Differential control by arterial and portal noradrenaline of hepatic carbohydrate metabolism: Evidence for an indirect hemodynamic mechanism

Hisayuki Miura, Kurt Jungermann, Andreas Gardemann – 1 December 1993 – In an earlier study it was found (a) that arterial noradrenaline caused increases in glucose and lactate output slower in onset, smaller in peak height and clearly longer in duration than those caused by portal noradrenaline and (b) that arterial noradrenaline was extracted to a much greater extent than portal noradrenaline.

The role of transjugular liver biopsy in fulminant liver failure: Relation to other prognostic indicators

Bruce W. Donaldson, Ramya Gopinath, Ian R. Wanless, M. James Phillips, Ross Cameron, Eve A. Roberts, Paul D. Greig, Gary Levy, Laurence M. Blendis – 1 December 1993 – Early and accurate diagnosis and prognosis of patients with fulminant liver failure is of critical importance for optimum management. We investigated the role of transjugular liver biopsy in the management of patients with fulminant liver failure and assessed its value in comparison with the recently proposed King's College criteria.

Plasma elimination of indocyanine green in the intact pig after bolus injection and during constant infusion: Comparison of spectrophotometry and high‐pressure liquid chromatography for concentration analysis

Peter Ott, Susanne Keiding, Ludvik Bass – 1 December 1993 – Indocyanine green is used to estimate liver blood flow rate and hepatic intrinsic clearance. However, its use as a test substance for studies of liver function has been limited by two puzzling kinetic observations: a biexponential plasma decay after bolus injection with an extremely slow late phase and an apparently steadily decreasing clearance value during constant infusion. These observations have been made with spectrophotometric concentration analysis.

Role of ethanol‐inducible cytochrome p‐450 2E1 in the development of hepatocellular carcinoma by the chemical carcinogen, N‐nitrosodimethylamine

Mikihiro Tsutsumi, Yoshiro Matsuda, Akira Takada – 1 December 1993 – Cytochrome P‐450 2E1 is a specific isozyme of cytochrome P‐450 induced by ethanol. P‐450 2E1 may also be the only enzyme that metabolizes N‐nitrosodimethylamine at a very low concentration. Because N‐nitrosodimethylamine is a procarcinogen, the possibility that induction of P‐450 2E1 by alcohol abuse may accelerate the carcinogenic action of a very small dose of N‐nitrosodimethylamine should be considered.

Transforming growth factor‐α expression during liver regeneration after partial hepatectomy and toxic injury, and potential interactions between transforming growth factor‐α and hepatocyte growth factor

Eric M. Webber, Mark J. Fitzgerald, Pamela I. Brown, Molly H. Bartlett, Nelson Fausto – 1 December 1993 – Transforming growth factor‐α and hepatocyte growth factor are important stimulators of hepatocyte proliferation. In this series of experiments we sought to measure the expression of transforming growth factor‐α mRNA by hepatocytes in response to toxic liver injury produced by carbon tetrachloride or galactosamine and to perform a more detailed analysis of transforming growth factor‐α expression after partial hepatectomy.

Human leukocyte antigen A1‐B8‐DR3‐DQ2‐DPB1*0401 extended haplotype in autoimmune hepatitis

Koji Manabe, Peter T. Donaldson, James A. Underhill, Derek G. Doherty, Giorgina Mieli‐Vergani, Ian G. McFarlane, Adrian L. W. F. Eddleston, Roger Williams – 1 December 1993 – Genetic susceptibility to autoimmune hepatitis is associated with the human leukocyte antigen haplotype A1‐B8‐DR3 and DR4. To date, only one study in Japan has considered the human leukocyte antigen DP locus in this disease, and no studies have been reported in whites.

Increased benzodiazepine‐like activity is neither necessary nor sufficient to explain acute hepatic encephalopathy in the thioacetamide‐treated rat

Peter Widler, Hans U. Fisch, Peter Schoch, Arthur Zimmermann, Thomas E. Schläpfer, Jürg Reichen – 1 December 1993 – Increased levels of natural benzodiazepine receptor agonists, produced in the body (endogenous) or ingested with food (exogenous) have been proposed as one of the factors causing hepatic encephalopathy in both experimental animals and human subjects. However, the divergent response of hepatic encephalopathy to benzodiazepine antagonists sheds doubt on this attractive hypothesis.

High plasma concentration of myeloperoxidase in cirrhosis: A possible marker of hypersplenism

Makoto Nakamuta, Masao Ohashi, Yuichi Tanabe, Kaichiro Hiroshige, Hajime Nawata – 1 December 1993 – Plasma myeloperoxidase levels in patients with cirrhosis were compared with those in patients with chronic hepatitis and healthy controls by means of a specific radioimmunoassay for myeloperoxidase. The mean concentration of plasma myeloperoxidase in cirrhotic patients (309.1 ± 17.2 ng/ml, n = 41) was markedly higher than that in chronic hepatitis patients (222.6 ± 17.2 ng/ml, n = 21) (p < 0.01) and normal controls (219.5 ± 5.7 ng/ml, n = 50) (p < 0.01).

Increase in prostanoid formation in rat liver macrophages (Kupffer cells) by human anaphylatoxin C3a

Gerhard P. Püschel, Ursula Hespeling, Martin Oppermann, Peter Dieter – 1 December 1993 – Human anaphylatoxin C3a increases glycogenolysis in perfused rat liver. This action is inhibited by prostanoid synthesis inhibitors and prostanoid antagonists. Because prostanoids but not anaphylatoxin C3a can increase glycogenolysis in hepatocytes, it has been proposed that prostanoid formation in nonparenchymal cells represents an important step in the C3a‐dependent increase in hepatic glycogenolysis.

Handling of epidermal growth factor and number of epidermal growth factor receptors are changed in aged male rats

Ulrich Marti – 1 December 1993 – In the aged liver, cell proliferation and induction of DNA synthesis by epidermal growth factor is impaired. Changes in the hepatic handling of epidermal growth factor may be important for these effects. I compared epidermal growth factor handling in the livers of young and old rats. Epidermal growth factor binding capacity of plasma membranes was reduced from 1.30 ± 0.15 to 0.51 ± 0.19 pmol/mg in young and old animals, respectively.

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