Samuel S. Lee, Richard Moreau, Antoine Hadengue, Raimondo Cerini, Abraham Koshy, Didier Lebrec – 1 November 1988 – To delineate the circulatory effects of glucagon in cirrhosis, we infused two moderately supraphysiological doses of this hormone into 19 patients with cirrhosis and determined hemodynamic responses. Patients were divided into a group with good liver function (Pugh Class A, n = 8) and poorer function (Pugh Class B and C, n = 11). All patients received glucagon at 10 ng per kg per min for 20 min, then 20 ng per kg per min for a further 20 min.

Gilles Pomier‐Layrargues, Pierre‐Michel Huet, Claire Infante‐Rivard, Jean‐Pierre Villeneuve, Denis Marleau, Lester Duguay, Serge Tanguay, Pierre Lavoie – 1 November 1988 – The objective of this study was to assess the prognostic value of spontaneous portosystemic shunting and liver function for survival and spontaneous hepatic encephalopathy after end‐to‐side portacaval shunt in cirrhotic patients. One hundred ninety‐eight patients with variceal hemorrhage as shown by endoscopy were evaluated.

Carol A. Sattler, Norimasa Sawada, Gerald L. Sattler, Henry C. Pitot – 1 November 1988 – Primary cultures of adult rat hepatocytes in a serum‐free medium were observed by time lapse cinematography to proceed through mitotis and cytokinesis. An ultrastructural study of these cultures is presented with electron micrographs of each stage of mitosis and cytokinesis. The cultured hepatocytes begin to enter prophase about 48 hr after plating and proceed through mitosis in approximately 70 min not including cytokinesis.

Giacomo Laffi, Fabio Cominelli, Marco Ruggiero, Sandra Fedi, Vincenzo P. Chiarugi, Giorgio La Villa, Massimo Pinzani, Paolo Gentilini – 1 November 1988 – Hemorrhagic disorders are common in patients with liver cirrhosis and result from several factors including impaired platelet function. We evaluated platelet aggregation and arachidonic acid metabolism in response to standard agonists in platelet‐rich plasma from 12 cirrhotic patients with mild impairment of liver function (Child A), 12 patients with severe liver dysfunction (Child B and C) and 12 healthy subjects.

1 November 1988

Keith D. Lindor, Russell H. Wiesner, E. Rolland Dickson, Henry A. Homburger – 1 November 1988 – Blastogenesis of autoreactive T lymphocytes in the autologous mixed lymphocyte reaction has been shown to be decreased in patients with primary biliary cirrhosis, but the mechanisms underlying this abnormality are not known.

Yolanta Kruszynska, Nicholas Williams, Michael Perry, Philip Home – 1 November 1988 – We have examined the hypothesis that insulin insensitivity in hepatic cirrhosis is related to abnormalities of glycogen deposition and skeletal muscle enzyme activities. Otherwise well patients with biopsy‐proven hepatic cirrhosis secondary to previous excess alcohol intake were studied.

Peter Schauder – 1 November 1988 – The effects of branched‐chain α‐ketoacids on flux through and activity state of the branched‐chain α‐ketoacid dehydrogenase complex were studied in hepatocytes prepared from chow‐fed, starved, and low‐protein‐diet‐fed rats. Very low concentrations of α‐ketoisocaproate caused a dramatic stimulation (50% activation at 20 μM) of α‐ketoisovalerate decarboxylation in hepatocytes from low‐protein‐fed rats. α‐Keto‐β‐methylvalerate was also effective, but less so than α‐ketoisocaproate.

Roger F. Butterworth, Joël Lavoie, Jean‐François Giguère, Gilles Pomier‐Layrargues – 1 September 1988 – The integrity of GABA‐A receptors and of central benzodiazepine receptors was evaluated in membrane preparations from prefrontal cortex and caudate nuclei obtained at autopsy from nine cirrhotic patients who died in hepatic coma and an equal number of age‐matched control subjects. Histopathological studies revealed Alzheimer Type II astrocytosis in all cases in the cirrhotic group; controls were free from neurological, psychiatric or hepatic diseases.

Neville L. Sandford, Ronald E. Saul – 1 September 1988 – Thirty‐six patients with advanced chronic liver disease of predominantly alcoholic etiology and with a documented history or current physical evidence of hepatic encephalopathy were studied and compared to 30 healthy controls. Assessment was made of their mental state, number connection test, venous blood ammonia, electroencephalography and visual evoked potentials with both pattern reversal and flash stimuli.