Both Ischemic and Pharmacological Preconditioning Decrease Hepatic Leukocyte/Endothelial Cell Interactions 1

Howell, James G.; Zibari, Gazi B.; Brown, Mark F.; Burney, Donna; Sawaya, David; Olinde, J. G.; Granger, D. Neil; McDonald, John C.

doi:10.1097/00007890-200001270-00017

Cited by 38 publications

(33 citation statements)

References 12 publications

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“…In fact, over the examined time range (0 -50 min), hepatic ischemia time closely correlated with ALT and AST levels (R 2 ϭ 0.941, P Ͻ 0.001, R 2 ϭ 0.957, P Ͻ 0.001, respectively). Furthermore, our AST and ALT results compared with the results of others using relatively similar ischemia times in rodents (19,36). Taken together, these results provide feasibility of using portal triad occlusion via a hanging-weight system for inducing highly reproducible and time-dose-dependent hepatic injury.…”

Section: Technique Of Portal Triad Occlusionsupporting

confidence: 75%

Use of a hanging-weight system for liver ischemic preconditioning in mice

Hart

Much²,

Köhler³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Hart ML, Much C, Kö hler D, Schittenhelm J, Gorzolla IC, Stahl GL, Eltzschig HK. Use of a hanging-weight system for liver ischemic preconditioning in mice. Am J Physiol Gastrointest Liver Physiol 294: G1431-G1440, 2008. First published April 24, 2008 doi:10.1152/ajpgi.00083.2008 represents a powerful experimental strategy to identify novel molecular targets to attenuate hepatic injury during ischemia. As a result, murine studies of hepatic IP have become an important field of research. However, murine IP is technically challenging, and experimental details can alter the results. Therefore, we systematically tested a novel model of hepatic IP by using a hanging-weight system for portal triad occlusion. This system has the benefit of applying intermittent hepatic ischemia and reperfusion without manipulation of a surgical clamp or suture, thus minimizing surgical trauma. Systematic evaluation of this model revealed a close correlation of hepatic ischemia time with liver damage as measured by alanine (ALT) and aspartate (AST) aminotransferase serum levels. Using different numbers of IP cycles and times intervals, we found optimal liver protection with four cycles of 3 min ischemia/3 min reperfusion as measured by ALT, AST, lactate dehydrogenase, and interleukin-6. Similarly, ischemiaassociated increases in hepatic infarct size, neutrophil infiltration, and histological injury were maximally attenuated with the above regimen. To demonstrate transcriptional consequences of liver IP, we isolated RNA from preconditioned liver and confirmed transcriptional modulation of known target genes (equilibrative nucleoside transporters, acute-phase complement genes). Taken together, these studies confirm highly reproducible liver injury and protection by IP when using the hanging-weight system for hepatic ischemia and intermittent reperfusion. Further studies of murine IP may consider this technique.

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Section: Technique Of Portal Triad Occlusionsupporting

confidence: 75%

Use of a hanging-weight system for liver ischemic preconditioning in mice

Hart

Much²,

Köhler³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Adenosine has been shown to inhibit neutrophil oxidative metabolism and adhesion to endothelial cells, to increase membrane stability and energy production by promoting glucose transport, and to reduce Ca 2ϩ influx through the activation of ATP-dependent K ϩ channels [72][73][74][75]. However, the role of all biochemical effects in adenosine-afforded protection is yet to be defined.…”

Section: Protective Mechanisms Of Early Ischemic Preconditioningmentioning

confidence: 99%

Microvascular dysfunction induced by reperfusion injury and protective effect of ischemic preconditioning

Cutrn

Perrelli

Cavalieri

et al. 2002

Free Radical Biology and Medicine

151

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Abstract-Hepatic ischemia/reperfusion injury has immediate and deleterious effects on the outcome of patients after liver surgery. The precise mechanisms leading to the damage have not been completely elucidated. However, there is substantial evidence that the generation of oxygen free radicals and disturbances of the hepatic microcirculation are involved in this clinical syndrome. Microcirculatory dysfunction of the liver seems to be mediated by sinusoidal endothelial cell damage and by the imbalance of vasoconstrictor and vasodilator molecules, such as endothelin (ET), reactive oxygen species (ROS), and nitric oxide (NO). This may lead to no-reflow phenomenon with release of proinflammatory cytokines, sinusoidal plugging of neutrophils, oxidative stress, and as an ultimate consequence, hypoxic cell injury and parenchymal failure. An inducible potent endogenous mechanism against ischemia/reperfusion injury has been termed ischemic preconditioning. It has been suggested that preconditioning could inhibit the effects of different mediators involved in the microcirculatory dysfunction, including endothelin, tumor necrosis factor-␣, and oxygen free radicals. In this review, we address the mechanisms of liver microcirculatory dysfunction and how ischemic preconditioning could help to provide new surgical and/or pharmacological strategies to protect the liver against reperfusion damage.

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“…The underlying mechanism is thought to rely on the modification of gene expression resulting in protein production as its effectors [110] . Various substances have been implicated as key effectors in liver IPC including adenosine [111][112][113][114] , protein kinase C [115][116][117] , NO [118][119][120][121] , heatshock proteins [122,123] , tyrosine kinases [124] , MAPKs [117] , oxidative stress [125,126] and NF-κB [127,128] . The beneficial effects of IPC on the liver following IRI include decrease in severity of liver necrosis [129] , antiapoptotic effects [130] , preservation of liver microcirculation [131,132] and improvement in survival rate [119] , and more recently, its role in liver regeneration is currently being evaluated.…”

Section: Ischaemic Preconditioning In Liver Regenerationmentioning

confidence: 99%

Role of ischaemic preconditioning in liver regeneration following major liver resection and transplantation

Gomez¹

2007

WJG

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Liver ischaemic preconditioning (IPC) is known to protect the liver from the detrimental effects of ischaemicreperfusion injury (IRI), which contributes significantly to the morbidity and mortality following major liver surgery. Recent studies have focused on the role of IPC in liver regeneration, the precise mechanism of which are not completely understood. This review discusses the current understanding of the mechanism of liver regeneration and the role of IPC in this setting. Relevant articles were reviewed from the published literature using the Medline database. The search was performed using the keywords "liver", "ischaemic reperfusion", "ischaemic preconditioning", "regeneration", "hepatectomy" and "transplantation". The underlying mechanism of liver regeneration is a complex process involving the interaction of cytokines, growth factors and the metabolic demand of the liver. IPC, through various mediators, promotes liver regeneration by up-regulating growthpromoting factors and suppresses growth-inhibiting factors as well as damaging stresses. The increased understanding of the cellular mechanisms involved in IPC will enable the development of alternative treatment modalities aimed at promoting liver regeneration following major liver resection and transplantation.

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Both Ischemic and Pharmacological Preconditioning Decrease Hepatic Leukocyte/Endothelial Cell Interactions 1

Cited by 38 publications

References 12 publications

Use of a hanging-weight system for liver ischemic preconditioning in mice

Use of a hanging-weight system for liver ischemic preconditioning in mice

Microvascular dysfunction induced by reperfusion injury and protective effect of ischemic preconditioning

Role of ischaemic preconditioning in liver regeneration following major liver resection and transplantation

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