نتایج جستجو برای: renal ischemia reperfusion injury
تعداد نتایج: 597757 فیلتر نتایج به سال:
conclusions pretreatment with epo and application of ipc significantly ameliorated the renal injury induced by bilateral renal ir. however, both treatments attenuated renal dysfunction and oxidative stress in kidney tissues. there were no significant differences between pretreatment with epo or application of ipc. materials and methods twenty four male wistar rats were allocated into four exper...
Introduction: Using brief episodes of ischemia and reperfusion (IR) prior to a more sustained IR insult – ischemic preconditioning (IPC) – can reduce IR injury of the heart, brain and many other tissues. The purpose of present study was to investigate the effect of 2min ischemic periods on subsequent rat renal IR injury. Methods: Male rat's renal IR injury was investigated in a right nephrectom...
conclusions treatment with epo and mel had a beneficial effect on renal ir injury. the results may also indicate that mel protects against morphological damage better than epo in renal ir injury. results ischemia-reperfusion significantly decreased the observed hb and hct values. the histopathological findings in the ir group confirmed that there was an increase in the hyaline cast and thickeni...
Background: Ischemia/reperfusion induced acute renal failure causes excretory functional disorders of nephrons. Ischemia/reperfusion injury is accompanied by generation of reactive oxygen species that leads to dysfunction, injury, and death of renal cells. Antioxidants of plant origin minimize the harmful effects of reactive oxygen species. The aim of this study was to determine the possible th...
renal ischemia-reperfusion (ir) contributes to the development of acute renal failure (arf). oxygen free radicals are considered to be principal components involved in the pathophysiological tissue alterations observed during renal ir. the purpose of this study was to investigate the combination effect of melatonin (mel) and erythropoietin (epo), which are a potent antioxidant and anti-apoptoti...
Objective(s):Bradykinin is a part of the kinin-kallikreinsystem which is involved in ischemia-reperfusion injury via B1 and B2 receptors.Noscapine is a non-competitive antagonist of bradykinin receptors. Noscapine has been reported to to be able to protect some organs against ischemia-reperfusion injury but its effect on renal ischemia-reperfusion injury (RIR) in rats is unknown. Therefore, the...
Background: The renal sympathetic nerve activity (RSNA) is enhanced in renal failure. Paraventricular nucleus in hypothalamus is an important central site to regulate sympathetic activity. There are angiotensin II (Ang) II receptors in this nucleus. The aim of this study was to evaluate the effects of angiotensin II in hypothalamic paraventricular nucleus (PVN) on renal ischemia-reperfusion inj...
objective(s):bradykinin is a part of the kinin-kallikreinsystem which is involved in ischemia-reperfusion injury via b1 and b2 receptors.noscapine is a non-competitive antagonist of bradykinin receptors. noscapine has been reported to to be able to protect some organs against ischemia-reperfusion injury but its effect on renal ischemia-reperfusion injury (rir) in rats is unknown. therefore, the...
introduction: this study was designed to evaluate the effects of treatment with flaxseed oil (fso) on renal ischemia-reperfusion (rir) injuries in rats. materials and methods: in this study, 32 wistar rats were randomly studied in four groups: co+ns (control group with normal saline administration), sh+ns (sham group with normal saline administration), rir+ns and rir+fso. fso (0.2 ml) was admin...
Background: Renal ischemia reperfusion (RIR) injury is a common clinical syndrome that affects renal function and significantly increases morbidity and mortality. Hydrogen sulfide (H2S) is an endogenously gaseous mediator that exhibits many cytoprotective effects. Recently, studies have shown that H2S have opposite effects in different doses. Therefore, in the current study we investigated the ...
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