The immunosuppressive effect of ursodeoxycholic acid: A comparative in vitro study on human peripheral blood mononuclear cells

Florence Lacaille, Khazal Paradis – 1 July 1993 – Ursodeoxycholic acid is an efficient treatment for putatively immune‐mediated liver diseases, but its mechanism of action is unknown. We studied human mononuclear cell proliferation as an in vitro model for cell‐mediated immunity in the presence of ursodeoxycholic acid, its glycoconjugate and tauroconjugate and chenodeoxycholic acid at concentrations of 5, 25 and 50 μmol/L.

Reduced gastric mucosal blood flow in patients with portal‐hypertensive gastropathy

Tadashi Iwao, Atsushi Toyonaga, Motoki Ikegami, Kazuhiko Oho, Michihiro Sumino, Hiroshi Harada, Munenori Sakaki, Hiroyuki Shigemori, Toshichika Aoki, Kyuichi Tanikawa – 1 July 1993 – Although congestive gastric mucosal circulation has been suggested in patients with portal‐hypertensive gastropathy, whether it is due to “active” (overflow) or “passive” (stasis) congestion is not known. To answer this question, we assessed regional gastric mucosal blood flow with laser Doppler flowmetry in 57 patients with portal hypertension and 30 controls.

Prior esophageal variceal bleeding does not adversely affect survival after orthotopic liver transplantation

Ka‐Sic Ho, Bret A. Lashner, Jean C. Emond, Alfred L. Baker – 1 July 1993 – Prior variceal bleeding may adversely affect the prognosis of orthotopic liver transplantation. We studied this question by evaluating all 175 adult patients undergoing orthotopic liver transplantation at our institution to determine risk factors associated with mortality after transplantation. Seventy patients demonstrated prior variceal bleeding, and of those, 32 had a course of sclerotherapy. Thirteen also had portal systemic shunts.

Cardiovascular hyporesponsiveness to norepinephrine, propranolol and nitroglycerin in portal‐hypertensive and aged rats

John Polio, Cornel C. Sieber, Emanuel Lerne, Roberto J. Groszmann – 1 July 1993 – Most studies testing vasoactive agents in portalhypertensive rats have been performed in young animals. To assess age‐related changes in hemodynamic responses to adrenergic stimuli, we examined (a) responsiveness to norepinephrine (0.14 to 12.0 μg ˙ kg−1 ˙ min−1) in young (3‐mo‐old) and aged (9‐mo‐old) sham‐operated and portal‐hypertensive rats and (b) response to propranolol (2 and 10 mg ˙ kg−1 body wt), nitroglycerin (3.6 mg ˙ kg−1 ˙ min−1) or saline solution in aged portal‐hypertensive rats.

Differences in the steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA during mitogen‐induced liver growth and compensatory regeneration

Pierpaolo Coni, Gabriella Simbula, Alessandra Carcereri de Prati, Marta Menegazzi, Hisanori Suzuki, Dittakavi S. R. Sarma, Giovanna M. Ledda‐Columbano, Amedeo Columbano – 1 June 1993 – The steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA were investigated in rat liver tissue after proliferative stimuli of different nature‐namely, compensatory regeneration induced by partial hepatectomy or carbon tetrachloride administration ‐ and direct hyperplasia induced by four different hepatomitogens: lead nitrate, ethylene dibromide, cyproterone acetate and nafenopin.

Effect of ursodeoxycholic acid on the kinetics of cholic acid and chenodeoxycholic acid in patients with primary sclerosing cholangitis

Gerda Rudolph, Richard Endele, Martin Senn, Adolf Stiehl – 1 June 1993 – Treatment of patients with cholestatic liver diseases with ursodeoxycholic acid has been shown to have beneficial effects that may be related to a shift in the balance between hydrophilic and hydrophobic bile acids in favor of hydrophilic bile acids. During treatment of patients with primary sclerosing cholangitis with ursodeoxycholic acid, plasma concentrations of some endogenous bile acids decrease.

Long‐term ethanol consumption alters the hepatic response to the regenerative effects of tumor necrosis factor‐α

Paul A. Akerman, Piera M. Cote, Shi Qi Yang, Craig McClain, Steve Nelson, Gregory Bagby, Anna Mae Diehl – 1 June 1993 – The pathogenesis of chronic alcoholic liver disease is uncertain, but it may reflect an impaired wound healing response to ethanol‐induced liver injury. Cellto‐cell communication such as that mediated by the cytokine tumor necrosis factor is necessary for successful liver regeneration and complete recovery from liver injury. Hence disruption of intercellular regenerative signaling may contribute to the pathogenesis of chronic alcoholic liver disease.

Reduction of cerebral perfusion precedes rise of intracranial pressure in rats with ischemic fulminant liver failure

Vijay Shah, Steve Webster, Jeanne Gottstein, Andres T. Blei – 1 June 1993 – In fulminant liver failure, brain edema may progress to intracranial hypertension. However, the rise in intracranial pressure is a late event in this sequence. We investigated the relationship between cerebral perfusion and development of intracranial hypertension in a well‐characterized model of fulminant liver failure, the rat subjected to hepatic devascularization (n = 11).

Brain indoles in human hepatic encephalopathy

Hanan Al Mardini, Emma J. Harrison, Paul G. Ince, Kim Bartlett, Christopher O. Record – 1 June 1993 – The neurotransmitter serotonin has a profound effect on the control of sleep; thus excess serotonin activity in the brain could be responsible for impaired consciousness in hepatic encephalopathy. Furthermore, an increased brain level of 5‐hydroxyindoleacetic acid has been a consistent finding in various animal models of the condition.

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