Assessment of Oxidative Stress in a Pancreatic Warm Ischemia-Reperfusion Model

Balén, E; Ferrer, J.; Zazpe, C.; Gourichon, David; Sáez, María José Pérez; Herrera, Javier; Lera, José Miguel

doi:10.1016/s0041-1345(97)01407-3

Cited by 3 publications

(3 citation statements)

References 2 publications

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“…In concordance with others [7, 16], we have shown a significant rise in amylase and lipase concentration in serum after IR. Melatonin abolished the increase of both enzymes after IR especially when the antioxidant was administered before ischemia.…”

Section: Discussionsupporting

confidence: 93%

“…Different experimental studies have shown that the induction of oxidative stress is the underlying mechanism of IR injury in pancreas [5–7]. Sanfey et al [8] showed that the treatment with enzymatic antioxidants [superoxide dismutase (SOD) and catalase (CAT)] reduces the histological signs of tissue damage (glandular edema) induced by IR in pancreas.…”

Section: Introductionmentioning

confidence: 99%

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Melatonin reduces apoptosis and necrosis induced by ischemia/reperfusion injury of the pancreas

Muñoz-Casares¹,

Padillo²,

Briceño³

et al. 2006

Journal of Pineal Research

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The pancreas is highly susceptible to the oxidative stress induced by ischemia/reperfusion (IR) injury leading to the generation of acute pancreatitis. Melatonin has been shown to be useful in the prevention of the damage by ischemia‐reperfusion in liver, brain, myocardium, gut and kidney. The aim of the study was to evaluate the cytoprotective properties of melatonin against injury induced by IR in pancreas. The obstruction of gastro‐duodenal and inferior splenic arteries induced pancreatic IR in male Wistar rats. Melatonin was intraperitoneally administered before or/and after IR injury. The animals were killed at 24 and 48 hr after reperfusion and there were evaluated parameters of oxidative stress (lipoperoxides, superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione), glandular endocrine and exocrine function (lipase, amylase, insulin) and cell injury (apoptosis and necrosis). The IR induced a marked enhancement of oxidative stress and impaired pancreatic function. The histological analysis showed that IR induced acute pancreatitis with the accumulation of inflammatory infiltrate, disruption of tissue structure, cell necrosis and hemorrhage. Melatonin administration before or after pancreatic IR prevented all tissue markers of oxidative stress, biochemical and histological signs of apoptosis and necrosis, and restored glandular function. No histological signs of pancreatitis were observed 48 hr after reperfusion in 80% of the animals treated with melatonin, with only a mild edematous pancreatitis being observed in the remaining rats. Preventive or therapeutic administration of melatonin protected against the induction of oxidative stress and tissue injury, and restored cell function in experimental pancreatic IR in rats.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Melatonin reduces apoptosis and necrosis induced by ischemia/reperfusion injury of the pancreas

Muñoz-Casares¹,

Padillo²,

Briceño³

et al. 2006

Journal of Pineal Research

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“…Many factors lead to the generation of oxygen-derived free radicals during the reperfusion period, including endothelial dysfunction, endogenous enzymes, and leucocyte recruitment [ 6 ]. The induction of oxidative stress is the major mechanism of I/R injury in pancreas transplantation [ 7 ]. Free radicals and proinflammatory cytokines could damage the cellular membrane and subcellular structures, which contain large amounts of phospholipids and protein, resulting in lipid peroxidation and subsequent structural and metabolic alterations, leading to cell apoptosis and necrosis.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen‐Rich Saline Protects against Ischemia/Reperfusion Injury in Grafts after Pancreas Transplantations by Reducing Oxidative Stress in Rats

Luo

Cheng

Ren

et al. 2015

Mediators of Inflammation

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Purpose. This study aimed to investigate the therapeutic potential of hydrogen-rich saline on pancreatic ischemia/reperfusion (I/R) injury in rats. Methods. Eighty heterotopic pancreas transplantations (HPT) were performed in syngenic rats. The receptors were randomized blindly into the following three groups: the HPT group and two groups that underwent transplantation and administration of hydrogen-rich saline (HS, >0.6 mM, 6 mL/kg) or normal saline (NS, 6 mL/kg) via the tail vein at the beginning of reperfusion (HPT + HS group, HPT + NS group). Samples from the pancreas and blood were taken at 12 hours after reperfusion. The protective effects of hydrogen-rich saline against I/R injury were evaluated by determining the changes in histopathology and measuring serological parameters, oxidative stress-associated molecules, and proinflammatory cytokines. Results. Administration of hydrogen-rich saline produced notable protection against pancreatic I/R injury in rats. Histopathological improvements and recovery of impaired pancreatic function were observed. In addition, TNF-α, IL-1β, and IL-6 were reduced markedly in the HPT + HS group. Additionally, there were noticeable inhibitory effects on the pancreatic malondialdehyde level and considerable recruitment of SOD and GPx, which are antioxidants. Conclusion. Hydrogen-rich saline treatment significantly attenuated the severity of pancreatic I/R injury in rats, possibly by reducing oxidative stress and inflammation.

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Current State of Pancreas Preservation and Implications for DCD Pancreas Transplantation

2013

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One of the main factors limiting potential uptake of pancreas transplantation, particularly in the United Kingdom, is the shortage of grafts. There has therefore been a recent expansion, particularly in the United Kingdom, in the utilization of grafts from donation after cardiac death (DCD) donors. These grafts are subjected to a greater ischemic insult and are arguably at higher risk of poor functional outcome. Although conventional preservation techniques may be adequate for donation after brain death (DBD) and low-risk DCD pancreases, as the number of DCD pancreas transplants increase and the threshold for rejecting organs decreases, the importance of optimal preservation techniques is going to increase. Over recent years, there have been significant advances in preservation techniques for DCD kidneys, improving the outcome of these marginal grafts. However, the use of such techniques for pancreas preservation is extremely limited and mainly historical. This overview describes the background and results of the established method of pancreas preservation for DBD, namely, cold static storage, and describes the use of the two-layer method. It also reviews pulsatile machine perfusion and normothermic perfusion for pancreas preservation techniques, which have shown promise in the preservation of DCD kidney grafts. The use of these techniques in pancreas preservation is predominantly historical but warrants reevaluation as to the feasibility of applying these techniques to DCD pancreas grafts not only for preservation but also for viability assessment. Further areas for development of pancreas preservation are discussed.

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Assessment of Oxidative Stress in a Pancreatic Warm Ischemia-Reperfusion Model

Cited by 3 publications

References 2 publications

Melatonin reduces apoptosis and necrosis induced by ischemia/reperfusion injury of the pancreas

Melatonin reduces apoptosis and necrosis induced by ischemia/reperfusion injury of the pancreas

Hydrogen‐Rich Saline Protects against Ischemia/Reperfusion Injury in Grafts after Pancreas Transplantations by Reducing Oxidative Stress in Rats

Current State of Pancreas Preservation and Implications for DCD Pancreas Transplantation

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