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Biomedical subjects

S Erlinger

Publications and source records attributed to S Erlinger.

At least 235 records · Page 13Linked to original sources

[Benign postoperative intrahepatic cholestasis].

The authors report the clinical, biochemical, histological and etiologic characteristics of 24 patients with the syndrome of benign intra-hepatic post-operative cholestasis. Jaundice appeared early in the post-operative period, from the first to the 12th post-operative day. All patients had received blood transfusions. In 23 patients, the post-operative course was complicated, chiefly by local infection or septicemia. Hyperbilirubinemia ranged from 2 to 28 mg per 100 ml and was mainly conjugated; serum alkaline phosphatase activity was normal or moderately elevated; in 3 patients, it was markedly elevated; serum glutamic-pyruvic transaminase activity was normal on 7 patients, moderatly increased in 15, and markedly increased in one. Liver histology was normal in 6 patients, and showed minimal lesions (cholestasis and slight portal inflammatory changes) in 3. Jaundice did not appear to modify the final outcome. It appears to be due both to increased production of bilirubin (as a result of blood transfusions) and to decreased excretion of bilirubin by the liver (as a result of the surgical operation and of infection).

Acute Kidney Injury↗

Influence of phenobarbital on bile composition in epileptic patients.

The influence of phenobarbital on bile composition was studied in 13 patients with epilepsy, treated with the drug in doses ranging from 0.05 to 0.30 g per day during 4 months to 50 years. Fourteen normal subjects matched for age and sex acted as controls. Expressed as percent of total lipids, biliary cholesterol (9.2 +/- SD 2.7 in the controls, 9.0 +/- SD 2.5 in the treated patients), phospholipid (23.3 +/- SD 6.1 in the controls, 20.5 +/- SD 5.9 in the treated patients) and bile acid concentrations (67.5 +/- SD 8.1 in the controls, 70.4 +/- SD 7.4 in the treated patients) did not differ significantly in the two groups. When represented on triangular coordinates, bile from the treated patients was not separated from that of controls. These studies indicate that long-term phenobarbital administration in the doses used for the treatment of epilepsy does not modify biliary lipid composition and do not suggest that this drug may be useful in the treatment of cholesterol gallstones in man.

Adolescent↗

[Postoperative intraabdominal suppurations due to Ristella. Clinical, bacteriological and therapeutic characteristics].

From 1972 to 1974, 8 intraabdominal postoperative suppurations due to Bacteroides have been observed at Hospital Beaujon. Three characteristic features of such infections have been analysed: the high frequency of associated jaundice; the difficulty of isolation of the Bacteroides; their specific sensitivity to some antibiotics. In 5 patients, jaundice related to the bacterial infection has been observed; jaundice was of the cholestatic type; it was mainly due to conjugated hyperbilirubinemia; in approximately 50 p.cent of the cases, serum alkalin phosphatases activity and serum glutamic-pyruvic transaminase activity were moderately elevated; the presence of jaundice did not seem to have any influence on the prognosis. The frequent association to Bacteroids of enterobacteria makes isolation of the Bacteroides difficult. The necessity of some precautions in the handling (storage at 4 degrees C or immediate inoculation in anaerobic conditions) is emphasized. Bacteroides are always resistant to penicillin and to the other broad spectrum antibiotics usually effective enterobacteria. They are sensitive to tetracyclins (5/8), lincomycin (2/4), clindamycin (2/3), rifampicin (8/8), pristinamycin (7/7), carbenicillin (3/3), erythromycin (8/8) and chloramphenicol (8/8).

Alkaline Phosphatase↗

Effect of lysine acetylsalicylate on biliary lipid secretion in dogs.

1. The influence of lysine acetylsalicylate on bile flow, erythritol clearance and bile salt, phospholipid and cholesterol secretion in bile was studied in unanaesthetized dogs fitted with a Thomas duodenal cannula. 2. Lysine acetylsalicylate induced a marked increase in bile flow and a parallel increase in erythritol clearance although the bile salt secretion remained unchanged; this suggests that the compound stimulated the formation of the canalicular (hepatocytic) bile salt-independent fraction of bile flow. 3. Lysine acetylsalicylate induced a significant decrease in biliary phospholipid and cholesterol secretion and the cholesterol saturation of bile was significantly reduced. 4. It is postulated that the decrease in phospholipid and cholesterol secretion resulted from the dilution of intracanalicular bile salts. This effect of lysine acetylsalicylate, and possibly of other bile salt-independent choleretics, may be of value in the treatment of cholesterol gallstones in man.

Animals↗

Influence of dehydrocholate and taurocholate on bromsulphthalein uptake, storage, and excretion in the dog.

The influence of dehydrocholate on bromsulphtalein relative-storage capacity, bilary transport maximum (Tm), and fractional transfer rates between plasma, liver and bile have been studied in unanaesthetized dogs. In six dogs, storage capacity, Tm, and fractional transfer rates from plasma to liver, liver to bile, and liver to plasma were measured during 0-15 M NaCL infusion and the measurements were repeated under a dehydrocholate infusion of 95 mumol. min-1, ie, an infusion rate approaching the known biliary Tm of bile salts. It was found that: (a) storage capacity and fractional transfer rates from plasma to liver significantly lower during dehydrocholate infusions (respectively 18-0 plus or minus SD 9-0 mg-mg-1. 100 ml-1 and 0-120 plus or minus SD 0-035 min-1) than during NaCL infusions (respectively 47-0 plus or minus 21-0 mg. mg-1. 100 ml-1 and 0-280 plus or minus SD 0-055 min-1; P smaller than 0-001); (b) Tm and fractional transfer rates from liver to bile were also significantly lower during dehydrocholate infusion (respectively 3-2 plus or minus SD 1-1 mg. min-1 and 0-013 plus or minus SD 0-004 min-1) than during NaCl infusion (4-8 plus or minus SD 1-1 mg. min-1 and 0-033 plus or minus SD 0-017 min-1; P smaller than 0-02); (c) in three additional experiments, taurocholate had similar effects on storage capacity and Tm. These findings suggest that competition occurred between bile salts and bromsulphthalein for hepaticuptake and storage. They support the hypothesis that the decreased disappearance rate and relative storage capacity of bromsulphtalein observed during biliary obstruction may be due to competition between bile salts and bromsulphthalein for hepatic uptake and storage.

Animals↗

Hepatocellular uptake of erythritol and mannitol in the dog.

The purpose of this study was to determine the initial space of distribution of [14C]erythritol (mol wt 122) and [14C]mannitol (mol wt 182) in the liver of the dog by the single-injection, multiple-indicator-dilution method. 22Na was used as the extracellular indicator and tritiated water (THO) was used as total liver water indicator. The indicators were simultaneously injected into the portal vein of anesthetized dogs and dilution curves were obtained at the outflow from the hepatic vein. It was found that hepatic venous dilution curves of [14C]erythritol and THO were practically identical in all experiments. In contrast, the dilution curves of [14C]mannitol were generally distinct from those of THO. Analysis of [14C]mannitol-dilution curves according to Goresky suggested that the observed difference between this solute and THO was the result of a limited permeability of the sinusoidal membrane to mannitol. It is concluded that [14C]erythritol has instantaneous and practically unrestricted access to total liver water. This finding supports the validity of using erythritol as a liver cell water marker. A larger solute, [14C]mannitol, has restricted access to total liver cell water because of a permeability barrier in the sinusoidal liver cell membrane, but its diffusion into the hepatocyte is also very rapid.

Animals↗

Barbituates and biliary function.

This paper reviews the principal effects of phenobarbital on biliary function. Phenobarbital administration is followed by an increase in bile flow. This is mainly due to an increase in the bile salt-independent fraction of canalicular bile flow possibly through an increase in canilicular Na+-K+ ATPase activity. In addition, bile salt excretion may be increased. This effect of barbiturates on choleresis appears to be independent of microsomal enzyme induction. Barbiturates increase the uptake, storage and excretion of various dyes, for example sulfobromophthalein. Phenobarbital increases bilirubin clearance by the liver; it enhances bilirubin-UDP-glucuronyl transferase activity; whether the influence on bilirubin clearance is related to the effect on the enzyme is unknown. The influence of phenobarbital on biliary lipids is markedly different from one species to the other. In the rhesus monkey and in the rat, the relative concentration of cholesterol is decreased; in the hamster it is increased, and in man it appears largely unaffected. These effects of phenobarbital have been utilized in the treatment of chronic unconjugated hyperbilirubinemia and of certain cholestatic syndromes. Phenobarbital alone has been useful, so far, in the treatment of cholesterol gallstones.

Adenosine Triphosphatases↗

Hepatocellular uptake of taurocholate in the dog.

The purpose of this study was to examine the hepatocellular extraction of taurocholate and to determine the kinetic characteristics of the uptake process. The uptake of taurocholate by the liver of the intact dog was studied by the multiple-indicator dilution method. 51Cr-labeled red blood cells (a vascular indicator), 125I-labeled albumin (an extravascular reference), and [14C]taurocholate were injected into the portal vein. Different doses of unlabeled taurocholate were included in the injection mixture. Hepatic venous dilution curves were obtained. As a consequence of the hepatic uptake, the outflow recovery of [14C]taurocholate was much reduced when compared to that of albumin, but its recovery increased with increasing doses of taurocholate, suggesting a progressive saturation of the uptake process. The analysis of the dilution curves fitted a three-compartment model system well and no return of the extracted taurocholate to the extracellular space could be detected. The initial space of distribution of taurocholate was 1.22 plus or minus 0.12 (SD) times greater than that of albumin. Analysis of the data for uptake was consistent with Michaelis-Menten kinetics. The calculated initial maximal velocity of uptake (Vmax) was 4.53 mumol times s--1 times 100 g of liver--1 and the dose yielding half-maximal velocity (DK) was 7.11 mumol times 100 g of liver--1. These results are consistent with the hypothesis that the uptake of taurocholate is carrier-mediated. The maximal vilocity of uptake was about six times the known maximal capacity of biliary secretion of taurocholate in the dog.

Albumins↗

Hepatocellular uptake of bile acids in the dog: Evidence for a common carrier-mediated transport system. An indicator dilution study.

The purpose of this study was to compare the uptake of taurocholate (TC) by the liver of the dog to that of taurochenodeoxycholate (TCDC) and to examine the influence of TCDC on TC uptake. The uptake of these bile acids by the liver of the intact was studied with the multiple indicator dilution method, using 51Cr-labeled red blood cells as a vascular indicator, 125I-labeled albumin as an extravascular reference, and one or two labeled bile acids. The analysis of the dilution curves fitted well a three-compartment model, and no return of the extracted bile acids to the extracellular space could be detected. The initial space of distributin of TC in the presence of a fixed dose of TCDC was 1.25 +/- 0.09 (SD) times greater than that of albumin. Analysis of the data for TC uptake in the presence of TCDC was consistent with Michaelis-Menten kinetics, as previously established for TC alone. The calculated initial maximal velocity of uptake (Vmax) of TC in the precence of TCDC was 4.92 +/- 1.36 (SD) mumoles per sec per 100 g of liver. This value is not significantly different from the Vmax previously calculated for TC alone. The apparent KD (dose of TC yielding half-maximal velocity) was 18.10 +/- 6.14 (SD) mumoles per 100 g of liver, a value significantly higher than that obtained in the absence of TCDC. A K1 (the Michaelis-type constant characterizing the inhibition of TC uptake by TCDC) of 2.71 +/- 1.08 (SD) mumoles of TCDC per 100 g of liver was calculated. These observations are consistent with competitive inhibition of TC uptake by TCDC, and thus with the existence of a common carrier-mediated transport system for TC and TCDC. Estimation of the kinetic characteristics of the two bile acids from dilution curves obtained simultaneously showed that the affinity for the carrier was higher for TCDC than for TC, but that the maximal capacity was lower for TCDC than for TC.

Animals↗

Increased sulfobromophthalein clearance in a patient receiving phenobarbital and other anticonvulsant drugs.

A marked increase in bromosulfophthalein, dibromosulfophthalein, and indocyanine green fractional clearance was found in a patient who had received phenobarbital for 30 years and other anticonvulsant agents for 6 years. This was related to a marked increase in hepatic blood flow, while hepatic extraction remained normal. These changes were associated with signs of hepatic microsomal enzyme induction (in particular a 2-fold increase in liver bilirubin UDP-glucuronyltransferase activity and hypertrophy of the smooth endoplasmic reticulum in the hepatocytes). Drug administration (especially phenobarbital) should be considered as a possible cause of increased bromosulfophthalein clearance in man.

Adult↗