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Biomedical subjects

S Erlinger

Publications and source records attributed to S Erlinger.

At least 37 records · Page 2Linked to original sources
PubMed1991

Inhibition by colchicine of biliary secretion of diethylmaleate in the rat: evidence for microtubule-dependent vesicular transport.

It has been proposed that a microtubule-dependent transport of vesicles derived from the Golgi apparatus may play a role in biliary secretion of bile salts and other cholephilic anions. To test this hypothesis, we examined the influence of colchicine and vinblastine, two microtubule inhibitors, on diethylmaleate-induced bile flow and on the biliary secretion of diethylmaleate, an organic anion whose glutathione conjugates may be secreted into bile through the Golgi apparatus and Golgi-derived vesicles. Rats were pretreated with colchicine or vinblastine, and diethylmaleate was injected intraperitoneally at doses of 28 to 400 mumol/100 gm body wt. Basal bile flow was unaffected by colchicine or vinblastine. In contrast, diethylmaleate-induced bile flow and the secretion into bile of diethylmaleate conjugates (estimated by the cation-anion gap in bile) were significantly lower in colchicine-treated and vinblastine-treated animals than in controls. Diethylmaleate-induced bile flow was reduced in proportion to diethylmaleate conjugate secretion. A linear relationship was seen between bile flow and biliary output of diethylmaleate conjugates: this relationship was similar in colchicine-treated or vinblastine-treated animals and in controls. At electron microscopy, diethylmaleate had induced distension of the Golgi saccules of the hepatocytes. In conclusion, colchicine and vinblastine inhibited the secretion into bile of diethylmaleate conjugates and diethylmaleate-induced bile flow. These results support the view that microtubule-dependent transport of Golgi-derived vesicles is involved in the biliary secretion of diethylmaleate and, perhaps, other cholephilic organic anions.

Animals↗
PubMed1991

Giant hemangioma of the liver with pain, fever, and abnormal liver tests. Report of two cases.

In conclusion, we report the cases of two patients with large hemangiomas of the liver, abdominal pain, increased ESR and fibrinogen, increased serum alkaline phosphatase and gamma-glutamyltransferase activity, and normal white blood cell counts. Clinical and biochemical abnormalities disappeared after surgical resection. Increased ESR and fibrinogen are probably related to thrombosis within the tumor. This mode of presentation may suggest a diagnosis of hepatocellular carcinoma.

Adult↗
PubMed1991

Effect of chronic administration of cyclosporin A on hepatic uptake and biliary secretion of bromosulfophthalein in rat.

Cyclosporin A (CyA) decreases bile flow and bile salt secretion in the rat. The purpose of this study was to examine the influence of CyA on the hepatic transport of bromosulfophthalein (BSP). Male Sprague-Dawley rats were injected with CyA at the daily dose of 10 mg/kg (treated animals) or solvent (controls) during three weeks. Hepatic uptake of BSP (assessed by the plasma disappearance curve of the dye) and biliary secretion during infusions (95.5 and 178 nmol/min/100 g) were examined in both groups. Administration of CyA resulted in a decrease in both bile flow and BSP biliary secretion at the two infusion rates used. BSP plasma disappearance rate was significantly lower in treated animals than in controls. Conjugation of the dye was unaffected by CyA. There was no modification in ALT activity or in liver histology. These data show that chronic administration of CyA in rats decreases both hepatic uptake and biliary secretion of BSP. Thus, the inhibitory effect of CyA on biliary secretion is not limited to bile salts but also is observed with other cholephilic substances.

Animals↗
PubMed1991

Acute infusions of bile salts increase biliary excretion of iron in iron-loaded rats.

The mechanisms of biliary excretion of iron are not well known. The aim of this study was to examine the effect of choleresis induced by several agents on biliary iron excretion in iron-loaded rats. Iron overload was obtained with a diet supplemented by 3% iron carbonyl during a 6-week period. Bile was collected with an external bile fistula. Biliary iron concentration was measured by atomic absorption spectrophotometry, and hepatic iron concentration was measured by a chemical method. Compared with controls, iron overload resulted in a 14-fold increase in hepatic iron concentration but only a 3.9-fold increase in biliary iron output. In iron-loaded rats, taurocholate infusion caused a 1.8-fold significant increase in biliary iron output. Dehydrocholate, given at the same dose, induced a significant but less pronounced (1.3-fold) increase in biliary iron output in spite of a higher bile flow. Taurochenodeoxycholate, tauroursodeoxycholate, and tauro-7-ketolithocholate induced an increase in biliary iron output similar to that observed with taurocholate. The canalicular bile salt-independent choleretic dihydroxydibutyl ether caused a significant but less pronounced increase in biliary iron output (1.4-fold). These results confirm that in iron-loaded rats biliary iron excretion is increased much less than hepatic iron concentration. They show that in iron loaded rats (a) bile salts can increase biliary iron secretion, and (b) this increase is related in part to choleresis and in part to bile salts themselves. This increase may be related to an interaction of iron with bile salt monomers and/or micelles.

Animals↗
PubMed1991

Severe monochlorobenzene-induced liver cell necrosis.

Benzene derivatives can induce severe liver cell necrosis in animals. A case of a 40-year-old man whose daily consumption of alcohol was 200 g and who had a severe monochlorobenzene-induced liver necrosis is described. Liver biopsy specimen showed centrilobular and mediolobular necrosis, similar to that in mice after experimental bromobenzene administration. Monochlorobenzene serum concentration, assayed from day 3 to day 15 after poisoning, decreased monoexponentially with a half-life of 40.3 hours. Prostaglandin E1 was administered from day 3 to day 8. The patient ultimately recovered. The mechanism of monochlorobenzene-induced liver injury and the possible aggravating role of chronic alcohol consumption are discussed.

Adult↗
PubMed1990

Bile acids mobilise internal Ca2+ independently of external Ca2+ in rat hepatocytes.

In the present study, we investigated the possible role of external Ca2+ in the rise of the cytosolic Ca+ concentration induced by the monohydroxy bile acid taurolithocholate in isolated rat liver cells. The results showed that: (a) the bile acid promotes the same dose-dependent increase in the cytosolic Ca+ concentration (half-maximal effect at 23 microM) in hepatocytes incubated in the presence of 1.2 mM Ca2+ or 6 microM Ca2+; (b) taurolithocholate is able to activate the Ca2(+)-dependent glycogen phosphorylase a by 6.3-fold and 6.0-fold in high and low Ca2+ media, respectively; (c) [14C]taurolithocholate influx is not affected by external Ca2+, and 45Ca2+ influx is not altered by taurolithocholate. These results establish that the effects of taurolithocholate on cell Ca2+ do not require extracellular Ca2+ and are consistent with the view that monohydroxy bile acids primarily release Ca2+ from the endoplasmic reticulum in the liver.

Aminoquinolines↗
PubMed1990

Cholangitis associated with cholecystitis in patients with acquired immunodeficiency syndrome.

Four patients with acquired immunodeficiency syndrome developed severe abdominal pain and fever due to acute acalculous cholecystitis. In all patients, preoperative laboratory data showed elevation of alkaline phosphatase and gamma-glutamyltransferase levels. Endoscopic or intraoperative cholangiography showed signs of intrahepatic and extrahepatic cholangitis. Cholecystectomy was performed and prompt relief of symptoms was achieved in all patients; no postoperative complication was observed. One patient did not develop any recurrence during an 18-month period of follow-up; two patients died 2 and 3 months after the operation. One patient developed recurrent abdominal pain and cholestasis 4 months after the operation, with dilatation of the common bile duct and papillary stenosis due to progression of cholangitis. These observations suggest that cholangitis is frequently associated with cholecystitis in patients with the acquired immunodeficiency syndrome. Its pathogenesis is not known.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Cholangiographic appearance simulating sclerosing cholangitis in metastatic adenocarcinoma of the liver.

Three patients with liver metastases and clinical and biochemical signs of cholestasis are reported in this study. In the three patients, cholangiography showed shifted and stretched intrahepatic bile ducts and multifocal strictures simulating intrahepatic primary sclerosing cholangitis. In two patients, histological examination showed periductal fibrosis or inflammation. Hepatic metastases should be included among the conditions considered to simulate intrahepatic primary sclerosing cholangitis during cholangiography.

Adenocarcinoma↗
PubMed1990

Influence of backward perfusion on ursodeoxycholate-induced choleresis in isolated in situ rat liver.

Ursodeoxycholate-induced bicarbonate-rich hypercholeresis was studied in isolated in situ forward- or backward-perfused rat livers. Both spontaneous bile flow and bile acid secretion were similar regardless of the direction of the perfusion. The choleretic effect of tauroursodeoxycholate infusion (400 nmol.min-1.100 g-1 body weight) was not significantly different in forward- or backward-perfused livers either. Ursodeoxycholate infusions at low rate (800 nmol.min-1.100 g-1 body weight) induced similar bile flow, bile acid output and bicarbonate output in both forward- and backward-perfused livers. Net ursodeoxycholate uptake, measured as [14C]ursodeoxycholate uptake over the bile acid infusion period (30 min), was not significantly different during forward- or backward-perfusion (4.8 and 5.1 mumol/g liver, respectively); i.e., approx. 67% of infused dose (approximately 7.5 mumol/g liver per 30 min). A 2-fold increase in the dose of ursodeoxycholate infusion (1600 nmol.min-1.100 g-1 b.wt.) induced additional enhancement in both bile flow and bicarbonate biliary secretion, but not in bile acid uptake or output, in forward-perfused livers. Moreover, infusion of the same dose of ursodeoxycholate to backward-perfused livers had a significantly lower choleretic effect (-29%, p less than 0.001) even though ursodeoxycholate uptake and biliary output were similar regardless of perfusion direction. Net ursodeoxycholate uptake, was only 2.4 mumol/g liver; i.e., approx. 16% of infused dose (approximately 15 mumol/g liver per 30 min). These findings indicate that a process related with the hepatic microanatomy may be involved in the hypercholeretic response to ursodeoxycholate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Role of intracellular organelles in the hepatic transport of bile acids.

The intracellular events associated with the vectorial transport of bile acids by the hepatocytes from the sinusoidal pole to the canalicular pole are reviewed. Binding to cytosolic proteins occurs. The role of this binding is to prevent efflux from the cytosol back into the blood. There is evidence from electron microscopy, from autoradiography and from immunoperoxidase observations that bile acids interact with the endoplasmic reticulum and the Golgi apparatus. There is also evidence that a carrier system or taurocholate exists on the Golgi membrane. We propose that a vesicular pathway involving the Golgi apparatus and dependent on the integrity of microtubules may play a role in bile acid transport in the cell. Inhibition of bile acid transport by microtubule poisons is consistent with this hypothesis. Finally, monohydroxylated, cholestatic bile acids such as lithocholate and taurolithocholate interact with the endoplasmic reticulum. This interaction results in a depletion of the endoplasmic reticulum calcium stores and an increase in intracellular ionized calcium. The relationship of this novel effect of bile acids to their cholestatic properties remains to be elucidated.

Actin Cytoskeleton↗
PubMed1990

Membranous obstruction of the inferior vena cava and hepatocellular carcinoma in a Caribbean patient.

Membranous obstruction of the inferior vena cava has been reported mainly in South Africa, Japan, and India; in 20-40% of patients the disease is complicated by hepatocellular carcinoma. We report a case of membranous obstruction of the inferior vena cava with hepatocellular carcinoma in a 43-year-old Caribbean man of Indian origin. The Caribbean islands may constitute another geographical area where the population is at risk for the development of membranous obstruction of the inferior vena cava and subsequent hepatocellular carcinoma.

Adult↗
PubMed1990

Retroperitoneal fibrosis after surgery for aortic aneurysm in a patient with periarteritis nodosa: successful treatment with corticosteroids.

A 54-year-old man with hepatitis B virus-related periarteritis nodosa developed retroperitoneal fibrosis with bilateral hydronephrosis 2.5 months after placement of an aortobifemoral prosthesis for abdominal aortic aneurysm. Retroperitoneal fibrosis disappeared after treatment with corticosteroids. This observation is interesting in the light of the hypothesis that retroperitoneal fibrosis is caused by vasculitis.

Aorta, Abdominal↗
PubMed1990

Effect of acid-base balance on biliary bicarbonate secretion in the isolated perfused guinea pig liver.

Secretin-induced choleresis is of ductal origin and involves bicarbonate transport. Its mechanism is unknown. To determine the relative effects of systemic pH, PCO2, and bicarbonate concentration on secretin-stimulated bicarbonate transport, states of acute metabolic and respiratory acidosis or alkalosis were created in isolated perfused guinea pig livers with or without secretin infusion. During spontaneous secretion conditions, biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.62) or perfusate PCO2 (23.9-59.7) but was significantly correlated with perfusate bicarbonate concentration (17.5-37.9 mM). Under secretion infusion (25 mU/min), bile flow and biliary bicarbonate concentration increased significantly (109 and 51%, respectively). Biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.60) but was significantly correlated both with perfusate bicarbonate concentration (14.6-36.8 mM) and PCO2 (25.8-54.3 mmHg). Spontaneous and secretin-induced bile flow were correlated with biliary bicarbonate concentration. The correlation between biliary bicarbonate secretion and PCO2 during secretin-induced choleresis supports the hypothesis that secretin-induced biliary bicarbonate secretion could, at least in part, involve a transport of H+ (or OH-) rather than HCO3- itself and that intracellular pH could play a role in the regulation of this secretion. Amiloride (5 X 10(-4) M) did not influence secretin-induced biliary bicarbonate secretion. This result suggests that the Na(+)-H+ exchange is not involved in bicarbonate secretion by ductular cells.

Acid-Base Equilibrium↗