Hematologic and plasma biochemical values for Tonkean macaques (Macaca tonkeana).

Hematologic and serum biochemical parameters were measured in 29 captive Tonkean macaques (Macaca tonkeana) to provide normative reference values for the species. Mean normal values and ranges were close to those reported in other species of macaques. Some significant variations related to age and sex were found.

Use of von Willebrand diseased kidney as donor in a pig-to-primate model of xenotransplantation.

Background: The coagulation process in hyperacute and delayed xenograft rejection is essential and depends upon platelet adhesion and aggregation. The initial binding of platelets to the damaged endothelium is due to the interaction of the platelet receptor glycoprotein Ib with von Willebrand factor (vWF), which is present on activated endothelial cells and bound to the subendothelial matrix. We hypothesized that the use of organs from animals with homozygous von Willebrand disease (vWD), severely deficient in vWF, might prevent the thrombosis encountered in delayed xenograft rejection.

Amelioration of hepatocellular integrity and inhibition of sinusoidal oxidative stress by N-acetylcysteine pretreatment in cold ischemia-reperfusion injury of rat liver.

Further improvements of donor liver preservation are still required in liver transplantation. In the present study, we investigated whether intraportal injection of N-acetylcysteine (NAC) 15 min before flush-out of UW solution (NAC pretreatment) improves liver dysfunction after cold preservation or has a protective effect on sinusoidal oxidative stress. The effect of NAC pretreatment was examined using an isolated perfused rat liver model.

Protective effects of N-acetylcysteine on hypothermic ischemia-reperfusion injury of rat liver.

We investigated whether intraportal injection of 150 mg/kg N-acetylcysteine (NAC) into rats reduced hepatic ischemia-reperfusion injury after 48 hours of cold storage and 2 hours of reperfusion. The organ was isolated and perfused to evaluate liver function. The control group received an intraportal injection of 5% dextrose.