Effects of albumin and Ringer’s lactate on production of lung cytokines and hydrogen peroxide after resuscitated hemorrhage and endotoxemia in rats

Zhang, Haibo; Voglis, Stefanos; Kim, Chang‐Ho; Slutsky, Arthur S.

doi:10.1097/01.ccm.0000065271.23556.ff

Cited by 46 publications

(35 citation statements)

References 42 publications

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“…These three clinically available parameters were used to test the effectiveness of volume expansion and tissue perfusion with different resuscitation fluids, and the difference in gas exchange or in lung edema formation. The results are consistent with several reports on the protective effects of albumin on I/R-induced organ dysfunction (Boura et al, 2003;Zhang et al, 2003;Su et al, 2007).…”

Section: Nf-κb P65 Activation Following T/hs Induction and Albumin Trsupporting

confidence: 82%

Albumin resuscitation protects against traumatic/hemorrhagic shock-induced lung apoptosis in rats

Zhang

Liang

Zhang

et al. 2008

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To determine the effects of albumin administration on lung injury and apoptosis in traumatic/hemorrhagic shock (T/HS) rats. Methods: Studies were performed on an in vivo model of spontaneously breathing rats with induced T/HS; the rats were subjected to femur fracture, ischemia for 30 min, and reperfusion for 20 min with Ringer's lactate solution (RS) or 5% (w/v) albumin (ALB), and the left lower lobes of the lungs were resected. Results: Albumin administered during reperfusion markedly attenuated injury of the lung and decreased the concentration of lactic acid and the number of in situ TdT-mediated dUTP nick-end labelling (TUNEL)-positive cells. Moreover, immunohistochemistry performed 24 h after reperfusion revealed increases in the level of nuclear factor κB (NF-κB), and phosphorylated p38 mitogen-activated protein kinase (MAPK) in the albumin-untreated group was down-regulated by albumin treatment when compared with the sham rats. Conclusion: Resuscitation with albumin attenuates tissue injury and inhibits T/HS-induced apoptosis in the lung via the p38 MAPK signal transduction pathway that functions to stimulate the activation of NF-κB.

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Section: Nf-κb P65 Activation Following T/hs Induction and Albumin Trsupporting

confidence: 82%

Albumin resuscitation protects against traumatic/hemorrhagic shock-induced lung apoptosis in rats

Zhang

Liang

Zhang

et al. 2008

J. Zhejiang Univ. Sci. B

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“…Studies in various animal models for acute ischemic organ damage have shown the protective effects of NO-Alb and PNA in treatment of ischemia-reperfusion tissue injury (28,31,40,43). In the present study, we examined the effects of NO-Alb on the acute lung injury induced by hypoxia-reoxygenation in transgenic sickle cell SAD mice.…”

Section: Discussionmentioning

confidence: 99%

Protective effects ofS-nitrosoalbumin on lung injury induced by hypoxia-reoxygenation in mouse model of sickle cell disease

Franceschi

Malpeli²,

Scarpa³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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. We investigated the effects of NO donor on hypoxia-induced acute lung injury that occurs when transgenic sickle cell SAD mice are exposed to chronic hypoxia, a model for lung vasoocclusive sickle cell events. In wild-type and SAD mice, intraperitoneal injection of S-nitrosoalbumin (NO-Alb) produced no significant hematologic changes under room air conditions, whereas it induced mild temporary hypotension and inhibition of platelet aggregation. NO-Alb administration (300 mg/kg ip twice a day, equivalent to 7.5 M NO) in wild-type and SAD mice exposed to 46 h of hypoxia (8% oxygen) followed by 2 h of normoxia resulted in 1) reduction of the hypoxiainduced increase in blood neutrophil count, 2) prevention of hypoxiainduced increased IL-6 and IL-1␤ levels in bronchoalveolar lavage, 3) reduction of the lung injury induced by hypoxia-reoxygenation, 4) prevention of thrombus formation, and 5) prevention of hypoxiainduced increase of lung matrix metalloproteinase-9 gene expression. These effects provide new insights into the possible use of NO-Alb in the treatment of acute lung injury in SCD. transgenic sickle cell SAD mice; hypoxic lung injury; nitric oxide; nitrite NITRIC OXIDE (NO) is a potent vasodilator, an inhibitor of vascular remodeling, and a modulator of the cascade of events involved in leukocyte, platelet, and endothelial activation (8,9,21). Sickle cell disease patients show reduced NO metabolites during either vasoocclusive crisis associated with severe pain or acute chest syndrome as well as a decreased exhaled NO, suggesting a possible role of a relative NO lung deficiency in the pathogenesis of sickle cell-related pulmonary complications (25).

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“…The method measures the total oxidative potential with the exception of O 2 − since this radical appears to be unable to oxidize DCFH directly (Zhu et al 1994). In contrast, in studies attempting to assess pulmonary oxidative stress, only hydrogen peroxide was measured either in BAL fluid (Zhang et al 2003;Xu et al 2004) or in breath condensate (Zuckerbraun et al 2005). Interestingly, the results from our study showed that the generation of ROS derives mainly from PMNs cells despite that macrophages are the dominant cells in the BAL fluid.…”

Section: Discussionmentioning

confidence: 99%

“…With few exceptions (Zhang et al 2003), in the case of ALI, ROS and cytokines have not been measured in combination at the site of their production, namely in the BAL fluid. Besides, the current study is the first one that investigates the biological oxidative and inflammatory pulmonary loads in relation to lung morphologic changes that follow resuscitation from hemorrhagic shock.…”

Section: Discussionmentioning

confidence: 99%

“…There has been only one study in the past focusing on the combined detection of cytokines and ROS in the BAL fluid from animals resuscitated from hemorrhagic shock (Zhang et al 2003). The aim of our study was to provide pathophysiological insights in the implication of the oxidative and inflammatory responses in the development of ischemia-reperfusion induced acute lung injury using the well-known model of hemorrhagic shock resuscitation.…”

mentioning

confidence: 99%

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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

Tasoulis

Livaditi

Stefanaki

et al. 2009

Tohoku J. Exp. Med.

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Effects of albumin and Ringer’s lactate on production of lung cytokines and hydrogen peroxide after resuscitated hemorrhage and endotoxemia in rats

Cited by 46 publications

References 42 publications

Albumin resuscitation protects against traumatic/hemorrhagic shock-induced lung apoptosis in rats

Albumin resuscitation protects against traumatic/hemorrhagic shock-induced lung apoptosis in rats

Protective effects ofS-nitrosoalbumin on lung injury induced by hypoxia-reoxygenation in mouse model of sickle cell disease

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

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