Preconditioned Hyperbaric Oxygenation Protects the Liver against Ischemia-Reperfusion Injury in Rats

Yu, Shi; Chiu, Jen‐Hwey; Yang, Shiaw Der; Yu, Huichuan; Hsieh, Cheng Chu; Chen, Pei Ju; Lui, Wing Yiu; Wu, Chew Wun

doi:10.1016/j.jss.2005.04.025

Cited by 77 publications

(69 citation statements)

References 32 publications

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“…The I/R process involves changes ranging from microvascular alterations to the activation of neutrophils, platelets, Kupffer cells and sinusoidal endothelial cells [7][8][9] . Thus, the objective of the present study was to investigate the effect of the use of HBO after an I/R process.…”

Section: Introductionmentioning

confidence: 99%

Effects of hyperbaric oxygen therapy on the liver after injury caused by the hepatic ischemia-reperfusion process

et al. 2014

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PURPOSE:To evaluate the effects of hyperbaric oxygen on rats submitted to hepatic ischemia and reperfusion. METHODS:Twenty-three Wistar rats were divided at random into 3 groups: SHAM, rats submitted to surgical and anesthetic stress without induction of hepatic ischemia/reperfurion; I/R, rats submitted to total ischemia of the hepatic pedicle for 25 min followed by 5 min of reperfusion; HBOI/R, rats submitted to 60 min of hyperbaric oxygen therapy at a pressure of 2 absolute atmospheres immediately after the experimental protocol of ischemia/reperfusion. Hepatic function was evaluated by quantitation of serum alanine aminotranferase (ALT) and aspartate aminotransferase (AST), and by mitochondrial function through the determination of states 3 and 4 of mitochondrial respiration, respiratory control ratio (RCR) and mitochondrial swelling. Data were analyzed by the Mann-Whitney test, with the level of significance set at p <0.05. RESULTS:There was a significant difference in state 3 values for the SHAM group vs I/R and I/R vs IRHBO, in state 4 values for the SHAM group vs I/R; and in mitochondrial swelling for the SHAM groups vs I/RHBO, SHAM vs I/R, and IR vs I/RHBO. CONCLUSION:The use of hyperbaric oxygen after I/R improved in a relative manner both the production of energy and the effects on the mitochondrial wall.

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Section: Introductionmentioning

confidence: 99%

Effects of hyperbaric oxygen therapy on the liver after injury caused by the hepatic ischemia-reperfusion process

et al. 2014

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“…These induced events can cause cellular damage by oxidizing lipids, proteins, and deoxyribonucleic acid (DNA), which, in turn, induce apoptosis (Narkowicz et al 1993). In addition, theincreased in HBO 2 -treated cells and animals in which it functioned as a chaperone of oxidative-damaged proteins (Wada et al 1996;Dennog et al 1999;Shyu et al 2004;Yu et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Comparison of the effects of 40% oxygen and two atmospheric absolute air pressure conditions on stress-induced premature senescence of normal human diploid fibroblasts

Oh¹,

Lee²,

Lee³

et al. 2008

Cell Stress and Chaperones

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The pressure during hyperbaric oxygen treatment may increase oxygen toxicity via an augmented oxygen pressure in the gas. Nevertheless, only a few reports have been published on the effect of cells grown under 2 atmospheric absolute (ATA) pressure. To evaluate the effect of pressure on oxygen toxicity and to study effects in addition to oxygen toxicity, we designed an experiment to compare the effects of normobaric mild hyperoxia (NMH, 40% oxygen) and hyperbaric air condition (HA, air with 2 ATA) on human diploid fibroblasts (HDF) in a hyperbaric incubator. HDFs in both the NMH and the HA condition had a similar oxidative stress response and exhibited premature senescence. To investigate differences in gene profiling in cells grown in the NMH and HA conditions, samples from cells exposed to each condition were applied to microarrays. We found no expression difference in genes related to aging and deoxyribonucleic acid damage, but the expression of genes including cell adhesion, stress response, and transcription were significantly increased in fibroblasts that were responsive to pressure. Among 26 statistically reliable genes, the expression of apoptosis related genes such as ADAM22, Bax, BCL2L14, and UBD, as well as tumor suppressor-related genes like Axin2 and ATF, and also mitogen-activated protein kinase-related genes like mitogen-activated protein kinase kinase kinase 1, histamine receptor, and RAB24, were significantly changed in cells responsive to pressureinduced oxidative stress.

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“…From previous studies, it seems that in tissues like rat heart [6,10] and liver [12] normobaric or hyperbaric oxygen can induce delayed tolerance against ischemic damage in shorter exposure time. For example Esmaili et al showed in an in vivo model of rat regional heart ischemia that 120 or 180 minutes of nearly pure oxygen pretreatment could induce delayed heart ischemic tolerance, [23] but our study demonstrates that in kidney, like the central nervous system, [4,7] it takes longer to make tissue tolerant against ischemiareperfusion damage.…”

Section: Discussionmentioning

confidence: 99%

“…This activation can protect tissues from subsequent ischemia-reperfusion injuries. [12] Hyperoxia, regardless of its underlying mechanisms, is potentially clinically applicable. According to a Gurer et al study, it seems that there is no early phase of hyperoxia-induced ischemic tolerance in rat renal tissue in exposure times up to six hours [13] ; thus, in the present study, we sought to investigate whether hyperoxic (≥ 95% O 2 ) pretreatment can induce delayed renal protection and to study the impact of the duration of hyperoxic exposure on the possible protection.…”

Section: Introductionmentioning

confidence: 99%

Hyperoxia-Induced Protection against Rat's Renal Ischemic Damage: Relation to Oxygen Exposure Time

et al. 2009

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Preconditioned Hyperbaric Oxygenation Protects the Liver against Ischemia-Reperfusion Injury in Rats

Cited by 77 publications

References 32 publications

Effects of hyperbaric oxygen therapy on the liver after injury caused by the hepatic ischemia-reperfusion process

Effects of hyperbaric oxygen therapy on the liver after injury caused by the hepatic ischemia-reperfusion process

Comparison of the effects of 40% oxygen and two atmospheric absolute air pressure conditions on stress-induced premature senescence of normal human diploid fibroblasts

Hyperoxia-Induced Protection against Rat's Renal Ischemic Damage: Relation to Oxygen Exposure Time

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