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N-acetylcysteine abrogates acute lung injury induced by endotoxin.

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الدخول التسجيل فى الموقع

1. Acute lung injury (ALI) or acute respiratory distress syndrome is a serious clinical problem with high mortality. N-Acetylcysteine (NAC) is an anti-oxidant and a free radical scavenger. It has been reported recently that NAC ameliorates organ damage induced by endotoxin (lipopolysaccharide; LPS)

Enhancement effects of hypercapnia on the acute lung injury caused by acid aspiration.

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Acid aspiration or intrapulmonary instillation of gastric particles causes lung inflammation leading to acute lung injury (ALI). Hypercapnia exerts different effects on ALI caused by various insults. The effects of hypercapnia on lung inflammation and injury due to acid aspiration are yet to be

Oxidative and nitrosative mediators in hepatic injury caused by whole body hyperthermia in rats.

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The involvement of oxidative and nitrosative mediators in liver injury caused by heat stress remains unclear. This study aimed to elucidate the role of endothelial nitric oxide synthase (eNOS), and inducible NOS (iNOS)-derived NO and nitrotyrosine in the whole-body hyperthermia (WBH)-induced liver

Nitric oxide mediates acute lung injury caused by fat embolism in isolated rat's lungs.

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BACKGROUND The involvement of nitric oxide (NO) in acute lung injury (ALI) induced by fat embolism (FE) has not been investigated. The present study elucidated the role of NO in ALI because of FE. METHODS FE was produced by introduction of fatty acid (corn oil micelles) into the isolated rat's

N-acetylcysteine attenuates the acute lung injury caused by phorbol myristate acetate in isolated rat lungs.

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Acute lung injury (ALI) caused by phorbol myristate acetate (PMA) is characterized by pulmonary edema and inflammatory cells infiltration. PMA-activated neutrophils in vivo and in vitro to release free radicals, pro-inflammatory cytokines, nitric oxide (NO) and other mediators. These mediators may

The protective effect of niacinamide on ischemia-reperfusion-induced liver injury.

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Reperfusion of ischemic liver results in the generation of oxygen radicals, nitric oxide (NO) and their reaction product peroxynitrite, all of which may cause strand breaks in DNA, which activate the nuclear enzyme poly(ADP ribose)synthase (PARS). This results in rapid depletion of intracellular

Inhibition of inducible nitric oxide synthase attenuates acute endotoxin-induced lung injury in rats.

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1. In the present study, we investigated the effects of the inducible nitric oxide (iNOS) inhibitors S-methylisothiourea (SMT) and l-N(6)-(1-iminoethyl)-lysine (l-Nil) on endotoxin-induced acute lung injury (ALI), as well as the associated physiological, biomedical and pathological changes, in

Endotoxin-induced acute lung injury is enhanced in rats with spontaneous hypertension.

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1. Acute lung injury (ALI), or acute respiratory distress syndrome, is a major cause of mortality in endotoxaemia. The present study tested whether the endotoxaemia-induced changes and associated ALI were enhanced in rats with established hypertension and to examine the possible mechanisms involved.

Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion.

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Poly (ADP-ribose) synthase or polymerase (PARS and PARP, respectively) is a cytotoxic enzyme which causes cellular damage. Nicotinamide, a compound of vitamin B complex, has been reported to exert an inhibitory effect on PARS or PARP. The present study tests the effects of nicotinamide on acute lung

Niacinamide abrogates the organ dysfunction and acute lung injury caused by endotoxin.

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Poly (ADP-ribose) synthabse (PARS) or polymerase (PARP) is a cytotoxic enzyme causing cellular damage. Niacinamide inhibits PARS or PARP. The present experiment tests the effects of niacinamide (NCA) on organ dysfunction and acute lung injury (ALI) following lipopolysaccharide (LPS). LPS was

Propofol exerts protective effects on the acute lung injury induced by endotoxin in rats.

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Acute lung injury (ALI) is a major culprit of mortality in endotoxemia. Propofol has been commonly used in critical ill patients for sedation. This experiment attempted to elucidate the effects and possible mechanisms of propofol on the ALI induced by endotoxin. Experimentations were carried out

Exercise training attenuates septic responses in conscious rats.

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OBJECTIVE To evaluate the effects of exercise training on the changes induced by endotoxin in arterial pressure, heart rate (HR), blood cells, biochemical factors, plasma nitrite/nitrate, methyl guanidine (MG), proinflammatory cytokines, and pathology of the heart, liver, and

The protective effect of curcumin on ischemia-reperfusion-induced liver injury.

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OBJECTIVE Reperfusion of the ischemic liver results in the generation of oxidative and nitrosative stresses and reaction product of peroxynitrite, which induce rapid cytotoxicity and liver injury. In this study we demonstrated that curcumin, an antioxidant, attenuated ischemia/reperfusion

N-acetylcysteine ameliorates lipopolysaccharide-induced organ damage in conscious rats.

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Lipopolysaccharide is strongly associated with septic shock, leading to multiple organ failure. It can activate monocytes and macrophages to release proinflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and nitric oxide (NO). The present

Endotoxin-induced acute lung injury and organ dysfunction are attenuated by pentobarbital anaesthesia.

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1. Acute lung injury (ALI) as a result of sepsis is a major cause of mortality. Certain anaesthetic agents have been reported to suppress pro-inflammatory cytokines and inducible nitric oxide (NO) synthase (iNOS) activities. We investigated the effects of pentobarbital on ALI and organ functions

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