Liver Transplant: Adenosine Metabolism and Apoptosis

Carlucci, Filippo; Marinello, Enrico; Gerunda, G.E.; Neri, Daniele; Rosi, F.; Floccari, F.; Tabucchi, Antonella

doi:10.1081/ncn-200027551

Cited by 2 publications

(1 citation statement)

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“…The liver can be damaged by liver resection, transplantation (Tx), viral infections, excessive alcohol intake, environmental toxins, and toxic medications and by many other causes. Among these causative factors hepatic resection with concomitant periods of ischemia and reperfusion is a common occurrence in resectional surgery [4][5][6][7], liver Tx [8][9][10][11], as well as reduced size liver (split liver or living donor liver) transplantation [12][13]. Most recently, an *Address correspondence to this author at the First Department of Surgery, Faculty of Medicine, Kagawa University, 1750-1, Ikenobe, Miki-cho, Kitagun, Kagawa 761-0793, Japan; Tel: +81-87-891-2186; Fax: +81-87-891-2187; E-mail: hossain@med.kagawa-u.ac.jp and akramhossain@yahoo.com experimental study has demonstrated that the liver is injured even by gentle in situ organ manipulation by touching, retracting and moving liver lobes gently during harvest which subsequently reduces graft survival afterwards [14].…”

Section: Introductionmentioning

confidence: 99%

The Role of Prostaglandins in Liver Ischemia-Reperfusion Injury

Hossain

Wakabayashi

Izuishi³

et al. 2006

CPD

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Ischemia reperfusion (IR) of the liver is a multifactorial process that, at least in part, is responsible for the morbidity associated with major liver surgery under occlusion of the portal triad with the Pringle maneuver, total vascular exclusion or after liver transplantation. Surgeons are confronted with IR injury (IRI) more often than they anticipate. Although the human body has its own defense system, understanding the pathophysiology of IRI is essential for the surgeon in preventing and/or treating the reperfusion injury in common clinical practice. Several endogenous mechanisms exist to overcome IRI and a large number of pharmacological agents have also been found to confer protection against ischemic injury in the liver. They either blocked the injurious pathways directly or they subjected the liver to preconditioning. Prostaglandins (PGs) are a group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase (COX) pathway. They are short-lived, hormone-like chemicals that regulate cellular activities on a moment-to-moment basis and are produced in most tissues of the body, although the liver has emerged as the major organ participating in the synthesis, degradation and elimination of arachidonate products of systemic origin. PGs are released through the prostaglandin transporter on the cell's plasma membrane. During the last decade intensive work on the cytoprotective effects of PGs on livers suffering from IRI have been well documented. Prostaglandins confer their protective effects on IR-injured livers mainly by inhibiting the generation of reactive oxygen species, preventing leukocyte migration, reducing the synthesis or production of membrane degradation products, improving hepatic insulin and lipid metabolism, and regulating the production of inflammatory cytokines and cell adhesion molecules. Production of PGs have been found essential also soon after partial hepatectomy for hepatocyte proliferation.

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