Work

Reperfusion injury following cold ischemia activates rat liver Kupffer cells.

Year: 1991

Type: article

Abstract: Liver transplantation is now an accepted therapy for end-stage liver disease.1 Organ preservation, transport, and subsequent transplantation involves a period of cold ischemia followed by reperfusion. Toxic oxygen radicals liberated at reperfusion can cause severe injury to the microvascular endothelial cell.2–6 It has recently been demonstrated that severe preservation injury to the endothelial cell results in an increased incidence of allograft rejection in liver transplantation.7 Although the exact reasons for this phenomenon are unclear, it is possible that endothelial cell injury may activate the neighboring Kupffer cell resulting in the production of inflammatory cytokines like interleukin-1 (IL-1) and tumor necrosis factor (TNF).8 The IL-1 and TNF thus produced can initiate the rejection cascade leading ultimately to graft failure.9–14 An isolated perfused rat liver (IPRL) model was used to investigate whether reperfusion injury following cold preservation can activate the Kupffer cell as measured by increased production of IL-1 and TNF.

Source: PubMed

Authors: P N Rao, T Liu, J T Synder, J L Platt, T E Starzl

Institution: University of Pittsburgh

Language: English

Topic: Organ Transplantation Techniques and Outcomes

Subfield: Surgery

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green

Funder: National Institute of Diabetes and Digestive and Kidney Diseases

Award: ORTHOTOPIC LIVER TRANSPLANTATION