Mary J. Ruwart, Bob D. Rush, Nanette M. Friedle, Jerzy Stachura, Andrzej Tarnawski – 1 July 1984 – Male rats were treated with subcutaneous vehicle or 16, 16‐dimethyl‐PGE2 (dmPGE2, 100 μg per kg), 24,18 and 0.5 hr prior to and 6, 24 and 30 hr after challenge with oral α1‐napthylisothio‐cyanate (ANIT, 30 mg per kg). Forty‐eight hours after challenge, rats were sacrificed by decapitation; serum and liver samples were taken for biochemical and histological analysis, respectively.

Kim Krogsgaard, Christian Gluud, Jens H. Henriksen, Per Christoffersen – 1 July 1984 – In 14 alcoholic patients, the degree of hepatic architectural destruction was graded (preserved architecture; nodules alternating with preserved architecture; totally destroyed architecture) and related to portal pressure. A positive correlation was found between the degree of architectural destruction and both wedged hepatic vein pressure (r = 0.72, p < 0.01) and wedged‐to‐free hepatic vein presure (r = 0.67, p < 0.02).

Donald L. Kaminski, Yashwant G. Deshpande – 1 July 1984 – The effect of prostacyclin on canine hepatic bile flow was evaluated. Utilizing chronic, unanesthetized bile fistula dogs, prostacyclin was found to significantly increase bile flow rates and bile bicarbonate and cyclic AMP concentration and output when compared to control values. The choleretic response was not due to the effect of the principal metabolic endproduct of prostacyclin, 6‐keto‐PGF1α, as this substance increased bile flow but did not increase bicarbonate or cyclic AMP concentrations in bile.

Bernhard H. Lauterburg, James D. Adams, Jerry R. Mitchell – 1 July 1984 – Hepatic glutathione turnover and the efflux of glutathione from the liver into bile and blood were measured in male Sprague‐Dawley rats in vivo. In fed rats the efflux of glutathione into blood, calculated from the hepatic arteriovenous concentration gradient and hepatic blood flow, amounted to 12.4 ± 1.4 nmoles min.gm liver. Together with the excretion of glutathione into bile (3.4 ± 0.4 nmoles per min.gm liver) total efflux accounted for the hepatic turnover of glutathione of 15.2 ± 0.9 nmoles per min.gm liver.

1 July 1984

Jürgen SchÖLmerich, Maria‐Sybille Becher, Karlheinz Schmidt, Rolf Schubert, Bernd Kremer, Susanne Feldhaus, Wolfgang Gerok – 1 July 1984 – To characterize the relative toxicity of different bile salts, isolated hepatocytes were incubated with different concentrations of one bile salt or with identical concentrations of different bile salts and their conjugates. Incubation lasted for 1 hr; samples were taken at different intervals and studied for enzyme release, urea synthesis and stimulation by glucagon, and by electron microscopy.

R. Gideon Shaw, Alice R. Johnson, Werner W. Schulz, Rainer N. Zahlten, Burton Combes – 1 July 1984 – Guinea pig nonparenchymal hepatic cells were isolated by enzymatic digestion and subsequent separation on a 17.5% metrizamide gradient. Endothelial cell and Kupffer cell‐enriched fractions were separated by centrifugal elutriation. Viability of both cell fractions was approximately 80%. Endothelial cells were cultured on a substratum of guinea pig liver collagen and 1% gelatin (1:1).

Charles S. Davidson, Raymond S. Koff – 1 July 1984

Geoffrey Farrell, Judith Baird‐Lambert, Mara Cvejic, Neil Buchanan – 1 July 1984 – A pharmacokinetic study of metronidazole disposition was performed in 10 patients with severe liver disease, the majority of whom also had impaired renal function. Following a single intravenous dose, systemic clearance of metronidazole was decreased by 66% in patients compared with healthy controls (p < 0.001). The apparent volume of distribution for metronidazole was also decreased in patients (by 21%), but the greater effect on clearance resulted in the elimination half‐life being prolonged 152%.

Peter Schauder, Karsten SchrÖDer, Lothar Herbertz, Klaus Langer, Ulrich Langenbeck – 1 July 1984 – Valine (62.5 mg per kg), leucine (70 mg per kg) and equal amounts of the calcium salts of the corresponding keto acids, i.e., α1‐ketoisovaleric acid (KIVA) and α1‐ketoisocaproic acid (KICA) were orally administered to patients with cirrhosis and to control subjects.Valine or leucine ingestion increased serum valine and leucine levels and the corresponding keto acids, KIVA and KICA, in cirrhotics and controls.