NDLI: Kamidono Endothelial nitric oxide synthase expression in ischemia-reperfusion injury after living related-donor renal transplantation

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Kamidono Endothelial nitric oxide synthase expression in ischemia-reperfusion injury after living related-donor renal transplantation

Content Provider	Semantic Scholar
Author	Ishimura, Takeshi Fujisawa, Masato Isotani, Shuji Iijima, Kazumoto Yoshikawa, Norishige Sadao
Abstract	Ischemia-reperfusion (I-R) injury in cadaveric renal transplantation may cause acute tubular necrosis or delayed initiation of graft function [30]. I-R injury was correlated with the incidence of acute rejection in several clinical series [8, 12, 21]. Experimental and clinical evidence has also identified I-R injury as an antigen-independent risk factor for chronic renal allograft failure [12, 13, 29, 35]. Nitric oxide (NO) appears to be a key link between I-R injury and the rate of tissue repair during injury response, the number of acute rejection episodes, and the occurrence of chronic allograft nephropathy [14]. A versatile intercellular messenger molecule associated with vasodilation and neurotransmission, NO is also involved in inflammation, tissue injury, and cell defense [19, 28]. Synthesis of NO is catalyzed by nitric oxygen synthase (NOS) [19], which has three known isoforms: endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS) [22, 23, 28]. The isoform predominantly involved in the recovery from I-R injury in the transplanted kidney is eNOS [28, 32]. The activity of eNOS after I-R can thus influence the ORIGINAL ARTICLE Transpl Int (2002) 15: 635–640 DOI 10.1007/s00147-002-0473-2
File Format	PDF HTM / HTML
Alternate Webpage(s)	https://page-one.springer.com/pdf/preview/10.1007/s00147-002-0473-2
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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