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Results for “LIVER CIRRHOSIS, EXPERIMENTAL”

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At least 127 records · Page 7Linked to original sources
PubMed2005

Melatonin prevents experimental liver cirrhosis induced by thioacetamide in rats.

Liver cirrhosis is a critical stage of chronic liver diseases that can produce liver failure, portal hypertension and hepatocarcinoma. Sustained oxidative stress plays a key role in cell damage and fibrosis induced during liver cirrhosis. We evaluated the effect of oxidative stress regulation by melatonin on the development of parenchymal destruction and stellate cell activation in experimental liver cirrhosis. Melatonin was administered to rats with liver cirrhosis induced by thioacetamide (TAA) for 1 or 3 months. Liver injury was assessed by serological analysis, as well as hematoxylin-eosin staining and the in situ apoptosis detection assay in liver sections. Oxidative stress was evaluated by lipoperoxide and reduced glutathione levels, and by the measurement of catalase and superoxide dismutase activities in liver and serum respectively. The activation of stellate cells was evaluated by alpha-smooth muscle actin expression in liver sections. Our results showed that TAA induced oxidative stress with extensive tissue damage and enhanced alpha-smooth muscle actin expression in liver. Melatonin prevented the oxidative stress-related changes associated with TAA toxicity. In conclusion, the study showed that melatonin prevents the tissue damage and fibrosis associated with TAA-induced liver cirrhosis in rats.

Animals↗
PubMed1995

Alterations of trace elements in kidney, spleen and lungs in treated and untreated experimental liver cirrhosis.

Repeated administration of carbon tetrachloride (CC1(4)) to the experimental animals not only produces liver cirrhosis but also pathological changes in different organs. The alteration of trace elements in the plasma and in the liver has been documented. Very limited studies were carried out regarding the alteration of trace elements in different organs in experimental animals subjected to CC1(4) toxicity and the influence of scavengers such as superoxide dismutase (SOD) and allopurinol as preventative measurements. Four groups of animals were studied: CC1(4) and allopurinol (group 1), CC1(4) and SOD (group 2), CC1(4) alone (group 3) and olive oil (group 4). Analysis of tissue concentrations of trace elements in different organ's tissues (e.g. lung, spleen and kidneys) were performed. Histopathological assessments were studied in all groups after 7 weeks of repeated administration of the solutions. Copper contents in the spleen and lungs were significantly high in group 2, while kidney copper contents were significantly high in all experimental groups. Selenium contents in the kidneys and lungs were significantly low in group 1, while it was significantly high in group 2 in all organs. Manganese contents in kidneys was significantly low in group 1 and significantly increased in group 2 in the case of spleen and lung. Lung zinc content was significantly increased in group 2. Spleen zinc decreased significantly only in group 3. Histopathological assessment indicated evidence of interstitial pneumonia in the group treated with allopurinol. The low levels of selenium predisposes to the development of interstitial pneumonia.

Allopurinol↗
PubMed1989

[The possibility of correcting metabolic disorders in experimental liver cirrhosis by cryodestruction and plasma-flow resection].

The first week after the cryodestruction, the resection of plasma flow and combined effect of the two methods causes metabolic changes, which later according to observations are normalized. The metabolic disturbances, which are connected with experimental liver cirrhosis under the combined cryodestructive effect and plasma flow resection are normalized three weeks after treatment. But there is no elimination of defects of free radical oxidation and there remains a decreased insulin binding capability of lymphocytes. All these processes should be taken into account in surgical treatment of liver cirrhosis.

Animals↗
PubMed1999

Enhanced tumor detection in the presence of liver cirrhosis: experimental study on the diagnostic value of a superparamagnetic iron oxide MR imaging contrast agent (NSR 0430).

The purpose of this study was to determine the diagnostic value of the superparamagnetic iron oxide NSR 0430 for the detection of focal liver lesions in the presence of advanced cirrhosis. Cirrhosis and growth of cholangiofibromas were induced in 22 rats by administration of thioacetamide. Sixteen non-cirrhotic animals served as controls. T1 and T2 relaxation times of liver and tumor tissue of 12 animals were measured spectroscopically. In 10 animals in vivo MRI was performed before and 1 hour after contrast administration, and then the tumor-to-liver contrast-to-noise ratio (CNR) was calculated. All specimens were evaluated histologically. After contrast administration, T1 and T2 values of liver tissue showed a significant decrease of 18% (P = 0.01) and 31% (P = 0.009), respectively, whereas relaxation times of tumor tissue did not change. On precontrast turbo spin-echo images, 40 tumors could be identified; after contrast administration, 95 lesions were visible. CNR increased significantly after contrast administration by 297% at a TE of 50 msec and by 254% at a TE of 90 msec. In conclusion, our in vitro and in vivo results demonstrate that administration of NSR 0430 substantially improves liver-to-tumor CNR and lesion detection on T2-weighted magnetic resonance images even in the presence of severe cirrhosis.

Animals↗
PubMed1991

[Pharmacological lowering of portal pressure in normal rats and in experimental liver cirrhosis].

Four pharmacons were tested on an acute portal pressure lowering effect in an experimental animal model with 25 normal and 25 rats with Thioacetamide-toxic liver cirrhosis. Invasive measurements of arterial and portal pressure were made under Hexobarbital-Sodium anaesthesia during 30 minutes after pharmacon application. The portal pressure of cirrhotic rats was under basic conditions 9.5 +/- 1.5 mm Hg and significant higher as in normal animals (5.3 +/- 0.9 mm Hg, p less than 0.01). After 10 mg/kg body mass Propranolol the portal pressure decreased in both animal groups small but not significantly over the whole measurement time. 1 mg/kg Verapamil lowered arterial middle pressure significantly, but increased portal pressure at all 15-20% in both animal groups. Application of 0.1 mg/kg Prazosin decreased the arterial middle pressure at all 5-15% and the portal pressure at all 20-30% in both study groups (both significantly). For Canrenoat-Potassium (20 mg/kg) no clear effect could by evaluated on portal pressure. The model of Thioacetamide-toxic cirrhosis of the rat offers conditions like cirrhosis in human medicine in order to study the effects of portal pressure lowering pharmacons. Propranolol and Prazosin decrease portal pressure and should by further investigated.

Acute Disease↗
PubMed2004

[Pathological study of the therapeutic effect of wen-yang herbs on experimental liver cirrhosis].

OBJECTIVE: To observe the pathological effect of wen-yang herbs on experimental hepatic fibrosis. METHODS: Thirty-two male Wistar rats were used in this study comprising four groups. To start with, 24 rats of three groups were given subcutaneous injection of CCl4 and drinking 10% alcohol so as to make the model of hepatic fibrosis. After the establishment of the pathologic model, the rats were divided into the model group, the pathological control group and the therapeutic group by randomization. The rats of the therapeutic group were given the herbal remedies via gastrogavage, q.d. x 30. The rats of the pathological control group were given normal saline via gastrogavage, q.d. x 30. Then liver tissue Hydroxyproline (Hyp) content was examined in these 3 groups and the normal group. Quantitative marks were done according to a modified semiquantitative scoring system (SSS). The results of SSS marks and Hyp contents were analysed using Pearson's coefficient of correlation. RESULTS: The Hyp content and SSS marks of the therapeutic group decreased remarkably as compared with those of the control group (P<0.01), and the SSS marks had a strong positive correlation with Hyp content (r=0.804). CONCLUSION: Wen-yang herbs can mitigate the rats' hepatic fibrosis and promote a recovery of their experimental illness.

Animals↗
PubMed1993

Comparative effect of nifedipine and S-adenosylmethionine, singly and in combination on experimental rat liver cirrhosis.

An experimental rat liver cirrhosis, by means of carbon tetrachloride and ethanol during 8 weeks, was employed to assay the effect of Nifedipine (a calcium antagonist blocker), S-Adenosylmethionine (a precursor of glutathione); singly and in combination on rat liver cirrhosis. A slight decrease of cirrhosis (N.S.) was observed with the pharmacological therapy employed singly. The combination therapy (Nifedipine+S-Adenosylmethionine) significantly inhibited liver cirrhosis (p < 0.01).

Animals↗
PubMed1987

Experimental liver cirrhosis does not influence reproductive performance of female rats and development of hepatic biotransformation in their offspring.

Experimental hepatic cirrhosis was produced in virgin female Wistar rats by thioacetamide (TAA) administration with the drinking water from the 4th up to the 6th month of life. Mating occurred 31 +/- 3 d after cessation of TAA treatment. At the time the body mass of cirrhotic rats was not different from that of untreated controls. Body mass gain during pregnancy, length of gestation, litter size and body mass of the newborns were not influenced by experimental cirrhosis. Lactation seems to be slightly decreased in TAA-dams in the first 5 postnatal days, reflected by lower growth rates of TAA- and control-pups nursed by TAA- in comparison to control-dams. Somatic development (body mass) and hepatic biotransformation (ethylmorphine N-demethylation and ethoxycoumarin O-deethylation) were not different in the TAA- and control-offspring up to adulthood. Liver mass was enhanced in TAA-offspring at birth, but not any longer in 10-d-old and older rats.

Animals↗
PubMed2005

Role of vascular nitric oxide in experimental liver cirrhosis.

One of the most important features of liver cirrhosis is the splanchnic and systemic arterial vasodilation, related to an increase in vascular capacity and an active vasodilation. This arterial vasodilation seems to be the consequence of the excessive generation of vasodilating substances, which also contributes to a lower than normal pressor response to circulating nervous or humoral substances. The following review analyzes the mechanisms responsible for the vascular hyporesponse to vasoconstrictors observed in the experimental models of liver cirrhosis. It has become increasingly clear that, among the great variety of substances studied, nitric oxide (NO) seems to be one of the main contributors to this vascular alteration, since elimination of the endothelium or inhibition of its synthesis corrects it. The mechanism by which NO interferes with the contractile apparatus in smooth muscle cells seems to be related to a direct effect on calcium entry from the extracellular space and release from the internal stores.

Animals↗
PubMed2005

Impact of antithrombin III on hepatic and intestinal microcirculation in experimental liver cirrhosis and bowel inflammation: an in vivo analysis.

AIM: To analyze the hepatic and intestinal microcirculation in an animal model of liver cirrhosis and inflammatory bowel disease (IBD) and to characterize the anti-inflammatory action of antithrombin III (ATIII) on leukocyte kinetics and liver damage. METHODS: Hepatic and intestinal microcirculation was investigated by intravital videomicroscopy. Standardized models of experimental chronic liver cirrhosis and bowel inflammation were employed. Animals were divided into four groups (n = 6/group): controls, animals with cirrhosis, animals with cirrhosis and IBD, animals with cirrhosis and IBD treated with ATIII. RESULTS: Cirrhosis facilitated leukocyte rolling and sticking in hepatic sinusoids (1.91+/-0.28 sticker/microm vs 0.5+/-0.5 sticker/microm in controls, P<0.05). The effect enhanced in animals with cirrhosis and IBD (5.4+/-1.65 sticker/microm), but reversed after ATIII application (3.97+/-1.04 sticker/microm, P<0.05). Mucosal blood flow showed no differences in cirrhotic animals and controls (5.3+/-0.31 nL/min vs 5.4+/-0.25 nL/min) and was attenuated in animals with cirrhosis and IBD significantly (3.49+/-0.6 nL/min). This effect was normalized in the treatment group (5.13+/-0.4 nL/min, P<0.05). Enzyme values rose during development of cirrhosis and bowel inflammation, and reduced after ATIII application (P<0.05). CONCLUSION: Liver cirrhosis in the presence of IBD leads to a significant reduction in mucosal blood flow and an increase in hepatic leukocyte adherence with consecutive liver injury, which can be prevented by administration of ATIII.

Animals↗
PubMed1985

The influence of an experimental liver cirrhosis upon the metabolism of diazepam and imipramine hydrochloride in the rat.

When either diazepam or imipramine hydrochloride was administered orally to rats with thioacetamide-induced hepatic cirrhosis, the biliary and faecal elimination of metabolites was significantly decreased compared with that in normal animals. However, renal excretion of metabolites of diazepam or imipramine was increased in the liver-damaged rats. Experiments in vitro showed that liver homogenates from cirrhotic rats metabolized diazepam or imipramine hydrochloride in qualitatively and quantitatively similar ways to those from normal rats. Clearance of radioactivity from the blood following i.v. administration of either diazepam or imipramine hydrochloride was prolonged in animals with experimental cirrhosis.

Animals↗
PubMed1991

The effect of D-penicillamine on CCl4-induced experimental liver cirrhosis.

The effect of D-penicillamine (Pe) on liver fibrosis-cirrhosis induced by chronic CCl4 and phenobarbital (Pb) administration in Fischer 344 male rats was studied. Morphometric analysis did not reveal a decrease in the amount of connective tissue fibers after Pe-treatment. Compared to the CCl4 and Pb-treated control groups, Pe had no significant effect on the concentrations of hydroxyproline, a parameter of collagen degradation, either; however, it increased the glycosaminoglycan concentrations. Lymphocyte stimulation by Con-A in the Pe-treated groups did not differ from that of the CCl4 and Pb-treated ones. According to our studies, Pe-treatment was ineffective in rats with liver fibrosis-cirrhosis induced by CCl4 and Pb administration. It seems that Pe can be effective only in the cirrhosis types accompanied by a considerable copper accumulation due to suppression of the toxic effects of copper.

Animals↗
PubMed1985

Systemic and splanchnic hemodynamic disturbances in conscious rats with experimental liver cirrhosis without ascites.

Rats with CCl4-induced cirrhosis of the liver show histological and clinical features that closely resemble those of the disease in humans. Metabolic cages were used and hemodynamic studies (15-micrograms radioactive microspheres) were performed on 10 conscious, nonascitic, cirrhotic rats and in 10 control rats. Compared with control animals, cirrhotic rats showed lower sodium excretion (0.80 +/- 0.07 vs. 1.01 +/- 0.07 meq/day), total solute excretion (12.52 +/- 0.79 vs. 19.38 +/- 3.7 mosmol/day), and increased aldosterone excretion. No differences were observed in urinary epinephrine and norepinephrine excretion. Cirrhotic rats showed also slight hypotension, increased cardiac output (48.97 +/- 3.94 vs. 26.97 +/- 2.3 ml X min-1 X 100 g-1) without tachycardia, and decreased total peripheral resistance, which was mainly attributed to reduced renal and skeletal muscle resistances with increased blood flow throughout these areas. Cirrhotic rats showed increased hepatic vascular resistances by both portal and arterial inputs with portal hypertension (16.15 +/- 1.01 vs. 9.60 +/- 0.77 cmH2O) but without differences in total hepatic blood flow or portal-systemic shunt rate with respect to control rats. Plasma renin content was not significantly different between the groups of rats. From these data it can be concluded that nonascitic, cirrhotic rats show a hyperdynamic circulatory state, which seems to be caused by a peripheral vasodilation of unknown mechanism; portal-systemic shunting does not seem to be a necessary condition for the hyperdynamic status at this early stage of the hemodynamic disturbances.

Animals↗