The Role of Oxygen-free Radicals in Ischemic Tissue Injury in Island Skin Flaps

Manson, Paul N.; Anthenelli, Robert M.; Im, Michael J.; Bulkley, Gregory B.; Hoopes, John E.

doi:10.1097/00000658-198307000-00017

Cited by 234 publications

(75 citation statements)

References 8 publications

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“…Reperfusion injury mediated by oxygen free radicals has been reported in heart (7), brain (5), intestine (8), liver (9), pancreas (10), kidney (6), and skin (11). Whereas reperfusion injury has also been reported after reexpansion of atelectatic lung (12) or reperfusion of a mechanically occluded pulmonary artery ( 13), investigators have generally felt that the lung is relatively immune from reperfusion injury because oxidative metabolism does not decrease and ATP levels do not fall until alveolar Po2 drops below 1 mmHg (14).…”

Section: Introductionmentioning

confidence: 99%

Role of reactive oxygen species in reperfusion injury of the rabbit lung.

et al. 1989

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We have developed a model of reperfusion injury in Krebs buffer-perfused rabbit lungs, characterized by pulmonary vasoconstriction, microvascular injury, and marked lung edema formation. During reperfusion there was a threefold increase in lung superoxide anion (0°) production, as measured by in vivo reduction of nitroblue tetrazolium, and a twofold increase in the release of 02 into lung perfusate, as measured by reduction of succinylated ferricytochrome c. Injury could be prevented by the xanthine oxidase inhibitor allopurinol, the 02 scavenger SOD, the hydrogen peroxide scavenger catalase, the iron chelator deferoxamine, or the thiols dimethylthiourea or Nacetylcysteine. The protective effect of SOD could be abolished by the anion channel blocker 4,4'-diisothiocyano-2,2'-stilbene disulfonic acid, indicating that SOD consumes 02 in the extracellular medium, thereby creating a concentration gradient favorable for rapid diffusion of 02 out of cells. Our results extend information about the mechanisms of reperfusion lung injury that have been assembled by studies in other organs, and offer potential strategies for improved organ preservation, for treatment of reperfusion injury after pulmonary thromboembolectomy, and for explanation and therapy of many complications of pulmonary embolism.

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Section: Introductionmentioning

confidence: 99%

Role of reactive oxygen species in reperfusion injury of the rabbit lung.

et al. 1989

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“…8) Numerous studies have successfully applied antioxidants for protection against flap necrosis and other related complications. 7,[9][10][11][12][13][14] Various natural antioxidants significantly improve flap survival. 11,[15][16][17] Strategic therapeutic approaches with antioxidants have been used to reduce the oxidative stress effects of diabetes.…”

mentioning

confidence: 99%

Effects of Systemic Chlorogenic Acid on Random-Pattern Dorsal Skin Flap Survival in Diabetic Rats

Bağdaş

Etoz

Inan

et al. 2014

Biological & Pharmaceutical Bulletin

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There has been considerable interest in understanding the effects of antioxidants in flap survival during diabetes. Previous studies showed that chlorogenic acid (CGA) exhibits potent antioxidant effects. We aimed to determine the effects of systemic CGA treatment on skin flap survival in an experimental random-pattern dorsal skin flap model in diabetic rats. Twenty-eight male Wistar rats were divided into four groups: phosphate buffered saline (PBS)-treated or CGA-treated nondiabetic rats, PBS-treated or CGA-treated diabetic rats. Diabetes was induced by streptozotocin (45 mg/kg). Caudally based bipedicled dorsal skin flaps were elevated. CGA (100 mg/kg) or PBS (mL/kg; as vehicle) was administered intraperitoneally once daily. On postoperative day 7, flap survival, regional blood perfusion and microangiography were evaluated. The malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and nitric oxide (NO) levels were evaluated from the flap tissue. Capillary density and vascular endothelial growth factor (VEGF) expression were assessed. Harmful effects of diabetes on flap survival were observed. CGA attenuated these effects and allowed greater survival and blood perfusion. CGA decreased MDA and NO levels and increased GSH and SOD levels. CGA elevated capillary density and VEGF expression. This study showed that peripherally administered CGA significantly improved flap survival in diabetic and nondiabetic rats.Key words antioxidant; chlorogenic acid; diabetes; dorsal skin flap; flap survival; oxidative stress Skin flaps are widely used in the repair of local tissue loss and the reconstruction of several tissue defects. Flap necrosis is frequently observed in flap tissues in the postoperative period and is an unwanted effect of healing. Many factors are known to play a role in this major complication such as ischemia, inadequate blood flow and disturbed venous drainage.

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“…Free-radical scavengers can convert toxic ROS into common and relatively harmless end products. Many antioxidants, such as superoxide dismutase (Manson et al, 1983), grape seed proanthocyanidin extract (Karaaslan et al, 2010), and melatonin (Gurlek et al, 2006), have been used to limit tissue injury. However, strategies that decrease oxidative status intensively may produce unwanted side effects because at low levels ROS function as signaling molecules to regulate apoptosis, cell proliferation and differentiation.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of hydrogen-rich saline on ischemia/reperfusion injury in rat skin flap

Zhao

Wang

Qin

et al. 2013

J. Zhejiang Univ. Sci. B

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Abstract:Objective: Skin damage induced by ischemia/reperfusion (I/R) is a multifactorial process that often occurs in plastic surgery. The mechanisms of I/R injury include hypoxia, inflammation, and oxidative damage. Hydrogen gas has been reported to alleviate cerebral I/R injury by acting as a free radical scavenger. Here, we assessed the protective effect of hydrogen-rich saline (HRS) on skin flap I/R injury. Methods: Abdominal skin flaps of rats were elevated and ischemia was induced for 3 h; subsequently, HRS or physiological saline was administered intraperitoneally 10 min before reperfusion. On postoperative Day 5, flap survival, blood perfusion, the accumulation of reactive oxygen species (ROS), and levels of cytokines were evaluated. Histological examinations were performed to assess inflammatory cell infiltration. Results: Skin flap survival and blood flow perfusion were improved by HRS relative to the controls. The production of malondialdehyde (MDA), an indicator of lipid peroxidation, was markedly reduced. A multiplex cytokine assay revealed that HRS reduced the elevation in the levels of inflammatory cytokines, chemokines and growth factors, with the exception of RANTES (regulated on activation, normal T-cell expressed and secreted) growth factor. HRS treatment also reduced inflammatory cell infiltration induced by I/R injury. Conclusions: Our findings suggest that HRS mitigates I/R injury by decreasing inflammation and, therefore, has the potential for application as a therapy for improving skin flap survival.

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The Role of Oxygen-free Radicals in Ischemic Tissue Injury in Island Skin Flaps

Cited by 234 publications

References 8 publications

Role of reactive oxygen species in reperfusion injury of the rabbit lung.

Role of reactive oxygen species in reperfusion injury of the rabbit lung.

Effects of Systemic Chlorogenic Acid on Random-Pattern Dorsal Skin Flap Survival in Diabetic Rats

Protective effect of hydrogen-rich saline on ischemia/reperfusion injury in rat skin flap

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