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Conjugate anti-endotoxin vaccines

100%

Lugowski C., Jachymek W., Niedziela T.

Bulletin of the Veterinary Institute in Puławy

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1998

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tom 42

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nr 1

2

Involvement of platelet activating factor in immediate heart response to lipopolysaccharide

100%

Jakubowski A., Olszanecki R., Chlopicki S.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 2

Although lipopolysaccharide (LPS) is recognized to induce a biphasic cardiovascular response its mechanism is not fully elucidated. In this study we analysed the involvement of PAF, TXA2 and cysteinyl leukotrienes (cysLTs) in the acute cardiovascular effects of LPS in the isolated rat heart as well as in delayed phase of LPS response using a surrogate cellular model of the induction of NOS-2 by LPS in mouse macrophages. Perfusion of rat hearts with LPS resulted, in an immediate fall in heart contractility and coronary flow by 2.5 ± 0.59 ml min-1 and 560 ± 81 mmHg sec-1, respectively. This response was fully blocked by platelet activating factor (PAF) antagonist - WEB 2170 and partially inhibited, by inhibitor of cyclooxygenase (indomethacin) or by inhibitor of thromboxane synthase (camonagrel). The inhibition of leukotriene synthesis (BAY x1005) or cysLTs receptors (BAY x7195) was without effect. Administration of stable PAF analog (methylcarbamyl-PAF - MC-PAF) alone, mimicked heart response to LPS. In cultured mouse macrophages, MC-PAF did not induce NOS-2 expression and when given with LPS it slightly potentiated NOS-2 induction by LPS. However, in presence of WEB 2170 NOS-2 induction by LPS was inhibited in a dose-dependent manner. Inhibition of cyclooxygenase and leukotriene pathways had no effect on NOS-2 induced by LPS. These results indicate that PAF and TXA2 but not cysLTs mediate the instant heart response induced by LPS, while PAF alone mediates a delayed NOS-2 induction by LPS. Accordingly, PAF may constitute the mediator that links acute and delayed phases of LPS-induced cardiovascular response.

3

Effect of ozonetherapy on structural patterns of selected rat organs in endotoxemic shock

84%

Madej P., Plewka A., Madej J. A., Kuryszko J., Plewka D., Szczepanik T., Kaminski M.

Acta Toxicologica

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2007

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tom 15

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nr 2

95-105

4

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

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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.

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Are NKT cells essential for endotoxic shock?

84%

Emoto M.

Archivum Immunologiae et Therapiae Experimentalis

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2003

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tom 51

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nr 4

6

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

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tom 58

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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.

7

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

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2008

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tom 59

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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.

8

Effects of vitamin E and prednisolone on biochemical and haematological parameters in endotoxaemic New Zealand white rabbits

84%

Yazar E., Col R., Konyalioglu S., Birdane Y. O., Elmas M., Bas A. L.

Bulletin of the Veterinary Institute in Puławy

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2004

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tom 48

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nr 2

Ograniczanie wyników

Conjugate anti-endotoxin vaccines

Involvement of platelet activating factor in immediate heart response to lipopolysaccharide

Effect of ozonetherapy on structural patterns of selected rat organs in endotoxemic shock

Ultrastructure of immediate microvascular lung injury induced by bacterial endotoxin in the isolated, no-deficient lung perfused with full blood

Are NKT cells essential for endotoxic shock?

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

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

Effects of vitamin E and prednisolone on biochemical and haematological parameters in endotoxaemic New Zealand white rabbits