The Effect of Chronic Ethanol Ingestion on Ethanol Metabolizing Enzymes in Isolated Periportal and Perivenous Rat Hepatocytes

Hannu Väänänen, Mikko Salaspuro, Kai Lindros – 1 September 1984 – Periportal (pp) and perivenous (pv) hepatocyte populations were separated using a two‐diree‐tional closed perfusion technique with selective addition of collagenase either to direct or retrograde perfusions (Vaananen, H. et al., Liver 1983; 3:131). The activity of GPT in hepatocytes from the pp‐area was 1.9 times higher than in cells from the pv‐area (p < 0.01).

An Enzyme‐Linked Immunosorbant Assay (ELISA) for Detecting Antimitochondrial Antibody

Marshall M. Kaplan, John V. Gandolfo, Elaine G. Quaroni – 1 July 1984 – We have developed an enzyme linked immunosorbant assay (ELISA) for antimitochondrial antibody. Polyvinyl microtiter plate wells are coated with partially purified rat kidney mitochondria, and excess protein binding sites are blocked with bovine serum albumin. Human serum, diluted 1:1,000, is incubated for 1 hr. Then β‐galactosidase‐goat‐anti‐human IgG (H+L) is added followed by the substrate, p‐nitrophenyl‐β‐D‐galactopyranoside. The plates are then read at 404 nM in a microelisa autoreader.

A Comparison of Liver Ultrastructure in Salicylate Intoxication and Reye's Syndrome

Jacqueline S. Partin, Cynthia C. Daugherty, A. James Mcadams, John C. Partin, William K. Schubert – 1 July 1984 – All childhood liver biopsy specimens from The Cincinnati Children's Hospital Research Foundation which had been prepared for light and electron microscopy were reviewed to identify biopsies from children with salicylate intoxication. Only two cases of primary salicylate intoxication were identified.

Noncirrhotic Portal Hypertension in Congenital Cytomegalovirus Infection

Fayez K. Ghishan, Harry L. Greene, Susan Halter, John A. Barnard, J. Roberto Moran – 1 July 1984 – The majority of infants with cytomegalovirus hepatitis have resolution of the disease with little evidence of fibrosis; there are only rare instances of cirrhosis. We report an infant with cytomegalovirus hepatitis who developed portal hypertension and hematemesis at 3 months of age. Liver biopsy showed resolution of the hepatitis but the presence of noncirrhotic sinusoidal fibrosis.

16,16‐Dimethyl‐PGE2 Protection Against α — Napthy lisothiocy anate – Induced Experimental Cholangitis in the Rat

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.

Correlation Between Liver Morphology and Portal Pressure in Alcoholic Liver Disease

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).

The Effects of Prostacyclin on Canine Hepatic Bile Flow

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.

Hepatic Glutathione Homeostasis in the Rat: Efflux Accounts for Glutathione Turnover

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.

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