Carlos Caramelo, Dolores Fernandez‐Muñoz, Juan C. Santos, Alicia Blanchart, Diego Rodriguez‐Puyol, José M. López‐Novoa, Luis Hernando – 1 January 1986 – General and splanchnic hemodynamics (radioactive microspheres), renal function, spontaneous and histamine‐mediated vasopermeability and albumin distribution space were studied in conscious control and nonascitic cirrhotic rats, before and after a moderate and sustained saline infusion (3% of body weight per 30 min + repletion of urinary losses).

Bernard Willems, Jean‐Pierre Villeneuve, P.‐Michel Huet – 1 January 1986 – Propranolol has been reported to reduce portal and wedged hepatic vein pressures in man and may be useful for the prevention of variceal bleeding. However, its mechanism of action remains unclear. We have examined the effect of propranolol on the systemic and hepatic circulations in dogs with chronic bile duct ligation and secondary biliary cirrhosis. Underanesthesia, eight dogs received four increasing doses of propranolol as an i.v. bolus followed by continuous infusion.

Yukihisa Nagafuchi, Professor Peter J. Scheuer – 1 January 1986 – β2−Microglobulin display was examined in 131 liver biopsies from patients with acute and chronic type B hepatitis, using an indirect immunoperoxidase method. Enhanced expression of β2−microglobulin on hepatocyte membranes was observed in patients with acute hepatitis, chronic active hepatitis with moderate to severe activity and cirrhosis, when compared with normal liver. In acute hepatitis, β2−microglobulin‐positive hepatocytes were mainly observed in perivenular areas in association with bridging necrosis.

1 January 1986

Andres T. Blei – 1 January 1986

Anton L. Boks, Emile J. P. Brommer, Solko W. Schalm, Huub H. D. M. Van Vliet – 1 January 1986 – In a study of severe, decompensated liver failure, we tried to find a correlation between hemorrhage and parameters ofhemostasis and fibrinolysis. Three groups of patients were studied: alcoholic cirrhosis; nonalcoholic cirrhosis, and acute liver failure without known prior liver disease. The two cirrhotic groups did not differ significantly from each other in coagulation or in fibrinolytic parameters, although liver function was more impaired in nonalcoholic cirrhosis.

Linus Chang, Peter Clifton, Philip Barter, Malcolm Mackinnon, M.D. – 1 January 1986 – Severe liver disease may be associated with a reduction in plasma concentration of high density lipoprotein and an impairment of plasma cholesterol esterification. These changes were confirmed in two patients with severe acute on chronic alcoholic liver disease.

Marc L. Berger, Harshika Bhatt, Burton Combes, Ronald W. Estabrook – 1 January 1986 – CCl4 is proposed to induce cellular injury through its metabolites that are generated by a cytochrome P‐450 dependent step. These free radical products can interact with membrane structures, thereby generating lipid peroxides. The latter process has been implicated as a major mechanism of CCl4 hepatoxicity, although this relationship has been difficult to demonstrate when using isolated hepatocyte preparations.

Maud I. Cleton, Jan W. Sindram, Louk H. P. M. Rademakers, Floris M. J. Zuyderhoudt, Willem C. De Bruijn, Joannes J. M. Marx – 1 January 1986 – Ferritin‐like particles were observed in bile canaliculi of patients with iron overload. These particles have been further investigated by: (1) a staining method enhancing the size and contrast of ferritin protein, and (2) electronprobe microanalysis detecting the presence of the elements iron and phosphorus.

Jean‐Charles Delchier, Paul Benfredj, Anne‐Marie Preaux, Jean‐Michel Metreau, Daniel Dhumeaux – 1 January 1986 – Gallbladder bile collected by duodenal intubation or during surgery was examined microscopically in patients who werefree of stones and in patients with proven stones. None of the 16 patients free of stones had cholesterol monohydrate crystals or calcium bilirubinate granules in bile.