Effect of hyperbaric hepatic hyperoxia on the liver of rats submitted to intermittent ischemia/reperfusion injury

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

doi:10.1590/s0102-86502014001300005

Cited by 4 publications

(2 citation statements)

References 25 publications

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“…Hyperbaric oxygen administration one day before I/R protected rat liver against subsequent I/R injury, and administration three days before I/R took no effects 16 . Several studies also supported that injury induced by I/R immediately after a short-time HBOT (less than 60 minutes) was more alleviated than I/R without HBOT, and this protection might mediate by HO-1 and be characterized by attenuated hepatocyte apoptosis and improvement of mitochondrial functions 17 - 20 . 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 .…”

Section: Hbot In Acute Liver Injurymentioning

confidence: 86%

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: 86%

Hyperbaric Oxygen Therapy in Liver Diseases

et al. 2018

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“… have reported that HBO pre‐conditioning protects the liver from mitochondrial dysfunction and decreases the levels of hepatic injury markers during the ischaemia and reperfusion processes. Although HBO pre‐conditioning has been proven to effectively eliminate ALT and to improve the expression of HO‐1, it cannot decrease the levels of aspartate aminotransferase (AST) and malondialdehyde (MDA) . Notably, the time of HBO exposure is also critical for determining whether the effects in hepatic IR models are beneficial or deleterious .…”

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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