of normal and experimentally-altered liver cells.
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PMID:Some morphometric evidence of hepatoprotective effects of (+)-cyanidanol-3. 258 92

In the present study, the effects of chloroquine and ethanol administration during gestation have been investigated on the developing rat fetus. Intragastric administration of chloroquine (700 mg/kg body weight) resulted in several structural abnormalities. The incidence of hepatomegaly was increased by 30%, the liquification of visceral organs was increased by 15% and a 9% higher incidence of cleft palate, wrist drop, clubbed foot and brain liquification was observed in the fetuses from the chloroquine-treated group compared to the corresponding controls. Fetuses from the chloroquine-treated group also showed a decrease of about 40% in the body weight and a 30% reduction in the ossification of the sternum. The teratogenic effects of oral ethanol administration in several respects were similar to those of the chloroquine. Ethanol, when administered as 30% of the total daily calories, resulted in growth retardation, resorption, still births, liquification of the brain, wrist drop and clubbed foot. Additionally, ethanol resulted in the inhibition of several metabolic pathways in the liver and brain of the developing fetuses. This included the inhibition of protein, RNA and DNA metabolism in the fetal livers and brains. The feto-toxic effects of these two xenobiotics and their possible molecular mechanisms have been discussed.
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PMID:Toxicological consequences of chloroquine and ethanol on the developing fetus. 262 56

Chronic consumption of ethanol often results in an increased rate of ethanol metabolism (metabolic tolerance) and in hepatomegaly. However, the extent of these changes is highly variable. We have found that these two phenomena are greatly influenced by age. We studied the effect of age on the development of metabolic tolerance and hepatomegaly and on the increase in hepatic oxygen consumption produced by chronic ethanol administration. The latter has been proposed to contribute to metabolic tolerance to ethanol. Ethanol was administered to female Sprague-Dawley rats with different initial ages (4, 6, 8, 11, and 17 weeks) for a 4-week period in a high-fat liquid diet. Control animals were pair-fed an isocaloric liquid diet in which ethanol was replaced with carbohydrate. Metabolic tolerance and hepatomegaly following chronic ethanol consumption were markedly dependent on the initial age of the animal, with young animals showing the largest increases. Although showing a similar general trend with age, the degree of metabolic tolerance was not linked proportionally with the degree of hepatomegaly. Perfused livers from young rats fed chronically with ethanol showed increases in ethanol metabolism and oxygen consumption, whereas no increase were observed in those from older animals. These findings support the hypothesis that an elevated rate of hepatic oxygen consumption contributes to metabolic tolerance. Total hepatic alcohol dehydrogenase activity was not increased by chronic ethanol consumption in any age group, demonstrating that an increase in the levels of this enzyme is not obligatory for metabolic tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of age on metabolic tolerance and hepatomegaly following chronic ethanol administration. 639 2

It has been shown that alcohol consumption disrupts liver microtubules, impairs protein secretion and leads to ballooning of the hepatocytes in rats. Ethanol-induced hepatomegaly was accounted for by an increase of the hepatocytes volume. To study whether these changes occur in human alcoholic liver disease, hepatic tubular protein and export protein content were measured in 29 cases of alcoholic liver disease and were compared with those of 37 cases of non-alcoholic liver disease and 5 cases of non-hepatobiliary disease. Hepatic polymerized tubulin was significantly decreased in alcoholic liver disease compared to non-alcoholic liver disease (p less than 0.01), while free tubulin was increased in alcoholic liver disease. Hepatic transferrin (one of the export proteins) content was significantly higher (p less than 0.01) and serum transferrin level was significantly lower (p less than 0.05) in alcoholic liver disease than in non-alcoholic liver disease. These findings indicated that even in humans, chronic alcohol consumption decreased hepatic microtubules by impairing polymerization of tubular protein and increased hepatic export protein content. This decrease in hepatic microtubules by chronic alcohol consumption may play an important role in the development of human alcoholic liver disease.
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PMID:Changes of hepatic microtubules and secretory proteins in human alcoholic liver disease. 663 57

The effect of ethanol on hepatic regeneration after partial hepatectomy was studied. Ethanol was administered in a nutritionally adequate liquid diet 4 times daily by gastric intubation. The dose of ethanol was selected to maintain a continuous level of ethanol in the animals throughout the experiment. Treatment was started 24 hours before the operation and continued for 6 days. Control animals were pair-fed on a diet in which ethanol was isocalorically replaced by carbohydrate. On the 1st, 2nd, 3rd and 5th day after the operation the incorporation of [3H]-labelled thymidine into liver DNA and [14C]-labelled leucine into liver proteins and the mitotic index of the regenerating liver was assessed. On the 2nd and 3rd day the incorporation of labelled thymidine into DNA in the regenerating livers of alcohol-fed animals was significantly (P less than 0.05) lower than in pair-fed controls. The inhibition was most pronounced (60%) on the 2nd day after the operation. This was associated with a significant (P less than 0.01) decrease in mitotic activity, which was most pronounced in the periportal area. At the end of the experiment, however, DNA content was similar both in ethanol-treated and in control livers. It is concluded that the continuous presence of ethanol retards DNA synthesis and cell division of regenerating rat liver after partial hepatectomy. The incorporation of [14C]-leucine into liver proteins was inhibited by ethanol on the second day of regeneration (P less than 0.01), and at the end of the experiment the livers of ethanol-fed rats contained more protein than the control livers. This accumulation of proteins was accompanied by hepatomegaly.
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PMID:Effects of ethanol on liver regeneration after partial hepatectomy in rats. 723 Sep 14

Acute ethanol exposure depresses cardiac electromechanical function, whereas chronic ethanol consumption leads to the development of a specific myopathic state. Chronic hypertension and aging have similar effects in the impairment of myocardial function. However, little is known about the effects of ethanol on cardiac mechanical function in hypertension. We studied the effect of age on baseline mechanical properties and the inotropic response to clinically relevant concentrations of ethanol (18 to 71 mmol/L) using papillary muscles from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) at 10 and 25 weeks of age. Mechanical parameters measured were peak tension developed, time to peak tension, time to 90% relaxation, and maximal velocities of tension development and tension decline. SHR exhibited elevated systolic pressure and body weight as well as cardiomegaly and hepatomegaly at 10 and 25 weeks of age. Baseline mechanical properties were similar in SHR and WKY muscles at 10 weeks, whereas at 25 weeks, SHR muscles developed less tension, and both maximal velocities of tension development and tension decline were markedly depressed. Ethanol exposure produced concentration-dependent negative inotropic effects in both groups at both ages. Ethanol (> 18 nmol/L) decreased peak tension developed in both groups at 10 weeks, although higher concentrations were required at 25 weeks. The negative inotropic effect of ethanol resulted in the shortening of time to 90% relaxation in both groups at 10 weeks and was associated with a slowing of maximal velocities of both tension development and tension decline. The results suggest that aging depresses baseline mechanical properties when coupled with hypertension. In addition, the magnitude of the negative inotropic effect of ethanol was attenuated in both groups at 25 weeks of age.
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PMID:Influence of age on the inotropic response to acute ethanol exposure in spontaneously hypertensive rats. 890 37

Diabetes is associated with ventricular dysfunction. Ethanol consumption increases the risk of cardiovascular disease among diabetics. Acetaldehyde (ACA), the main ethanol metabolite, depresses cardiac contraction and contributes to ethanol-induced cardiac dysfunction. This study examined the influence of gender and diabetes on ACA-induced myocardial dysfunction. Adult male and female rats were made diabetic with streptozotocin (55 mg/kg). Left ventricular papillary muscles were isolated and stimulated to contract at 0.5 Hz. The mechanical parameters measured were peak tension development, time-to-peak tension (TPT), time-to-90% relaxation (RT90), and maximum velocities of tension development and decline (+/-VT). TPT and RT90 were comparably similar between genders. The +/-VT appeared to be slower in myocardium from female rats when compared to that of male counterparts, although the difference was not significant. Experimental diabetes elicited severe hyperglycemia, cardiac hypertrophy, hepatomegaly, and renal hypertrophy in both male and female animals. Myocardial mechanical properties exhibited prolonged TPT and RT90 in diabetic myocardium from both genders. The +/-VT was significantly reduced by diabetes in male but not in female myocardium. Acute ACA exposure decreased myocardial tension development and the +/-VT and shortened TPT and RT90 in myocardium from normal and diabetic rats of both genders. The ACA-induced depressant response on tension development was slightly enhanced by the diabetic state. In conclusion, these data suggest that the development of diabetes-induced myocardial dysfunction is similar between male and female animals and that the ACA-induced myocardial depressant action may be affected by diabetes but not by gender.
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PMID:The influence of gender, diabetes, and acetaldehyde on the intrinsic contractile properties of isolated rat myocardium. 1221 95