نتایج جستجو برای: ischemia reperfusion injury iri
تعداد نتایج: 382967 فیلتر نتایج به سال:
Hochegger K, Schätz T, Eller P, Tagwerker A, Heininger D, Mayer G, Rosenkranz AR. Role of / and / T cells in renal ischemia reperfusion injury. Am J Physiol Renal Physiol 293: F741–F747, 2007. First published June 13, 2007; doi:10.1152/ajprenal.00486.2006.—T cells have been implicated in the pathogenesis of renal ischemia-reperfusion injury (IRI). To date existing data about the role of the T c...
BACKGROUND Endothelial dysfunction contributes to ischemia-reperfusion injury (IRI) and is reduced by ischemic preconditioning (IPC). IPC may involve activation of ATP-sensitive potassium channels (K(ATP)). We determined whether modulation of K(ATP) channels occurs in endothelial IPC in humans. METHODS AND RESULTS IRI of the forearm was induced by inflating a blood pressure cuff to 200 mm Hg ...
Ischemia reperfusion injury (IRI) in organ transplantation remains a serious and unsolved problem. Organs that undergo significant damage during IRI, function less well immediately after reperfusion and tend to have more problems at later times when rejection can occur. Biliverdin has emerged as an agent that potently suppress IRI in rodent models. Since the use of biliverdin is being developed...
Cyclooxygenase-2 (COX-2) is a mediator of hepatic ischemia and reperfusion injury (IRI). While both global COX-2 deletion and pharmacologic COX-2 inhibition ameliorate liver IRI, the clinical use of COX-2 inhibitors has been linked to increased risks of heart attack and stroke. Therefore, a better understanding of the role of COX-2 in different cell types may lead to improved therapeutic strate...
Ischemia-reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI) and evidence supporting the involvement of both innate and adaptive immunity in renal IRI has accumulated in recent years. In addition to leukocytes, kidney endothelial cells promote inflammation after IRI by increasing adhesion molecule expression and vascular permeability. Kidney tubular epithelial cells...
BACKGROUND Renal ischemia-reperfusion injury (IRI) increases the rates of acute kidney failure, delayed graft function, and early mortality after kidney transplantation. The pathophysiology involved includes oxidative stress, mitochondrial dysfunction, and immune-mediated injury. The anti-oxidation, anti-apoptosis, and anti-inflammation properties of baicalin, a flavonoid glycoside isolated fro...
Background: Ischemia reperfusion injury (IRI) during liver transplantation carries a substantial risk for graft damage, and other major organ injury. Strategies to minimize IRI in the grafted are of paramount importance. Remote ischemic preconditioning (RIP) is recently described technique that can offer protective effect against IRI. Patients Methods: In this prospective randomized study, cons...
Crush syndrome is characterized by ischemia/reperfusion injury (IRI). The protective effect of nitrite on experimentally induced IRI has been demonstrated in the heart, kidney, liver, and skeletal muscle. IRI in tissues and systemic organs occurs due to the massive generation of reactive oxygen species and subsequent systemic inflammation. Therefore, ischemic pre and postconditioning are perfor...
Recent studies have shown the remarkable gender differences in the susceptibility or expression of many diseases. The mechanism underlying the gender differences is unclear. In the present study, we evaluated the effects of gender differences and different ischemia time on the renal ischemia-reperfusion injury (IRI). The IRI was induced in the bilateral kidneys of 156 male and 30 female BALB/c ...
Background Seventy-two hours of preoperative fasting (F) or 2 weeks of 30% dietary restriction (DR) offers robust protection against renal ischemia-reperfusion injury (IRI) in mice. However, the mechanism remains to be elucidated. We hypothesize that immunomodulation plays a pivotal role. Innate immunity, especially the complement system, is crucial in the pathophysiology of IRI. Therefore, we ...
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