Combined use of adenosine and amrinone inhibits reperfusion injury of rat liver.

  title={Combined use of adenosine and amrinone inhibits reperfusion injury of rat liver.},
  author={Kunihiro Katsuragi and Shigekazu Takemura and Yukiko Minamiyama and H Tanaka and Kazuhiro Hirohashi and Masayasu Inoue and Hideki Kinoshita},
  journal={Pathophysiology : the official journal of the International Society for Pathophysiology},
  volume={8 1},
  • K. KatsuragiS. Takemura H. Kinoshita
  • Published 1 August 2001
  • Biology, Medicine, Chemistry
  • Pathophysiology : the official journal of the International Society for Pathophysiology

Dynamic changes of post-ischemic hepatic microcirculation improved by a pre-treatment of phosphodiesterase-3 inhibitor, milrinone.

Pretreatment with a Phosphodiesterase-3 Inhibitor, Milrinone, Reduces Hepatic Ischemia-Reperfusion Injury, Minimizing Pericentral Zone-Based Liver and Small Intestinal Injury in Rats

A hepatic IRI model caused zone 3-based LI and SII, which were attenuated by intraportal administration of milrinone, and the 7-day survival rate was significantly elevated in the IR+milrinone group as compared with that of the IR group.



Post-ischemic intraportal adenosine administration protects against reperfusion injury of canine liver.

The results suggest that intraportally infused adenosine attenuates reperfusion injury of the liver, presumably by suppressing the activation of neutrophils and oxidative stress.

Protective effect of preconditioning on the injury associated to hepatic ischemia‐reperfusion in the rat: Role of nitric oxide and adenosine

It is suggested that, in preconditioning, adenosine stimulates NO production to protect against the injury associated with ischemia‐reperfusion.

Limitations of Exogenous L-Arginine in Exerting a Cytoprotective Effect on Hepatic Ischemia/Reperfusion Injury

The results suggest that exogenous L -arginine produced a relatively small amount of NO and therefore resulted in a slight decrease of hepatic I/R injury.

Cyclic GMP but not cyclic AMP prevents renal platelet accumulation after ischemia-reperfusion in anesthetized rats.

The present findings provide further evidence that cGMP-mediated drugs may afford effective antiplatelet action in an in vivo model of ischemia-reperfusion injury and demonstrate that modulation of the platelet function by cG MP agents can be dissociated from their blood pressure lowering effects.

The beneficial effect of dibutyryl cyclic adenosine monophosphate on warm ischemic injury of the rat liver induced by cardiac arrest.

DBcAMP pretreatment appeared to protect the liver from warm ischemic injury by increasing the intracellular cAMP concentration and stabilizing the cell membranes of endothelial cells and hepatocytes.

Adenosine inhibits ischemia-reperfusion-induced leukocyte adherence and extravasation.

It is found that intra-arterial administration of adenosine (2 microM) significantly attenuated the I/R-induced increases in intestinal capillary permeability and the number of extravasated leukocytes during the ischemic period was significantly reduced byadenosine.

Endothelial release of nitric oxide contributes to the vasodilator effect of adenosine in humans.

Adenosine-induced vasodilation in humans is mediated, at least in part, by endothelial release of NO, and the transducing mechanism is not known, but it does not appear to involve the activation of either ATP-dependent or quinidine-sensitive potassium channels.

Adenosine: a physiological modulator of superoxide anion generation by human neutrophils

Data indicate that adenosine (at concentrations that are present in plasma) acting via cell surface receptors is a specific modulator of superoxide anion generation by neutrophils.

Adenosine enhances nitric oxide production by vascular endothelial cells.

The results suggest that adenosine stimulates, by a receptor-mediated mechanism, the production of NO by arterial, but not by venous, endothelial cells.