Ischemic Preconditioning and Intermittent Clamping Increase the Tolerance of Fatty Liver to Hepatic Ischemia-Reperfusion Injury in the Rat

Saidi, Reza F.; Chang, Jennifer; Brooks, S E; Nalbantoglu, ILKe; Adsay, Volkan; Jacobs, Michael J.

doi:10.1016/j.transproceed.2007.09.044

Cited by 23 publications

(33 citation statements)

References 21 publications

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“…31 The lung is frequently damaged by proinflammatory mediators released from the injured liver after liver IR, as the lungs are the first capillary bed that is reached by the blood after leaving the hepatic circulation. [3][4][5][6][7] was recently found to act as a potent proinflammatory cytokine and participated in the development of systemic inflammatory response, when it was released into the extracellular environment. 32,33 HMGB1 was also found to be involved in many other types of ALI, such as endotoxin, ventilator, and hemorrhage-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, HMGB1 was reported to be released from macrophages and monocytes after exposure to proinflammatory cytokines. [36][37][38][39] Given that proinflammatory cytokines might be transported to lung tissue after liver I/R injury, [3][4][5][6][7] lung cells might be activated by proinflammatory cytokines and then release HMGB1. 40,41 For this reason, we examined HMGB1 mRNA in the lung tissue, and found that HMGB1 mRNA was significantly increased in the lung tissue after liver I/R injury.…”

Section: Discussionmentioning

confidence: 99%

“…After 90 min of warm ischemia, the clamps were removed to allow reperfusion for 18 h. The rats received approximately 5 ml of NS intraperitoneally before closure of the incision. 6,7,29 And, the rats were allowed to regain consciousness during TLR4-mediated ALI after liver I/R injury Z Yang et al reperfusion period. The sham procedure was performed identically without vascular occlusion.…”

Section: Experimental Animals and Groupsmentioning

confidence: 99%

“…Since the lungs are the first capillary bed that is reached by the blood after leaving the hepatic circulation, one proposed mechanism is that ALI may be induced by proinflammatory mediators released from the injured liver into system circulation. [3][4][5][6][7] High-mobility group box protein 1 (HMGB1), originally identified as a DNA-binding protein, is a proximal trigger that is sufficient to induce the release of other cytokines classically associated with mediating inflammatory responses, including tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), and interleukin-6 (IL-6). 8 Interestingly, HMGB1 was rapidly mobilized and released into system circulation by hepatocytes in the setting of liver I/R injury.…”

mentioning

confidence: 99%

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TLR4 as receptor for HMGB1-mediated acute lung injury after liver ischemia/reperfusion injury

Yang

Deng

et al. 2013

Laboratory Investigation

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Acute lung injury (ALI) frequently occurs after liver transplantation and major liver surgery. Proinflammatory mediators released by damaged liver after liver ischemia/reperfusion (I/R) injury might contribute to this form of ALI, but the underlying mechanisms have not been well characterized. High-mobility group box protein 1 (HMGB1), a recently identified proinflammatory cytokine, was found to be significantly higher in the serum after liver I/R injury. This study investigated whether HMGB1 was involved as a stimulating factor, and whether its downstream Toll-like receptor 4 (TLR4), p38 mitogen-activated protein kinase (p38MAPK), and activator protein-1 (AP-1) signaling pathways act as mediators in the development of liver I/R injury-induced ALI. Extensive ALI and lung inflammation was induced in a rat model of liver I/R injury. Serum HMGB1 was significantly higher after liver I/R injury, and more importantly, expression of HMGB1 mRNA and protein in the lung tissue was also significantly increased. We further found that liver I/R injury enhanced the expression of TLR4 mRNA and protein, and the activity of p38MAPK and AP-1 in the lung tissue. Inhibition of TLR4 expression in the lung tissue by infection with pGCSIL-GFP-lentivirus-expressing small hairpin RNAs targeting the TLR4 gene (TLR4-shRNA lentivirus) significantly attenuated ALI, lung inflammation, and activity of p38MAPK and AP-1 in the lung tissue. These findings indicate that HMGB1 might contribute to the underlying mechanism for liver I/R injuryinduced ALI and that its downstream TLR4, p38MAPK, and AP-1 signaling pathways are potentially important mediators in the development of ALI.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Experimental Animals and Groupsmentioning

confidence: 99%

mentioning

confidence: 99%

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TLR4 as receptor for HMGB1-mediated acute lung injury after liver ischemia/reperfusion injury

Yang

Deng

et al. 2013

Laboratory Investigation

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“…IPC has been proven to have a protective effect on many tissues, as well as an effect on attenuating postischemic cardiac dysfunction [1][2][3]. In 1991, the adenosine A1 receptor was found to trigger ischemic preconditioning in rabbit hearts [4], and it has now been shown that this preconditioning protection is receptor mediated [5].…”

Section: Introductionmentioning

confidence: 99%

Landiolol does not enhance the effect of ischemic preconditioning in isolated rat hearts

Katoh

Okada

et al. 2010

J Anesth

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Translational strategies to minimize transfusion requirement in liver surgery and transplantation: Targeting ischemia‐reperfusion injury

Saidi

Kenari

2014

Transfusion‐Free Medicine and Surgery

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Ischemic Preconditioning and Intermittent Clamping Increase the Tolerance of Fatty Liver to Hepatic Ischemia-Reperfusion Injury in the Rat

Cited by 23 publications

References 21 publications

TLR4 as receptor for HMGB1-mediated acute lung injury after liver ischemia/reperfusion injury

TLR4 as receptor for HMGB1-mediated acute lung injury after liver ischemia/reperfusion injury

Landiolol does not enhance the effect of ischemic preconditioning in isolated rat hearts

Translational strategies to minimize transfusion requirement in liver surgery and transplantation: Targeting ischemia‐reperfusion injury

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