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
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
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
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
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
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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