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1
Content available remote

Lung protection in cardio-pulmonary bypass

100%
Salameh A., Greimann W., Vollroth M., Dhein S., Bahramsoltani M., Dahnert I.
Journal of Physiology and Pharmacology
|
2017
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tom 68
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nr 1
2
Content available remote

Endotoxaemia in rats: role of leucocyte sequestration in rapid pulmonary nitric oxide synthase-2 expression

100%
Gebska A., Olszanecki R., Korbut R.
Journal of Physiology and Pharmacology
|
2005
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tom 56
|
nr 2
Nitric oxide (NO), depending on the amount, time and source of generation may exert both, protective and deleterious actions during endotoxic acute lung injury (ALI). Evaluation of the expression and localization of NOS isoforms in the lung of lipopolysaccharide (LPS) - treated rats may contribute to understanding the role of NO in pathogenesis of ALI. Tissue samples (lung, heart, liver, kidney and spleen) as well as peripheral blood polymorphonuclear cells (PMNs) were collected from control male Wistar rats and LPS - treated animals, 15, 30, 60, 120 and 180 min after LPS injection (2 mg kg-1 min-1 for 10 minutes, i.v.). Levels of NOS-2 and NOS-3 mRNA and protein in tissues and PMNs were estimated by RT-PCR, Northern blotting and Western blotting. Additionally, myeloperoxidase (MPO) activity in tissue samples was assayed. NOS-3 mRNA as well as protein were detected in lungs of control animals; pulmonary NOS-3 expression was not influenced by LPS. The induction of NOS-2 mRNA in rat lungs and in PMNs isolated from peripheral blood was observed 15 minutes after LPS challenge. In contrast, increase of NOS-2 mRNA in the heart, kidneys, liver and spleen was observed 2-3 hours after LPS injection. In all tissues rise in NOS-2 mRNA was followed after 1-2 hours by increase of NOS-2 protein. Importantly, progressive leukocyte sequestration in the lung parenchyma that started as early as 15 min after LPS injection was revealed only in the lungs; in other organs no significant changes in MPO activity were detected up to 180 min after LPS injection. In conclusion, infusion of LPS caused much more rapid expression of NOS-2 in lungs as compared to the heart, kidneys, liver and spleen. Early induction of NOS-2 may depend on the LPS-stimulated rapid neutrophil sequestration within lung vasculature and fast induction of NOS-2 in sequestrated neutrophils.
3
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N-acetylcysteine effectively diminished meconium-induced oxidative stress in adult rabbits

84%
Mokra D., Drgova A., Mokry J., Antosova M., Durdik P., Calkovska A.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 1
4

Effects of ketamine, propofol, and ketofol on proinflammatory cytokines and markers of oxidative stress in a rat model of endotoxemia - induced acute lung injury

84%
Gokcinar D., Ergin V., Cumaoglu A., Menevse A., Aricioglu A.
Acta Biochimica Polonica
|
2013
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tom 60
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nr 3
Intravenous lipopolysaccharide (LPS) leads to acute lung injury (ALI) in rats. The purpose of this study was to examine the anti-inflammatory and antioxidant efficacy of ketamine, propofol, and ketofol in a rat model of ALI. We induced ALI in rats via intravenous injection of LPS (15 mg kg-1). The animals were randomly separated into five groups: control, LPS only, LPS + ketamine (10 mg·kg-1·h-1), LPS + propofol (10 mg·kg-1·h-1), LPS + ketofol (5 mg·kg-1·h-1 ketamine + 5 mg·kg-1·h-1 propofol). LPS resulted in an increase in the release of pro-inflammatory cytokines, mRNA expression related with inflammation, production of nitric oxide, and lipid peroxidation. Ketamine prevented the increase in markers of oxidative stress and inflammation mediators, both in plasma and lung tissue. Propofol decreased the levels of cytokines in plasma and lung tissue, whereas it had no effect on the IL-1-beta level in lung tissue. Ketamine downregulated mediators of lung tissue inflammation and reduced the level of circulating cytokines and protected lung tissue against lipid peroxidation. Ketofol decreased the level of TNF-α and IL-1β in plasma, as well as expression of cyclooxygenase-2 mRNA and the nitrate/nitrite level in lung tissue. The results of this investigation support the hypothesis that ketamine may be effective in preventing ALI.
5
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Ultrastructure of immediate microvascular lung injury induced by bacterial endotoxin in the isolated, no-deficient lung perfused with full blood

84%
Chlopicki S., Walski M., Bartus J. B.
Journal of Physiology and Pharmacology. Supplement
|
2005
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tom 56
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nr 4
47-64
NOS-2-derived NO is involved in hypotension, vasoplegia, metabolic disorders and lung injury in endotoxic shock. On the other hand, NOS-3-derived NO protects against LPS-induced lung injury. We have previously shown that NO limits lung injury in the isolated blood-perfused rat lung. Here we characterize the ultrastructure of microvascular lung injury induced by LPS in the absence of endogenous NO and summarize our data on the mechanisms of immediate lung response to LPS in the presence and absence of endogenous NO. Injection of LPS (from E.Coli, 300 µg/ml) into the isolated blood-perfused rat lung induced an immediate transient constriction of airways and vessels that was not associated with lung edema and pulmonary microcirculation injury. In contrast, in the presence of the NOS inhibitor L-NAME (300 µg/ml), LPS produced an enhanced constriction of airways and vessels, which was accompanied by profound lung edema and capillary-alveolar barrier injury, as evidenced by optic and electron microscopy. Microvascular lung injury was confirmed by the following findings: edema of pulmonary endothelium with low electronic density of endothelial cytoplasm, presence of protein-rich fluid and numerous erythrocytes in alveolar space, concentric figures of damaged tubular myelin of surfactant (myelin-like bodies), edema of epithelium type I cells with low electronic density of their cytoplasm and alterations in ultrastructure of basal membrane of vascular-alveolar barrier. Interestingly, epithelial type II cells did not show signs of injury. It is worth noting that capillary-alveolar barrier injury induced by L-NAME+LPS was associated with sequestration of platelets and neutrophils in pulmonary microcirculation and internalization of LPS by neutrophils. In conclusion, in the absence of endogenous nitric oxide LPS induces injury of microvascular endothelium and vascular-alveolar barrier that leads to fatal pulmonary edema. Mechanisms of immediate lung response to LPS in presence of NO and those leading to acute microvascular lung injury in response to LPS in absence of NO are summarized. In our view, immediate lung response to bacterial endotoxin represents a phylogenetically ancient host defence response involving complement-dependent activation of platelets and neutrophils and subsequent production of lipid mediators. This response is designed for a quick elimination of bacterial endotoxin from the circulation and is safeguarded by endothelial NO.
6
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Effects of surfactant/budesonide therapy on oxidative modifications in the lung in experimental meconium-induced lung injury

84%
Mikolka P., Kopincova J., Tomcikova-Mikusiakova L., Kosutova P., Antosova M., Calkovska A., Mokra D.
Journal of Physiology and Pharmacology
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2016
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tom 67
|
nr 1
7
Content available remote

Complement activation contributes to ventilator-induced lung injury in rats

84%
Petersen B., Busch T., Gaertner J., Haitsma J. J., Krabbendam S., Ebsen M., Lachmann B., Kaisers U. X.
Journal of Physiology and Pharmacology
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2016
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tom 67
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nr 6
8
Content available remote

Protective effects of early treatment with lipoic acid in LPS- induced lung injury in rats

84%
Goraca A., Jozefowicz-Okonkwo G.
Journal of Physiology and Pharmacology
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2007
|
tom 58
|
nr 3
A lipopolysaccharide (LPS) stimulates the synthesis and releases several metabolites from phagocytes which can lead to an endotoxic shock characterized by multiple organ injury with the earliest to occur in the lungs. Among LPS-induced metabolites, reactive oxygen species are considered to play a crucial pathogenetic role in the lung damage. In this study, the effect of early administration of an antioxidant, alpha-lipoic acid (LA), on pulmonary lipid peroxidation, lung hydrogen peroxide (H202) concentration, and lung sulfhydryl group content was evaluated in rats with endotoxic shock induced by administration of LPS (Escherichia coli 026:B6, 30 mg/kg, i.v.). In addition, lung edema was assessed with wet-to-dry lung weight (W/D) ratio. Animals were treated intravenously with normal saline or LA 60 mg/kg or 100 mg/kg 30 min after LPS injection. After a 5 h observation, animals were killed and the lungs were isolated for measurements. Injection of LPS alone resulted in the development of shock and oxidative stress, the latter indicated by a significant increase in the lung thiobarbituric acid reacting substances (TBARS) and H202 concentrations, and a decrease in the lung sulfhydryl group content. The increase in the W/D ratio after the LPS challenge indicated the development of lung edema in response to LPS. Administration of LA after the LPS challenge resulted in an increase in the sulfhydryl group content and a decrease in TBARS and H202 concentration in the lungs as compared with the LPS group. An insignificant decrease in the W/D ratio was observed in rats treated with either dose of LA. These results indicate that the LPS-induced oxidative lung injury in endotoxic rats can be attenuated by early treatment with LA. Administration of LA could be a useful adjunct to conventional approach in the management of septic shock.
9

Assessment of neutrophil components as markers of lung injury in the course of bovine respiratory tract infections

84%
Wessely-Szponder J., Bobowiec R., Martelli F., Wojcik M., Kosior-Korzecka U.
Polish Journal of Veterinary Sciences
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2004
|
tom 07
|
nr 3
To define the role of activated neutrophils in lung injury during bovine respiratory tract infections (BRTI) their in vitro function was investigated. As a means to achieve this goal the comparison of secretory action between neutrophils from the BRTI group and control was made on the basis of elastase, myeloperoxidase (MPO), alkaline phosphatase (ALK-P) release, and nitric oxide production. We noted that there is an interdependence between secretory response of neutrophils and clinical severity of BRTI. The release of elastase was greater in the BRTI group than in the control group (49.17 ±4.41 versus 46.43 ±4.95% of the total content). Neutrophils from infected heifers exhibited a significantly (p<0.05) higher value of MPO release than from healthy heifers and reached 39.23 ± 10.18 versus 25.54 ± 8.41% of the total content. ALK-P containing granules released significantly (p<0.001) more enzyme in the group with BRTI than in the control group (22.42 ± 6.27 versus 13.74 ± 2.01% of the total enzyme content). The level of nitrite accumulation rose in the culture of cells isolated from heifers with BRTI from 4 ± 0.53 μM after 0.5h to 6.9 ± 0.52 μM after 72 h. Our data suggest that during BRTI the increase of neutrophil secretory action results in augmentation of enzyme release including elastase, MPO and ALK-P, and the nitrite production. During an excessive secretory response of neutrophils all these factors contribute to lung injury and worsen the course of a disease and might be recognised as markers of lung injury. Moreover, such a destructive action of neutrophils must be taken into account during the introduction of new methods of BRTI treatment.
10

X-band and S-band EPR detection of nitric oxide in murine endotoxaemia using spin trapping by ferro-di[N-[dithiocarboxy]sarcosine]

84%
Plonka P. M., Wisniewska M., Chlopicki S., Elas M., Rosen G. M.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr 3
Ammonium salt of N-(dithiocarboxy)sarcosine (DTCS) chelated to ferrous salt was tested as an NO-metric spin trap at room temperature for ex vivo measurement of NO production in murine endotoxaemia. In a chemically defined in vitro model system EPR triplet signals of NO-Fe(DTCS)2 were observed for as long as 3 hours, only if samples were reduced with sodium dithionite. This procedure was not necessary for the ex vivo detection of NO in endotoxaemic liver homogenates at X-band or in the whole intact organs at S-band, whereas only a weak signal was observed in endotoxaemic lung. These results suggest that in endotoxaemia not only high level of NO, but also the redox properties of liver and lung might determine the formation of complexes of NO with a spin trap. Nevertheless, both S- and X-band EPR spectroscopy is suitable for NO-metry at room temperature using Fe(DTCS)2 as the spin trapping agent. In particular, S-band EPR spectroscopy enables the detection of NO production in a whole organ, such as murine liver.
11
Content available remote

Beneficial effect of alpha-lipoic acid on lipopolysaccharide-induced oxidative stress in bronchoalveolar lavage fluid

84%
Goraca A., Skibska B.
Journal of Physiology and Pharmacology
|
2008
|
tom 59
|
nr 2
Lipopolysaccharide (LPS) from gram-negative bacteria is a major factor that contributes to multiple organ failure including lung injury. Among LPS-induced metabolites, reactive oxygen species are considered to play a crucial pathogenic role in the lung damage. In this study, the effect of early administration of an antioxidant, a-lipoic acid (LA), on bronchoalveoar lavage fluid (BALF) lipid peroxidation, hydrogen peroxide (H2O2), sulphydryl group (-SH) concentration and total protein concentration was evaluated in rats with endotoxic shock induced by administration of LPS (Escherichia coli 026:B6, 30 mg/kg, i.v.). The animals were treated intravenously with normal saline or LA (60 mg/kg or 100 mg/kg i.v.) 30 min after LPS injection. Five hours after LPS or saline administration, the animals were sacrificed and BALF was obtained for measurements. The results showed that the levels of oxidative markers, thiobarbituric acid reactive substances (TBARS) and H2O2 were increased significantly in BALF, whereas they were decreased significantly on treatment with LA. The concentrations of -SH groups were significantly increased and total protein concentration was insignificantly decreased in the LPS/LA group. There was no difference in oxidative stress reduction between 60 mg/kg and 100 mg/kg doses. These results indicate that early administration of lipoic acid provides protective effects against endotoxin-induced oxidative stress in the lung and supports the idea that alpha-lipoic acid is a free radical scavenger and a potent antioxidant.
12

Adult respiratory distress syndrome and alveolar epithelium apoptosis: an histopathological and immunohistochemical study

67%
Toth S., Pingorova S., Jonecova Z., Morochovic R., Pomfy M., Vesela J.
Folia Histochemica et Cytobiologica
|
2009
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tom 47
|
nr 3
13

The effect of TNFalpha on the production of nitric oxide by neutrophils isolated from heifers in the course of bovine respiratory disease

67%
Wessely-Szponder J.
Electronic Journal of Polish Agricultural Universities. Series Veterinary Medicine
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2007
|
tom 10
|
nr 4
14

IGFBP7 aggravates sepsis-induced acute lung injury by activating the ERK1/2 pathway

67%
Xu Q., Wang J.
Folia Histochemica et Cytobiologica
|
2020
|
tom 58
|
nr 4
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