Protective effects of hyperbaric oxygen and iloprost on ischemia/reperfusion-induced lung injury in a rabbit model

Bozok, Şahin; İlhan, Gökhan; Yılmaz, Yakup; Dökümcü, Z; Tümkaya, Levent; Karamustafa, Hakan; Karakişi, Sedat Ozan; Ergene, Şaban; Şener, Ebru

doi:10.1186/2047-783x-17-14

Cited by 18 publications

(18 citation statements)

References 33 publications

(37 reference statements)

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“…The experimental procedure for I/R-induced ALI was conducted according to published protocols with minor modifications 39-41 . Rats were randomized into sham-operated, and lung I/R groups with or without rhMG53 treatment.…”

Section: Methodsmentioning

confidence: 99%

Treatment of acute lung injury by targeting MG53-mediated cell membrane repair

et al. 2014

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Injury to lung epithelial cells has a role in multiple lung diseases. We previously identified mitsugumin 53 (MG53) as a component of the cell membrane repair machinery in striated muscle cells. Here we show that MG53 also has a physiological role in the lung and may be used as a treatment in animal models of acute lung injury. Mice lacking MG53 show increased susceptibility to ischemia-reperfusion and over-ventilation induced injury to the lung when compared with wild type mice. Extracellular application of recombinant human MG53 (rhMG53) protein protects cultured lung epithelial cells against anoxia/reoxygenation-induced injuries. Intravenous delivery or inhalation of rhMG53 reduces symptoms in rodent models of acute lung injury and emphysema. Repetitive administration of rhMG53 improves pulmonary structure associated with chronic lung injury in mice. Our data indicate a physiological function for MG53 in the lung and suggest that targeting membrane repair may be an effective means for treatment or prevention of lung diseases.

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Section: Methodsmentioning

confidence: 99%

Treatment of acute lung injury by targeting MG53-mediated cell membrane repair

et al. 2014

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“…Excessive production of ROS causes lipid peroxidation in cell membranes and oxidative damage to DNA and proteins (16). A number of agents, such as N-acetylcystein, calcium dobesilate, aprotinin, erdosteine or magnesium sulfate have been proposed to be useful against lung injury induced by I/R (17)(18)(19)(20)(21).…”

Section: Discussionmentioning

confidence: 99%

Antioxidative effects of adrenomedullin and vascular endothelial growth factor on lung injury induced by skeletal muscle ischemia-reperfusion

Gl¹,

Kirişçi²,

Dursun³

et al. 2013

BLL

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Abstract:Purpose: The aim of this study was to investigate the effects of adrenomedullin (AM) and vascular endothelial growth factor (VEGF) on lung injury as a remote organ following skeletal muscle ischemia-reperfusion injury in a rat model. Materials and methods: Thirty-six Wistar rats were randomized into six groups (n=6). Laparotomy was performed in all groups under general anesthesia. Nothing else was done in Group S (Sham). Ischemia reperfusion group (Group I/R) underwent ischemia and reperfusion performed by clamping and declamping of the infrarenal abdominal aorta for 120 minutes, respectively. Group VEGF and Group AM received intravenous infusion of VEGF (0.8 μg/kg) or AM (12 μg /kg) respectively, without ischemia and reperfusion. Group IR+VEGF and Group IR+AM received intravenous infusion of VEGF (0.8 μg/kg) or AM (12 μg /kg) respectively immediately after 2 hours period of ischemia. At the end of reperfusion period. Lung tissue samples were taken for biochemical examination. Total oxidant status (TOS) and total antioxidant status (TAS) levels in lung tissue were determined by using a novel automated method. p<0.05 was considered as statistically signifi cant. Results: TOS levels were signifi cantly higher in Group I/R, when compared with groups S, AM and VEGF (p=0.004, p=0.011, p=0.017, respectively) and signifi cantly lower in groups I/R+AM and I/R+VEGF, when compared with Group I/R (p=0.018, p=0.006, respectively). TAS levels were signifi cantly higher in Group I/R, when compared with groups S, AM and VEGF (p=0.006 p=0.016, p=0.016, respectively) and signifi cantly lower in Group I/R+AM, when compared with Group I/R (p=0.016). Conclusion: These fi ndings indicate that AM and VEGF acted effectively on the prevention of lung injury induced by skeletal muscle ischemia-reperfusion injury in a rat model (Fig. 2, Ref. 30). Full Text in PDF www.elis.sk.

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“…al., [5] studies showed that HBO and IL reduces lipid peroxidation minimizing the injury after reperfusion. The combined therapy is shown to be more effective than either treatment given alone.…”

Section: Hyperbaric Oxygen (Hbo) and Iloprost (Il) Therapymentioning

confidence: 99%

“…The aim of the present review is to display the role of those treatments and their level of success, reporting the effective ones in reducing the extension of the injury caused by reperfusion and its aspects [1,2,3,5,6,7,8,11,12,13,15,16,17,18].…”

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confidence: 99%

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Treatment of Post-Revascularization Syndrome: brief communication

Freitas¹,

Martins²,

Lima³

et al. 2015

Int Arch Med

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Post-Revascularization Syndrome (PRS), also described as, Ischemic Reperfusion Injury (IRI), is the main cause of failure in the revascularization of limbs. The etiology of Port-Revascularization Syndrome is not fully known, but it is accepted as a multifactorial chain with a time-dependent molecular and structural change of the affected tissues. Current clinical treatments of PRS are supportive only notwithstanding numerous intervention strategies have been proposed aiming at reducing IRI. The present perspective aimed to explain all the available treatments in studies of IRI, and their potential effects in the future medicine. Since there are almost no articles covering this topic, we believe that this perspective will clarify the necessity of more researchers and studies on IRI. Our main findings leads to believe that there are many possible therapies for ischemic reperfusion injury, but most of them are still not used in practical scenarios because of it small samples studies, or in vitro techniques or the clinical trials are still not concluded. Although, significant work remains to be done. Contact information:Modesto Leite Rolim Neto. modestorolim@yahoo.com.br KeywordsPost-Revascularization Syndrome; Treatment; Review.Post-Revascularization Syndrome (PRS), also described as, Ischemic Reperfusion Injury (IRI), is the main cause of failure in the revascularization of limbs and the transfer of free flaps with 'non reflow' phenomenon [1]. It involves microcirculatory collapse during revascularization following an ischemic insult, that constitutes an acute inflammatory process by which cells are damaged first by temporary ischemia, hypoxia and accumulation of toxic metabolites and later by reperfusion [2,3]. It may result from thrombotic occlusion, embolism, trauma or surgical intervention through tourniquet application and subsequent restoration of blood flow.

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Protective effects of hyperbaric oxygen and iloprost on ischemia/reperfusion-induced lung injury in a rabbit model

Cited by 18 publications

References 33 publications

Treatment of acute lung injury by targeting MG53-mediated cell membrane repair

Treatment of acute lung injury by targeting MG53-mediated cell membrane repair

Antioxidative effects of adrenomedullin and vascular endothelial growth factor on lung injury induced by skeletal muscle ischemia-reperfusion

Treatment of Post-Revascularization Syndrome: brief communication

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