High Concentrations of Reactive Oxygen Species in the BAL Fluid Are Correlated with Lung Injury in Rabbits after Hemorrhagic Shock and Resuscitation

Tasoulis, Marios Konstantinos; Livaditi, Olga; Stefanaki, Charikleia; Paneris, Pantelis; Prigouris, Panagiotis; Flevari, Aikaterini; Goutas, Nikos; Vlachodimitropoulos, Dimitrios; Villiotou, Vassiliki; Douzinas, Emmanuel E.

doi:10.1620/tjem.219.193

Cited by 21 publications

(10 citation statements)

References 29 publications

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“…ROS are produced by activated cytokines (Tasoulis et al;2009). ROS can cause several damages to lung tissue such as DNA damage, protein oxidation, and lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Antioxidant and Anti-Inflammatory Effects of Rhamnazin on Lipopolysaccharide-Induced Acute Lung Injury and Inflammation in Rats

Xiao-ping

et al. 2017

Afr J Tradit Complement Altern Med

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Background: Acute Lung Injury (ALI) results into severe inflammation and oxidative stress to the pulmonary tissue. Rhamnazin is a natural flavonoid and known for its antioxidant and anti-inflammatory properties. Materials and methods:The antioxidative and anti-inflammatory properties rhamnazin were tested for protection against the acute lung injury. We investigated whether rhamnazin improves the lipopolysaccharide (LPS)-induced ALI in an animal model (rat). We also studied the probable molecular mechanism of action of rhamnazin. Rhamnazin was injected intraperitoneally (i.p.) (5, 10 and 20 mg/kg) two days before intratracheal LPS challenge (5mg/kg). The changes in lung wet-to-dry weight ratio, LDH activity, pulmonary histopathology, BALF protein concentration, MPO activity, oxidative stress, cytokine production were estimated. Results:The results showed a significant attenuation of all the inflammatory parameters and a marked improvement in the pulmonary histopathology in the animal groups pretreated with rhamnazin. The rhamnazin pretreated group also showed activation of Nrf2 pathway and attenuation of ROS such as H2O2, MDA and hydroxyl ion. These results indicated that rhamnazin could attenuate the symptoms of ALI in rats due to its strong antioxidant and anti-inflammatory properties. Conclusion:The results strongly demonstrated that rhamnazin provides protection against LPS-induced ALI. The underlying mechanisms of its anti-inflammatory action may include inhibition of Nrf2 mediated antioxidative pathway.

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“…ROS are produced by activated cytokines (Tasoulis et al;2009). ROS can cause several damages to lung tissue such as DNA damage, protein oxidation, and lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Antioxidant and Anti-Inflammatory Effects of Rhamnazin on Lipopolysaccharide-Induced Acute Lung Injury and Inflammation in Rats

Xiao-ping

et al. 2017

Afr J Tradit Complement Altern Med

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“…Additional studies combining the TBX model and clinical data should allow the development of a wound biomarker panel which could predict wound healing outcome as well as estimate the impact of tissue injury on various organ systems, in particular the gastrointestinal tract. Considerable work has been done analyzing post-traumatic bronchoalveolar lavage fluid and these studies have also shown higher levels of TNF-α, IL-1β and IL-6, though primarily in hemorrhagic shock models of various species (24). The cellular origins of specific inflammatory mediators of trauma are still unclear in both clinical and experimental realms.…”

Section: Discussionmentioning

confidence: 99%

“…Considerable work has been done analyzing post-traumatic bronchoalveolar lavage fluid and these studies have also shown higher levels of TNF-a, IL-1b and IL-6, though primarily in hemorrhagic shock models of various species. 24 The cellular origins of specific inflammatory mediators of trauma are still unclear in both clinical and experimental realms. In this unique model, whether the inflammatory mediators were of donor or host origin remains to be determined, but future studies could definitively determine this by trans-implanting genetically modified TBX harvested from specific transgenic mice or utilizing specific transgenic host mice.…”

Section: Discussionmentioning

confidence: 99%

Novel model of peripheral tissue trauma-induced inflammation and gastrointestinal dysmotility

Tsukamoto

Antonic

Hajj

et al. 2011

Neurogastroenterology &Amp; Motility

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Background Trauma is a leading cause of death and although the gut is recognized as the “motor” of post-traumatic systemic inflammatory response syndrome and multiple organ failure, studies on the gastrointestinal tract are few. Our objectives were to create a precisely controllable tissue injury model in which gastrointestinal motility, systemic inflammation and wound fluid can be analyzed. Methods A non-narcotic murine trauma model was developed by the subcutaneous dorsal trans-implantation of a devitalized donor syngeneic harvested tissue-bone matrix (TBX), which was precisely adjusted to % total body weight and studied after 21 hrs. Gastrointestinal transit histograms were plotted after the oral administration of non-digestible FITC-dextran and geometric centers calculated. Organ bath evaluated jejunal circular muscle contractility. Multiplex electrochemiluminescence measurements of serum and TBX wound fluid inflammatory mediators were performed. Key Results Increasing TBX amounts progressively delayed transit, whereas TBX heat denaturation or decellularization prevented ileus and death. In the TBX17.5% model, jejunal muscle contractility was suppressed and a systemic inflammatory response developed as significant serum elevations in IL-6, keratinocyte cytokine and IL-10 compared to sham. Additionally, inflammatory responses within the wound fluid showed elevated levels of preformed IL-1β and TNF-α, whereas, 21 hours after implantation IL-1β, IL-6 and keratinocyte cytokine were significantly increased in the wound. Conclusions & Inferences A novel donor tissue-bone matrix trauma model was developed that is precisely adjustable and recapitulates important clinical phenomena. The non-narcotic model demonstrated that increasing tissue injury progressively caused ileus, initiated a systemic inflammatory response and developed inflammatory changes within the wound.

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“…The production of ROS was measured by flow cytometry using dichlorohydrofluiresceine diacetate (DCFH-DA) (Molecular Probes, Oregon, USA) as a probe as previously described [44]. The results were expressed as geometric mean of the fluorescence intensity (GMFI) for the neutrophils and monocytes of peripheral blood.…”

Section: Methodsmentioning

confidence: 99%

Nitrosative and Oxidative Stresses Contribute to Post-Ischemic Liver Injury Following Severe Hemorrhagic Shock: The Role of Hypoxemic Resuscitation

et al. 2012

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PurposeHemorrhagic shock and resuscitation is frequently associated with liver ischemia-reperfusion injury. The aim of the study was to investigate whether hypoxemic resuscitation attenuates liver injury.MethodsAnesthetized, mechanically ventilated New Zealand white rabbits were exsanguinated to a mean arterial pressure of 30 mmHg for 60 minutes. Resuscitation under normoxemia (Normox-Res group, n = 16, PaO2 = 95–105 mmHg) or hypoxemia (Hypox-Res group, n = 15, PaO2 = 35–40 mmHg) followed, modifying the FiO2. Animals not subjected to shock constituted the sham group (n = 11, PaO2 = 95–105 mmHg). Indices of the inflammatory, oxidative and nitrosative response were measured and histopathological and immunohistochemical studies of the liver were performed.ResultsNormox-Res group animals exhibited increased serum alanine aminotransferase, tumor necrosis factor - alpha, interleukin (IL) -1β and IL-6 levels compared with Hypox-Res and sham groups. Reactive oxygen species generation, malondialdehyde formation and myeloperoxidase activity were all elevated in Normox-Res rabbits compared with Hypox-Res and sham groups. Similarly, endothelial NO synthase and inducible NO synthase mRNA expression was up-regulated and nitrotyrosine immunostaining increased in animals resuscitated normoxemically, indicating a more intense nitrosative stress. Hypox-Res animals demonstrated a less prominent histopathologic injury which was similar to sham animals.ConclusionsHypoxemic resuscitation prevents liver reperfusion injury through attenuation of the inflammatory response and oxidative and nitrosative stresses.

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High Concentrations of Reactive Oxygen Species in the BAL Fluid Are Correlated with Lung Injury in Rabbits after Hemorrhagic Shock and Resuscitation

Cited by 21 publications

References 29 publications

Antioxidant and Anti-Inflammatory Effects of Rhamnazin on Lipopolysaccharide-Induced Acute Lung Injury and Inflammation in Rats

Antioxidant and Anti-Inflammatory Effects of Rhamnazin on Lipopolysaccharide-Induced Acute Lung Injury and Inflammation in Rats

Novel model of peripheral tissue trauma-induced inflammation and gastrointestinal dysmotility

Nitrosative and Oxidative Stresses Contribute to Post-Ischemic Liver Injury Following Severe Hemorrhagic Shock: The Role of Hypoxemic Resuscitation

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