Portal Hyperperfusion after Extended Hepatectomy Does Not Induce a Hepatic Arterial Buffer Response (HABR) but Impairs Mitochondrial Redox State and Hepatocellular Oxygenation.

Background & Aims: Portal hyperperfusion after extended hepatectomy or small-for-size liver transplantation may induce organ dysfunction and failure. The underlying mechanisms, however, are still not completely understood. Herein, we analysed whether hepatectomy-associated portal hyperperfusion induces a hepatic arterial buffer response, i.

Cilostazol improves hepatic blood perfusion, microcirculation, and liver regeneration after major hepatectomy in rats.

Major hepatectomy or small-for-size liver transplantation may result in postoperative liver failure. So far, no treatment is available to improve liver regeneration. Herein, we studied whether cilostazol, a selective phosphodiesterase III inhibitor, is capable of improving liver regeneration after major hepatectomy.

The phosphodiesterase 3 inhibitor cilostazol does not stimulate growth of colorectal liver metastases after major hepatectomy.

Liver failure after extended hepatectomy represents a major challenge in the surgery of hepatic colorectal metastasis. A previous study has indicated that inhibition of phosphodiesterase type 3 (PDE 3) stimulates liver regeneration. However, little is known whether PDE 3 inhibitors, such as cilostazol, also stimulate the growth of remnant metastases.

Negative pressure wound therapy for the treatment of the open abdomen and incidence of enteral fistulas: a retrospective bicentre analysis.

Introduction. The open abdomen (OA) is often associated with complications. It has been hypothesized that negative pressure wound therapy (NPWT) in the treatment of OA may provoke enteral fistulas.

Silver acetate coating promotes early vascularization of Dacron vascular grafts without inducing host tissue inflammation.

Background: Silver acetate is frequently used as an antimicrobial coating of prosthetic vascular grafts. However, the effects of this coating on the early inflammatory and angiogenic host tissue response still remain elusive. Therefore, the aim of the present in vivo study was to analyze the biocompatibility and vascularization of silver acetate-coated and uncoated vascular grafts during the initial phase after implantation.

Split-liver procedure and inflammatory response: improvement by pharmacological preconditioning.

Background: Final outcome of split-liver (SL) transplantation is impaired due to an increased rate of vascular complications and primary non-function. Herein, we hypothesized that an in situ split-liver procedure induces an inflammatory response and a deterioration of graft quality. We further studied whether graft quality can be improved by pharmacologic preconditioning.

P-selectin glycoprotein ligand-1-mediated leukocyte recruitment regulates hepatocellular damage in acute obstructive cholestasis in mice.

Objective: Leukocytes mediate hepatocellular injury in obstructive cholestasis. The aim of the present study was to define the role of P-selectin glycoprotein ligand-1 (PSGL-1) in cholestasis-induced leukocyte recruitment and liver damage.

Methods: C57BL/6 mice were pre-treated with an anti-PSGL-1 antibody or a control antibody prior to bile duct ligation (BDL) for 12 h.

The Rho-kinase inhibitor Y-27632 inhibits cholestasis-induced platelet interactions in the hepatic microcirculation.

Bile duct obstruction is associated with hepatic accumulation of leukocytes and liver injury. Emerging data suggest that platelets may play an important role in tissue damage and inflammation. Herein, we characterized the platelet response in cholestatic liver injury and evaluated the role of Rho-kinase signaling.

Rho-kinase inhibitor attenuates cholestasis-induced CXC chemokine formation, leukocyte recruitment, and hepatocellular damage in the liver.

Background: In the present experimental study, we analyzed the role of Rho-kinase during obstructive cholestasis by studying the effect of the Rho-kinase inhibitor Y-27632 on hepatic CXC chemokine formation, leukocyte recruitment and hepatocellular damage.

Materials And Methods: C57BL/6 mice underwent bile duct ligation (BDL) to induce obstructive cholestasis. Mice were pretreated with Y-27632 (1 and 10mg/kg) or the vehicle PBS.

Infectious port complications are more frequent in younger patients with hematologic malignancies than in solid tumor patients.

Background: We assessed longevity and complications of totally implantable venous access devices in oncology patients.

Methods: 197 patients received a total of 201 port devices via the subclavian vein for delivery of chemotherapy between January 1, 2005, and December 31, 2006. We reviewed the patient charts for port-related complications and risk factors until July 31, 2007.

Cholestatic liver damage is mediated by lymphocyte function antigen-1-dependent recruitment of leukocytes.

Background: The role of specific adhesion molecules in cholestasis-induced leukocyte recruitment in the liver is not known. Therefore, the aim of our experimental study was to evaluate the role of lymphocyte function antigen-1 (LFA-1) in cholestatic liver injury.

Methods: C57BL/6 mice underwent bile duct ligation for 12 hours.