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Renal damage in rats induced by myocardial ischemia/reperfusion: Role of nitric oxide

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dc.creator Vardi, Nigar
dc.creator Cicek, Ekrerm
dc.creator Ozer, Mehmet Kaya
dc.creator Parlakpinar, Hakan
dc.creator Acet, Ahmet
dc.creator Cigremis, Yilmaz
dc.date 2006-10-01T00:00:00Z
dc.date.accessioned 2021-12-03T11:31:57Z
dc.date.available 2021-12-03T11:31:57Z
dc.identifier 8c614489-6e1f-4bce-bb89-6d2a299b884c
dc.identifier 10.1111/j.1442-2042.2006.01540.x
dc.identifier https://avesis.sdu.edu.tr/publication/details/8c614489-6e1f-4bce-bb89-6d2a299b884c/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/93248
dc.description Background: It has been demonstrated that myocardial ischemia/reperfusion (MI/R) causes renal damage. However, the mechanism underlying this damage in kidneys during revascularization of myocardium is unclear. Direct renal ischemia/reperfusion has been implicated in the induction of inducible nitric oxide synthase (iNOS) that leads to increase production of nitric oxide (NO). Recently, excessive production of NO has been found to be involved in causing renal injury by formatting peroxinitrite (ONOO(-)). The aim of this study was to investigate whether NO has a role in this damage, using aminoguanidine (AMG), a known iNOS inhibitor and an antioxidant, in rats undergoing MI/R.
dc.language eng
dc.rights info:eu-repo/semantics/closedAccess
dc.title Renal damage in rats induced by myocardial ischemia/reperfusion: Role of nitric oxide
dc.type info:eu-repo/semantics/article


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