Effect of dexmedetomidine on hepatic ischemia–reperfusion injury in the setting of adult living donor liver transplantation

Fayed, Nirmeen A.; Sayed, Eman; Saleh, Sherif; Ehsan, Nermen A.; Elfert, Asem

doi:10.1111/ctr.12713

Cited by 37 publications

(36 citation statements)

References 94 publications

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“…The carbonic anhydrase inhibitor acetazolamide protects against cold hepatic IR injury by decreasing the MAPK signal and up‐regulating eNOS . Dexmedetomidine alleviates hepatic IR injury by suppressing intercellular adhesion molecule 1 and improving post‐operative liver function . Additionally, Chinese medicines have also been shown to conserve liver function in LT models.…”

Section: Pre‐conditions For Lt To Eliminate Cold Hepatic Ir Injurymentioning

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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Section: Pre‐conditions For Lt To Eliminate Cold Hepatic Ir Injurymentioning

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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“…Hepatic ischaemia–reperfusion injury is the major cause of liver injury, which is of clinical concern, especially following diverse hepatectomy and living donor liver transplantation. 1 Ischaemia–reperfusion injury, which involves complex inflammatory pathways, is a significant cause of liver damage and an important factor in a variety of diseases, injuries, and following transplantation surgery. 2 , 3 As liver ischaemia ends and reperfusion begins, oxidative stress is one of the first changes to take place and it regulates an oxidative stress-mediated apoptosis signalling pathway.…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-gallate protects against hepatic ischaemia–reperfusion injury by reducing oxidative stress and apoptotic cell death

et al. 2016

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ObjectiveTo investigate the protective effects of epigallocatechin-3-gallate (EGCG), a major polyphenol source in green tea, against hepatic ischaemia–reperfusion injury in mice.MethodsThe partial hepatic ischaemia–reperfusion injury model was created by employing the hanging-weight method in C57BL/6 male mice. EGCG (50 mg/kg) was administered via an intraperitoneal injection 45 min before performing the reperfusion. A number of markers of inflammation, oxidative stress, apoptosis and liver injury were measured after the ischaemia–reperfusion injury had been induced.ResultsThe treatment groups were: sham-operated (Sham, n = 10), hepatic ischaemia–reperfusion injury (IR, n = 10), and EGCG with ischaemia–reperfusion injury (EGCG-treated IR, n = 10). Hepatic ischaemia–reperfusion injury increased the levels of biochemical and histological markers of liver injury, increased the levels of malondialdehyde, reduced the glutathione/oxidized glutathione ratio, increased the levels of oxidative stress and lipid peroxidation markers, decreased B-cell lymphoma 2 levels, and increased the levels of Bax, cytochrome c, cleaved caspase-3, and cleaved caspase-9. Pretreatment with EGCG ameliorated all of these changes.ConclusionThe antioxidant and antiapoptotic effects of EGCG protected against hepatic ischaemia–reperfusion injury in mice.

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“…It applies its antiinflammatory effects by lowering the serum levels of catecholamines and releasing IL-10 and TNF-α (15). Fayed et al (10)found that DEX injection during anesthesia and after the completion of surgery for patients undergoing liver transplantation (LD Liver Transplantation) has a protective effect on hepatic ischemia-reperfusion injury (IRI), reduces the serum levels of lactate by facilitating the reperfusion of the transplanted tissue, facilitates the weaning and extubation of these patients and reduces their length of stay in ICU. In addition to the mechanisms mentioned in previous studies, other mechanisms of this drug in reducing the tissue ischemia are as follows:…”

Section: Discussionmentioning

confidence: 99%

“…Administration of DEX exerted protective effects against hepatic ischemiareperfusion injury (IRI) in adult living donor liver transplantation. It results in suppression of ICAM-2, improved scores of histopathalogic assessment, and augmentation of live function tests after surgery (10). Patients with liver transplantation, have a high risk of post-surgery delirium.…”

Section: α2-mentioning

confidence: 99%

Use of Dexmedetomidine in Liver Disease: A Systematic Review and Meta-Analysis

et al. 2019

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Introduction: Dexmedetomidine is a sedative and analgesic medication that is frequently used postoperatively in children after liver transplantation, hepatic dysfunction and liver failure. Objectives: The aim of this systematic review was to determine the role of dexmedetomidine in liver disease. Methods: We systematically reviewed the literature from PubMed, Embase, Scopus, ProQuest, Web of Science, and The Cochrane Library from January 1980 to June 2019. The search strategy included a combination of Mesh and free keywords such as liver transplantation, liver diseases, liver failure, and dexmedetomidine. Results: From a total of 741 articles, 7 studies were included in this systematic review. In the selected studies, a total of 218 patients in the control and treatment groups were studied. Based on the Fixed effect model, MAP changes in the intervention group were 1.89 units less than the control group, which was not statistically significant (pooled mean difference =-1.89, 95% CI:-6.28 to 2.5, P value = 0.39). Conclusions: DEX injection prior to anesthesia potentially had a protective effect on liver and intestinal function during hepatectomy with vascular occlusion.

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Effect of dexmedetomidine on hepatic ischemia–reperfusion injury in the setting of adult living donor liver transplantation

Abstract: Dexmedetomidine exerted protective effects against hepatic IRI during adult LDLiver transplantation, as indicated by suppression of ICAM-1, better scores of histopathological assessment, and augmented post-operative liver function tests.

Cited by 37 publications

References 94 publications

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

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

Epigallocatechin-3-gallate protects against hepatic ischaemia–reperfusion injury by reducing oxidative stress and apoptotic cell death

Use of Dexmedetomidine in Liver Disease: A Systematic Review and Meta-Analysis

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