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Biomedical subjects

S Erlinger

Publications and source records attributed to S Erlinger.

286 records · Page 16Linked to original sources
PubMedDate not supplied

Effect of systemic pH, PCO2 and bicarbonate concentration on biliary bicarbonate secretion in the rat.

The effect of acute metabolic or respiratory acid-base disturbances on biliary bicarbonate secretion was examined in bile fistula rats. Animals were infused with ursodeoxycholate at a rate that stimulates bicarbonate secretion (1 mumole . min-1 X 100 gm-1), in control conditions and during acute acid-base disturbances. Metabolic acidosis or alkalosis were induced by HCl or NaHCO3 infusions, and respiratory acidosis or alkalosis were created respectively by adding CO2 to the inspired gas or by hyperventilation in artificially ventilated animals. Biliary bicarbonate concentration was always higher than plasma bicarbonate concentration. During metabolic disturbances, changing the plasma bicarbonate concentration from 9.2 to 30.2 mM stimulated biliary bicarbonate secretion by 113%. During respiratory disturbances, changing the plasma PCO2 from 25.5 to 59.8 mm Hg also increased biliary bicarbonate secretion by 89%. Biliary bicarbonate output was thus independent of plasma pH. When all animals were considered, bile flow was positively correlated with biliary bicarbonate concentration (r = 0.71, p less than 0.001). Acetazolamide significantly decreased ursodeoxycholate-induced bile flow and bicarbonate secretion by 20 and 22%, respectively. These results support the hypothesis that there is a relationship between ursodeoxycholate-induced bicarbonate secretion and bile flow. They are also consistent with the view that ursodeoxycholate-stimulated biliary bicarbonate secretion in the rat is strongly affected by plasma bicarbonate and PCO2, but not by plasma pH, and involves carbonic anhydrase.

Acetazolamide↗
PubMedDate not supplied

Disappearance of liver cell adenoma: CT and MR imaging.

We report the disappearance of liver cell adenoma, documented by computed tomography (CT) and magnetic resonance (MR) imaging. A 42-year-old woman with a diagnosis of hepatic adenoma was followed up by CT and MR imaging after cessation of oral contraceptive use. At the time of diagnosis, the adenoma was 4 cm in diameter and appeared hypervascular on CT. At MR imaging, the lesion was hypointense on T1-weighted sequences, and hyperintense on T2-weighted sequences. The lesion disappeared 4 years after cessation of oral contraceptive use. We conclude that in nonoperated patients CT scans and MR imaging are useful for following the evolution, and documenting the regression, of liver cell adenomas.

Adenoma, Liver Cell↗
PubMedDate not supplied

[Different effects of taurocholate and ursodeoxycholate on the maximal rate of biliary sulfobromophthalein secretion in hamsters].

Because of the special physiochemical properties of ursodeoxycholate and its tauroconjugate, the effect of these two bile acids on the maximal biliary secretory rate of sulfobromophtalein was compared to that of taurocholate in the hamster. It was confirmed that taurocholate increased the maximal biliary secretory rate of the dye, while it was shown that ursodeoxycholate did not. When the bile acids were infused before sulfobromophtalein, the maximal biliary secretory rate of the dye was significantly higher under taurocholate infusion than under tauroursodeoxycholate and ursodeoxycholate infusions. Under the same conditions, the biliary bile acid output was only slightly decreased by the dye under taurocholate infusion, while it was reduced by approximately one-half under urso- and tauroursodeoxycholate infusions. These observations indicate that ursodeoxycholate is unable to increase the maximal biliary secretory rate of sulfobromophthalein (in contrast to taurocholate). It is suggested that urso- and tauroursodeoxycholate interact with sulfobromophthalein during hepatic transport and that these two bile acids may be transported by the liver by mechanisms different from those of taurocholate.

Animals↗
PubMedDate not supplied

Mechanisms of hepatic transport and bile secretion.

The transport processes responsible for bile flow are reviewed. Canalicular bile acid-dependent flow is the result of active transport of bile acids by the hepatocyte into bile canaliculi. Bile acids are taken up by at least two transport systems whose mRNAs have been expressed in Xenopus oocytes: a Na(+)-dependent system, named NTCP, and a Na(+)-independent system, named OATP. Bile acids are then secreted into bile by two other transport systems, an ATP-dependent system and an "electrogenic" voltage-dependent system. It is not known whether these two systems are mediated by the same protein or by two different proteins. Canalicular bile acid-independent flow is mainly the result of the secretion of glutathione into bile. The canalicular membrane contains also several proteins of the MDR (Multi Drug Resistance) family. MDR1 is responsible for biliary secretion of cationic drugs. MDR2 plays a major role in the secretion of phospholipids. A third MDR related protein has been shown recently to be the canalicular carrier of organic anions, like bilirubin and dyes (the canalicular Multiple Organic Anion Transporter, or cMOAT). Biliary epithelial cells secrete a bicarbonate rich solution, mostly in response to secretion. This secretion depends on the presence on the apical membrane of these cells of the CFTR, a chloride channel activated by cAMP, and of a chloride/bicarbonate exchanger. Knowledge of these transport systems should allow a better understanding of the mechanisms involved in cholestasis.

Animals↗
PubMedDate not supplied

[Clinical picture and evolution of hepatitis C].

Hepatitis C is becoming the main cause of cirrhosis and primary liver carcinoma. Infection by hepatitis C virus (HCV) generally induces an asymptomatic acute hepatitis. HCV infection becomes chronic in about 80% of cases. In a minority of the subjects, chronic HCV infection is asymptomatic with persistent viremia and normal liver tests. These asymptomatic subjects have minimal liver histologic lesions and a good prognosis. In a majority of the subjects, chronic HCV infection is associated with chronic hepatitis with increased serum transaminases levels. Among the patients with chronic hepatitis, the majority have a mild liver disease with a moderate increase in serum transaminases levels and, at liver histology, minimal lesions; a minority (about 20%) have a more severe liver disease and will develop cirrhosis after 5 to 20 years. In patients with HCV related cirrhosis, the incidence of hepatocellular carcinoma is high (around 5% per year). The factors influencing the evolution of HCV infection are not known. Alcohol is certainly an important factor which increases the risk of development of fibrosis then cirrhosis. Virus related factors, such as genotype and level of replication, might also be important. Autoimmune diseases have been reported in association with hepatitis C. HCV infection is a major cause of mixed cryoglobulinemia associated with vasculitis or glomerulonephritis. A relationship between HCV and auto-immune diseases such as thyroiditis or Gougerot syndrome has been suggested but not demonstrated. HCV infection is frequent in patients with porphyria cutanea tarda; in these patients, HCV related liver disease might trigger the expression of the metabolic disease.

Acute Disease↗