Reversal of type 1 hepatorenal syndrome with the administration of midodrine and octreotide

Paolo Angeli, Roberta Volpin, Giorgio Gerunda, Raffaella Craighero, Paola Roner, Roberto Merenda, Piero Amodio, Antonietta Sticca, Lorenza Caregaro, Alvise Maffei‐Faccioli, Angelo Gatta – 30 December 2003 – The aim of the study was to verify the effects of the administration of an inhibitor of the release of endogenous vasodilators together with a vasoconstrictor agent in patients with hepatorenal syndrome (HRS). This new medical perspective was compared with a traditional medical approach for HRS, such as the infusion of nonpressor doses of dopamine to produce renal vasodilation.

Deranged blood coagulation equilibrium as a factor of massive liver necrosis following endotoxin administration in partially hepatectomized rats

Satoshi Mochida, Masahiro Arai, Akihiko Ohno, Fumio Yamanobe, Keiko Ishikawa, Atsushi Matsui, Ikuo Maruyama, Hisao Kato, Kenji Fujiwara – 30 December 2003 – Activated Kupffer cells provoke massive liver necrosis after endotoxin stimulation through microcirculatory disturbance caused by sinusoidal fibrin deposition in rats undergoing 70% hepatectomy. In these rats, serum activities of purine nucleoside phosphorylase (PNP) and alanine transaminase (ALT) were increased at 1 and 5 hours, respectively, following endotoxin administration.

Contribution of increased mitochondrial free Ca2+ to the mitochondrial permeability transition induced by tert‐butylhydroperoxide in rat hepatocytes

Aaron M. Byrne, John J. Lemasters, Anna‐Liisa Nieminen – 30 December 2003 – Previously, we showed that the oxidant chemical,tert‐butylhydroperoxide (t‐BuOOH), induces a mitochondrial permeability transition (MPT) in intact hepatocytes, causing lethal cell injury. Here, we investigated the role of mitochondrial free Ca2+ in t‐BuOOH cytotoxicity to 1‐day‐cultured rat hepatocytes using confocal microscopy of autofluorescence and parameter‐indicating fluorophores.

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