Hyperoxic preconditioning in partial liver ischemia

Margarido, Maria Rita; Silveira, Marina Rodrigues Garcia da; Vanni, José Carlos; Féres, Omar; Castro‐e‐Silva, Orlando

doi:10.1590/s0102-86502014001300004

Cited by 3 publications

(3 citation statements)

References 22 publications

(25 reference statements)

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“…Yet the protection of HBOT in hepatic I/R injury still remains controversial. Margarido, M. R. et al 15 reported that HBOT during the ischemic period did not prevent the installation of mitochondrial edema induced by hepatic I/R. Moreover, HBOT preconditioning gains more controversies.…”

Section: Hbot In Acute Liver Injurymentioning

confidence: 99%

“…However, a 120-minute HBOT immediately before I/R surgery did not protect against injury, with higher liver malondialdehyde (MDA) and nitric oxide (NO) levels compared to the 60-minute HBOT 18 . Besides, two studies showed that HBOT preconditioning for 60 and 90 minutes even aggravated liver I/R injury via enhanced neutrophil accumulation 15 , 21 . No effects on mitochondrial functions by a 60-minutes HBOT preconditioning were also reported 22 .…”

Section: Hbot In Acute Liver Injurymentioning

confidence: 99%

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Hyperbaric Oxygen Therapy in Liver Diseases

et al. 2018

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Hyperbaric oxygen therapy (HBOT) is an efficient therapeutic option to improve progress of lots of diseases especially hypoxia-related injuries, and has been clinically established as a wide-used therapy for patients with carbon monoxide poisoning, decompression sickness, arterial gas embolism, problematic wound, and so on. In the liver, most studies positively evaluated HBOT as a potential therapeutic option for liver transplantation, acute liver injury, nonalcoholic steatohepatitis, fibrosis and cancer, especially for hepatic artery thrombosis. This might mainly attribute to the anti-oxidation and anti-inflammation of HBOT. However, some controversies are existed, possibly due to hyperbaric oxygen toxicity. This review summarizes the current understandings of the role of HBOT in liver diseases and hepatic regeneration. Future understanding of HBOT in clinical trials and its in-depth mechanisms may contribute to the development of this novel adjuvant strategy for clinical therapy of liver diseases.

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Section: Hbot In Acute Liver Injurymentioning

confidence: 99%

Section: Hbot In Acute Liver Injurymentioning

confidence: 99%

Hyperbaric Oxygen Therapy in Liver Diseases

et al. 2018

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“…. The protective effects of liver injury in HBO pre‐conditioning remain controversial because this pre‐treatment does not increase hepatocellular energy metabolism or repair mitochondrial oedema after hepatic IR . Intriguingly, Losada et al .…”

Section: Pre‐treatments With Un‐physiological Oxygen Content Before Hmentioning

confidence: 99%

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

Hu¹

2017

J Cellular Molecular Medi

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The liver, the largest organ with multiple synthesis and secretion functions in mammals, consists of hepatocytes and Kupffer, stem, endothelial, stellate and other parenchymal cells. Because of early and extensive contact with the external environment, hepatic ischaemia reperfusion (IR) may result in mitochondrial dysfunction, autophagy and apoptosis of cells and tissues under various pathological conditions. Because the liver requires a high oxygen supply to maintain normal detoxification and synthesis functions, it is extremely susceptible to ischaemia and subsequent reperfusion with blood. Consequently, hepatic IR leads to acute or chronic liver failure and significantly increases the total rate of morbidity and mortality through multiple regulatory mechanisms. An increasing number of studies indicate that mitochondrial structure and function are impaired after hepatic IR, but that the health of liver tissues or liver grafts can be effectively rescued by attenuation of mitochondrial dysfunction. In this review, we mainly focus on the subsequent therapeutic interventions related to the conservation of mitochondrial function involved in mitigating hepatic IR injury and the potential mechanisms of protection. Because mitochondria are abundant in liver tissue, clarification of the regulatory mechanisms between mitochondrial dysfunction and hepatic IR should shed light on clinical therapies for alleviating hepatic IR‐induced injury.

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miR-155 Aggravates Liver Ischemia/reperfusion Injury by Suppressing SOCS1 in Mice

Tan

Jiang

et al. 2018

Transplantation Proceedings

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Hyperoxic preconditioning in partial liver ischemia

Cited by 3 publications

References 22 publications

Hyperbaric Oxygen Therapy in Liver Diseases

Hyperbaric Oxygen Therapy in Liver Diseases

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

miR-155 Aggravates Liver Ischemia/reperfusion Injury by Suppressing SOCS1 in Mice

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