Effect of lipo-PGE1 on ischemia–reperfusion injury and endothelin-1 concentrations after canine partial liver transplantation

Seo, Ki Youl; Chung, Ku Yong; Kim, Yu Seun; Moon, Il Hwan; Choi, Ko-Eun

doi:10.1016/s0041-1345(02)03973-8

Cited by 3 publications

(3 citation statements)

References 3 publications

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“…A randomized clinical orthotopic liver Tx study has also shown that PGI 2 augmented graft survival by increasing hepatic splanchnic oxygenation [36]. Experimental canine partial liver Tx has also shown the hepatoprotective effect of lipo-PGE 1 against IR injury [35]. Another novel method, LRLT has been established recently which has several advantages over cadaver Tx.…”

Section: (H) Prostaglandins In Liver Surgery and Regenerationmentioning

confidence: 99%

“…But IR injury is inevitable in liver Tx performed by any method [30][31][32][33]. PGE 1 seems to be effective in ameliorating IR injury after orthotopic liver transplantation (OLT) clinically [34] and canine partial liver allotransplantation experimentally [35]. PGI 2 also reduced reperfusion injury of the graft after clinical OLT by improving hepatic splanchnic oxygenation [36].…”

Section: Introductionmentioning

confidence: 99%

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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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Section: (H) Prostaglandins In Liver Surgery and Regenerationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Role of Prostaglandins in Liver Ischemia-Reperfusion Injury

Hossain

Wakabayashi

Izuishi³

et al. 2006

CPD

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“…It has been shown to decrease liver I/R injury after warm ischemia [5] and cold preservation of liver grafts [6], and to improve portal blood flow after cold ischemia [7]. While this protective effect has been well-established experimentally [5][6][7][8][9][10][11][12][13][14], the clinical benefits of PGE1 following liver transplantation are not clear-cut [13,14]. Clinically, PGE1 administration during liver transplantation decreased intensive care unit stay, shortened hospitalization, and lowered serum creatinine in two randomized clinical trials [13,14], but did not improve patient or graft survival [15].…”

Section: Introductionmentioning

confidence: 99%

The Effect of Intraportal Prostaglandin E1 on Adhesion Molecule Expression, Inflammatory Modulator Function, and Histology in Canine Hepatic Ischemia/Reperfusion Injury

Hafez

Moussa

Nesim

et al. 2007

Journal of Surgical Research

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Drug Therapy in the Heart Transplant Recipient

2005

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With improving survival, the heart transplant recipient faces an increasing number of medical problems caused by both aging and the cumulative complications of immunosuppressive drugs. 1 The availability of new drugs to treat infection, obesity, hypertension, hyperlipidemia, renal insufficiency, diabetes, osteoporosis, gout, and malignancies has resulted in the heart transplant recipient and their physicians facing an almost overwhelming number of important drug-drug interactions. In parts 1 through 3 of this series, we reviewed commonly used immunosuppressive drugs and their pharmacology, as well as the common medical problems faced by the heart transplant recipient. In this article, we provide an overview of the mechanisms of common and important potential drug-drug interactions and guidelines for avoiding these interactions. Principles of Drug-Drug InteractionsThe risk for drug-drug interactions is increased by advanced age, polypharmacy, medications with a narrow therapeutic index, or medications requiring intensive monitoring. All of these factors except advanced age are present in the heart transplant recipient. A 10-fold interpatient variability may exist in the magnitude of a drug interaction resulting from patient-related and drug-related factors. 2 Patient-related factors predisposing to drug interactions include concomitant diseases, genetics, diet, and environmental exposures. For example, commonly used immunosuppressants, antifungal agents, and lipid-lowering medications are metabolized through the cytochrome P450 (CYP450) enzyme system and effluxed from cells by the multiple drug resistance transporter protein p-glycoprotein (P-gp). Both systems are found in the liver and gastrointestinal tract and exhibit genetic polymorphism. 2 The CYP450 enzymes belong to a superfamily of oxygenases; the primary purpose of these oxygenases is to add a functional group to a drug to increase its polarity and to promote its excretion from the body. If enzymes possess Ͼ40% homology, they are grouped together into families designated by an Arabic numeral (eg, the CYP1 family). Families are further divided into subfamilies, which are designated by a letter after the number (eg, CYP2C and CYP2D subfamilies); members of each subfamily have Ͼ55% homology with each another. Individual members are given an additional number (eg, CYP3A4) to identify a specific enzyme pathway. 2 CYP3A4 is particularly important because 60% of oxidized drugs, including the calcineurin inhibitors (CIs) cyclosporine (CSA) and tacrolimus (TAC), sirolimus (SIR), and everolimus (EVER), undergo biotransformation through this particular enzyme system. 3 P-gp is a membrane-bound glycoprotein belonging to the superfamily of ATP-binding cassette transporters. Like the CYP450 enzyme system, P-gp acts in a protective capacity by "effluxing" drug from the cell membrane or cytoplasm. P-gp density is highest within the small intestine, proximal tubules of the kidney, and biliary canalicular membranes. Some medications such as CIs and SIR use both the CYP450...

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Effect of lipo-PGE1 on ischemia–reperfusion injury and endothelin-1 concentrations after canine partial liver transplantation

Cited by 3 publications

References 3 publications

The Role of Prostaglandins in Liver Ischemia-Reperfusion Injury

The Role of Prostaglandins in Liver Ischemia-Reperfusion Injury

The Effect of Intraportal Prostaglandin E1 on Adhesion Molecule Expression, Inflammatory Modulator Function, and Histology in Canine Hepatic Ischemia/Reperfusion Injury

Drug Therapy in the Heart Transplant Recipient

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