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The British Society of Gastroenterology Gut: first published as 10.1136/gut.25.10.A1129 on 1 October 1984. Downloaded from Gut, 1984, 25, A1129-A1193 The British Society of Gastroenterology The 1984 Annual Meeting of the Society was held at the University of Liverpool under the presidency of Dr R B McConnell. One hundred and thirty four oral and 94 poster communications were presented in the scientific sessions; the abstracts of these are printed below. reflecting differences in susceptibility of the diagnosis and monitoring the progression of LIVER protein moieties of the ligands to pro- disease or response to treatment. W1-14 teolysis. This model produced a good statis- tical and graphical fit to both sets of data without the need for exocytosis. The data W3 WI show that ligands entering the cell by a com- Intrahepatic shunting and its relationship to Metabolism of mannose-terminated glyco- mon receptor may subsequently be proces- portal pressure and blood flow proteins by hepatic sinusoidal cells sed differently. M MCLAREN, J FLEMING, S KARRAN, AND I J A SUMMERFIELD, M E TAYLOR, AND M S LEAN- TAYLOR (University Surgical Unit, South- ING (Departments of Medicine and Physics, W2 ampton) It has been suggested that in cir- Royal Free Hospital, London) Mannose Dynamic scintigraphy in cirrhosis rhosis intrahepatic shunting between all (Man-) terminated glycoproteins are these major blood vessels occurs. The rapidly cleared from the blood by receptors M MCLAREN. J FLEMING. S KARRAN, AND I relationship of the degree of shunting to the on hepatic sinusoidal cells. In earlier studies TAYLOR (University Surgical Unit, South- level of portal pressure is not known but if a using acid precipitation to estimate the ampton) Dynamic hepatic scintigraphy manipulation of shunting results in a fall in catabolism of the glycoproteins, measure- yields information related to portal pressure this could have therapeutic http://gut.bmj.com/ ment artifacts led to models requiring haemodynamic and reticuloendothelial implications. A study was undertaken to exocytosis of whole ligand. In these studies function in liver disease by measuring the assess the relationship of portal venous the fate of glycoprotein was assessed in rats mesenteric fraction of liver blood flow (M shunting to blood flow and portal pressure. by measuring radioactivity in blood, liver, F) and the liver:spleen activity ratio (L:S Cirrhosis, assessed by histological and bile and other tissues over 40 minutes after ratio). It has been used to study 45 patients biochemical criteria, was induced in 45 male an intravenous injection of 57 pmol with liver cirrhosis, 24 of whom had bled Wistar rats by intragastric administration of radioiodinated glycoprotein. Ligand from varices. Control data were provided either carbon tetrachloride (n=25) or catabolism was measured by gel filtration. by 30 subjects with normal liver function. dimethlynitrosamine (n=20). Effective on September 30, 2021 by guest. Protected copyright. With these data a new compartmental For the overall group of cirrhotic patients liver blood flow (ELBF) and its relative model was formulated. The metabolism of the median MF was 0-28 compared with a arterial/venous components were measured 125I-agalactoorosoinucoid (1251I-AGOR) control value of 0-56 (p<0-001) and the L:S using Tc99m sulphur colloid, portal pres- and ' I-mannose 36-bovine serum albumin ratio was 1-5 compared with 4-75 sure was recorded manometrically and the (125I-Man36BSA) was studied. Both ligands (p<0-001). The sensitivity in the diagnosis degree of shunting obtained by intraportal accumulated principally in liver but more of cirrhosis was 84% for the MF and 89% injection of Co57 microspheres. '25I-AGOR (-30%) than 125I-Man36BSA for the L:S ratio. This increases to >95% by Both portal hypertension (median con- (-10%) accumulated in other sites. Uptake calculating the geometric mean of MFxL:S trol 9cm saline, cirrhosis 16-5cm saline parameters indicated that Man36BSA (0-78 ratio. Within the group of patients with cir- p<0-001) and shunting (median control min) had a higher affinity for the cell recep- rhosis the median MF for patients who had 0 3%, cirrhosis 23-0% p<0-001) increased tor thanr AGOR (0-50 min). Iritracellular gastrointestinal bleeding was 0-22 com- significantly in cirrhosis. There was no sig- transport of ligand from the cell membrane pared with 0-33 for non-bleeders nificant correlation between shunting and to the lysosome was estimated by a trans- (p=0-035), and the L:S ratio was 0-95 com- either a decrease in ELBF (r=0.3) or a port parameter (Tau) in the model. This pared with 1-9 (p=0-003). decrease in its venous component (r=0-36). was much greater for Man36BSA (-3 min) These data indicate a significant reduc- There was, however, a significant corre- than for AGOR (-0 min). These data may tion in the venous flow to the liver and a sig- lation between the increase in shunting and indicate that the rate of receptor-ligand nificant increase in functional splenomegaly an increase in portal pressure, r=0-67 uncoupling of Man36BSA is slower than for not only in patients with cirrhosis when p<0.001. The results do not indicate any AGOR. Furthermore, the rate of compared with controls but also between direct relationship between the develop- catabolism of Man36BSA (0-27 min) was those who have or have not bled from var- ment of shunting and changes in measured twice that of AGOR (0-12 min) probably ices. The value of such information lies in flow but intrahepatic portal venous shunt- A1129 Gut: first published as 10.1136/gut.25.10.A1129 on 1 October 1984. Downloaded from A1130 The British Society of Gastroenterology ing does increase with rising portal pres- in normal subjects, haemophiliac and von liver blood flow. The present study sure. Willebrand patients, mainly by raising the examines the simultaneous pharmacokine- concentration of all components of factor tics of two separate anions ICG and "4C- VIII complex. DDVAP, however, also glycocholate. Extraction ratios were esti- W4 shortens bleeding time in uraemics, and is mated by analysis of the biexponential Defective sulfoxidation combined with rapid used for prophylaxis and treatment of plasma disappearance curves and liver carbon oxidation in the liver may predispose bleeding, despite already raised factor VIII blood flow calculated. to chlorpromazine jaundice. concentrations. The latter is also seen in cir- Ten healthy volunteers fasted and rhotics, but the effects of DDVAP in such received a single oral dose of cimetidine 400 E ELIAS, R H WARING, AND S C MITCHELL patients is not well reported. We have mg, ranitidine 150 mg or placebo in random (Department of Medicine, QE Hospital studied the effect of a 15 minute intravenous order on three occasions one week apart. Medical School, Birmingham, Department infusion of 0*3,ug/kg DDVAP at one and Two hours later clearances measured for of Biochemistry, University, Birmingham, three hours post infusion as compared with ICG (ml/min/kg) were: cimetidine, 6 9+ and the Department of Pharmacology, St baseline values of prothrombin, partial 2-9; ranitidine, 7-9+3-1; placebo, 7-1±1-6; Mary's Hospital Medical School, London) thromboplastin (PTTK), thrombin and and for '4C-glycocholate: cimetidine, 8-4+ Chlorpromazine is a major tranquillising bleeding times factors VII, IX, X, XI, XII, 2.3; ranitidine, 8 1±2 2; and placebo, 8-6+ agent which is known to be metabolised in VIIIC, VIIIRAG, VIIIR-Cof, fibrinogen, 1-9. Similarly there was no difference in the man to give both hydroxylated and sul- fibrin monomers (FM) and degradation calculated extraction ratios or liver blood foxide metabolites. We proposed on the products (FDP), euglobulin lysis time and flow. basis of in vitro work that rapid conversion fibrin plate assay. Results to date are for six Using the same technique, it has recently of chlorpromazine (CPZ) to hydroxy- patients: five with parenchymal liver dis- been suggested that cimetidine but not metabolites and/or slow metabolism to the ease (prothrombin ratio of 1-3 or more) and ranitidine may reduce liver blood flow after relatively non-toxic sulphoxides might be one patient with non-malignant obstructive chronic administration secondary to inhibi- the underlying cause of CPZ hepatotoxic- jaundice. All were vit K replete. Abnormal tion of enzyme activity and reduction of ity. This hypothesis was investigated using and normal bleeding times were shortened intrinsic clearance. The lack of effect of a S-carboxymethyl-cysteine (SCMC) and by about 30% at both one and three hours. single dose of cimetidine on liver blood flow debrisoquine as probes for in vivo sulphur- At the same time PTTK was shortened to would be compatible with this hypothesis as and carbon oxidation-capacity respectively. within the normal range, and increases in this study neither H2 receptor antagonist Both these drugs are known to show a wide above baseline concentrations were seen for caused significant alteration of liver blood range of metabolism in normal populations. factors VIIIC by 26-106 lu/1, VIIIRAG by flow in normal subjects. Urinary metabolites and unchanged com- 50-95iu/1 and VIIIRiCof by 80-12Oiu/1. pound concentrations (0-8 h) were deter- There were also increases in factors XI and mined after oral SCMC (750 mg) and XII. There was no change in other factors, W7 http://gut.bmj.com/ debrisoquine sulphate (10 mg) in consecu- prothrombin time, fibrinogen, FM, or FDP. Hepatobiliary fibrocystic diseases tive days in three subjects who had fully No side effects were encountered. The recovered from prolonged jaundice after reduction in bleeding time is probably J A SUMMERFIELD, J CADAFALCH, AND S SHER- exposure to CPZ (twice in one subject). All because of increases in the components of LOCK (Academic Department ofMedicine, three subjects showed very low capacity for factor VIII complex.
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