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4 edition of The use of hypertonic preconditioning in hepatic ischemia-reperfusion injury found in the catalog.

The use of hypertonic preconditioning in hepatic ischemia-reperfusion injury

George D. Oreopoulos

The use of hypertonic preconditioning in hepatic ischemia-reperfusion injury

by George D. Oreopoulos

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Published by National Library of Canada in Ottawa .
Written in English


Edition Notes

Thesis (M.Sc.) -- University of Toronto, 2000.

SeriesCanadian theses = -- Thèses canadiennes
The Physical Object
FormatMicroform
Pagination2 microfiches : negative. --
ID Numbers
Open LibraryOL21784451M
ISBN 100612541436
OCLC/WorldCa50754828

Ischemic preconditioning is one of the therapeutic interventions aiming at preventing ischemia/reperfusionrelated injury. Numerous experimental studies and a few clinical series have shown that during liver resections, ischemic preconditioning is a promising strategy for optimizing the postoperative outcome. Moreover, various types of pharmacological intervention as well as different . -Lipoic acid preconditioning reduces ischemia-reperfusion injury of the rat liver via the PI3-kinase/Akt pathway Christian Mu¨ller,1* Friedrich Du¨nschede,2* Elke Koch,1 Angelika M. Vollmar,1 and Alexandra K. Kiemer1 1Department of Pharmacy, Center of Drug Research, University of Munich, Munich; and 2Department of Surgery, University of Mainz, Mainz, Germany.

Abstract. Hepatic ischemia/reperfusion (I/R) injury is a frequently encountered complication in a variety of clinical scenarios including liver transplantation, major hepatic resection, abdominal trauma surgery and hemorrhagic shock. While liver transplantation remains the sole treatment option for patients with end-stage liver disease, there are numerous limitations to liver transplantation including the scarcity of donor livers and a rise in livers that are unsuitable to transplant such as those with excess steatosis. Fatty livers are susceptible to ischaemia-reperfusion (IR) injury during transplantation and IR injury.

Intestinal Ischemic Preconditioning as a “Remote Preconditioning” to the Hepatic Ischemia/Reperfusion; Impact of Gut Protection and Signal Cross-Talk Between the Liver and the Gut. Jaeschke H. Molecular mechanisms of hepatic ischemia-reperfusion injury and preconditioning. Am J Physiol Gastrointest Liver Physiol. ; (1):G15–G Liu Z, Xu Z, Shen W, Li Y, Zhang J, Ye X. Effect of pharmacologic preconditioning with tetrandrine on subsequent ischemia/reperfusion injury in rat liver.


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The use of hypertonic preconditioning in hepatic ischemia-reperfusion injury by George D. Oreopoulos Download PDF EPUB FB2

Ischemia/reperfusion (I/R) injury of the liver is known to occur in many clinical scenarios, including major trauma with blood loss and extensive liver resections for tumor. 1, 2 Experimental studies have defined a multistep process that culminates in the development of liver inflammation and hepatocellular necrosis.

The initial phase involves activation of Kupffer cells with the production Cited by: Ischemia/reperfusion (I/R) of the liver occurs in many clinical scenarios including trauma, elective surgery, and transplantation.

Events initiated by this process can lead to inflammation in the liver, culminating in local injury as well as distant organ by: 1. Context. Ischemia reperfusion injury (IRI) is defined as the phenomenon during which cellular damage in an organ, caused by hypoxia, is paradoxically exacerbated after the restoration of oxygen delivery ().It is a dynamic process which involves the two interrelated phases of local ischemic insult and inflammation-mediated reperfusion injury ().

Cited by:   During ischemic preconditioning, brief periods of tissue ischemia are used to render tissue resistant to injury resulting from prolonged ischemia and reperfusion, so-called ischemia–reperfusion injury.

Hepatic ischemia–reperfusion injury plays a major role in hepatic resection and shock, particularly during liver transplantation.1, 2, 3, 4Cited by: 1.

The Pringle maneuver, which is conducted by temporarily clamping hepatic vascular inflow, is a widely used technique to reduce bleeding during hepatectomy, but it has the potential to induce liver damage in association with hepatic ischemia-reperfusion injury (IRI).

IRI is an important cause of morbidity and mortality in patients who have Author: Doyeon Kim, Ji Won Choi, Sangbin Han, Mi Sook Gwak, Gaab Soo Kim, Su Yeon Jeon, Sun Ryu, Tae Soo Hah. did not use hepatic vascular occlusion. One of the techniques used to attenuate ischemia-reperfusion syndrome (IRS) is ischemic preconditioning ().

The goal of our study was to determine in the experiment the optimal model of vascular clamping which causes minimum pathological changes in liver without depressing its regeneration functions.

Keywords: Kupffer cells, Hepatic macrophages, Ischemia-reperfusion injury, Liver transplantation, Pattern recognition receptors, Tumor necrosis factor-α INTRODUCTION With improvements in surgical procedures, immunosuppression techniques and perioperative care, liver transplantation (LT) has evolved into a definitive treatment for all types of.

1. Introduction Hepatic ischemia-reperfusion injury (IRI) is one of the most common complications associated with liver transplantation, hepatic lobectomy, massive trauma, or hemorrhagic shock [], which is unavoidable and usually leads to postoperative liver failure [4,5].

Hepatic ischemia/reperfusion injury (IRI) is an unavoidable course in liver transplantation, during which the immune response of inflammation plays a leading part.

MicroRNAb-5p (miRb-5p. BACKGROUND Ischemic preconditioning (IPC) has been shown to protect the liver against ischemia-reperfusion (I/R) injuries. However, ischemic post-conditioning has received little attention. The aim of the present study was to quantify and compare the hepato-protective properties of IPC and IPO, for the first time, using unbiased design-based stereological methods.

Ischemia-reperfusion (I/R) injury is a phenomenon in which cellular damage in a hypoxic organ is accentuated following the oxygen restoration [1, 2, 3], being a major pathophysiological event and cause of morbidity and mortality in liver resections and transplantation [].Despite the attempts to solve this problem, hepatic I/R is an unresolved problem.

C. Peralta, G. Hotter, D. Closa, et tive effect of preconditioning on the injury associated to hepatic ischemia-reperfusion in the rat: role of nitric oxide and adenosine Hepatology, 25 (), pp. Background. Ischemic preconditioning (IP) and intermittent inflow occlusion (IO) have provided beneficial outcomes in hepatic resection.

However, comparison of these two procedures against warm hepatic ischemia-reperfusion injury has not been studied enough. Congestion–reperfusion injury (CRI) is a common complication after living donor liver transplantation, which has not been fully understood.

It causes more severe inflammatory response as compared with ischemia–reperfusion injury (IRI). Ischemic preconditioning (IPC) has been endowed with powerful protective properties toward IRI. For this purpose, Fe liver preconditioning was assessed in a model of partial hepatic IR injury in the rat, either without or with pretreatment with the antioxidant N-acetylcysteine (NAC) [15], the results of which were correlated with parameters related to oxidative stress, and NF-[kappa]B activity.

Materials and Methods Remote ischemic preconditioning (RIPC) is known to have a protective effect against hepatic ischemia-reperfusion (IR) injury in animal models.

However, the underlying mechanism of action is not clearly understood. This study examined the effectiveness of RIPC in a mouse model of hepatic IR and aimed to clarify the mechanism and relationship of the ATP-sensitive potassium channel (KATP) and.

Keywords:Liver, ischemia/reperfusion injury, antioxidants, tumor necrosis factor alpha, cytoprotective cytokines, growth factors, nitric oxide, adenosine, apoptosis inhibitors. Abstract: Ischemia and reperfusion (I/R) injury develops when blood flow is interrupted for a long period of time and then restarted.

In the liver, this type of damage. The ischemia-reperfusion (I/R) injury is an important cause of liver damage occurring during surgical procedures that include hepatic resections and liver transplantation. Hepatic steatosis is a major risk factor after liver surgery because steatotic livers tolerate poorly I/R injury.

The occurrence of postoperative liver failure after hepatic resection in a steatotic liver exposed to.

Introduction. Although liver transplantation, as the only effective therapeutic method for end-stage liver disease, has been widely applied, unavoidable hepatic ischemia-reperfusion injury (IRI) is still challenging for clinicians because of the increased risk for hypohepatia, primary graft failure, allograft vasculopathy, acute rejection reactions, and damage to other major organs 1, 2.

Ischemia–reperfusion (I/R) injury of the liver occurs in many clinical cases. Many steps are associated with hepatic I/R injury, including the release of many inflammatory molecules and infiltration of neutrophils into the liver. Recent studies revealed that hypertonic saline (HTS) has a strong anti-inflammatory effect and can inhibit a varity of neutrophil functions.

Ischemic preconditioning (IPC) may protect the liver from ischemia reperfusion injury by nitric oxide formation. This study has investigated the effect of ischemic preconditioning on hepatic microcirculation (HM), and the relationship between nitric oxide metabolism and HM in preconditioning.Liver ischemia-reperfusion injury (IRI) is a major complication of hemorrhagic shock, liver transplantation, and other liver surgeries.

It is one of the leading causes for post-surgery hepatic dysfunction, always leading to morbidity and mortality. Several strategies, such as low-temperature reperfusion and ischemic preconditioning, are useful for ameliorating liver IRI in animal models.Hepatic IR (ischemia reperfusion) injury is a commonly encountered obstacle in the post‐operative management of hepatic surgery.

Hepatic IR occurs during ‘Pringle maneuver’ for reduction of blood loss or during a brief period of cold storage followed by reperfusion of liver grafts.