NO: More Than Just a Vasodilator in Lung Transplantation

Karamsetty, M. R.; Klinger, James R.

doi:10.1165/ajrcmb.26.1.f223

Cited by 16 publications

(9 citation statements)

References 48 publications

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“…NOS1 and NOS3 are regulated by the intracellular calcium/calmodulin level and are also often referred to as constitutive NOS (cNOS). Expression of NOS2 is calcium independent and responds to proinflammatory cytokines, such as interleukin 1 (IL-1), IL-6, interferon , and tumor necrosis factor (TNF-) directly and via nuclear factor-B (NF B) [1][2][3]. Epithelial NOS2 is thought to be the major source of increased fractional NO in exhaled air (FeNO) in inflammatory conditions such as asthma and FeNO can therefore be used as a marker of airway inflammation in asthma [4].…”

Section: No/l-arginine Metabolismmentioning

confidence: 99%

Alterations in L-Arginine Metabolism After Lung Transplantation~!2009-11-12~!2010-03-25~!2010-05-04~!

Mehl¹,

Grasemann²

2010

TONOJ

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Since the discovery of nitric oxide (NO) in biological systems more than 20 years ago, it became widely accepted that endogenous NO plays a key role in the regulation of a variety of physiological processes. NO is involved in reperfusion injury and chronic rejection after solid organ transplantation. Arginase is an enzyme that competes with NO synthases for the common substrate L-arginine. Increased arginase activity alters L-arginine metabolism and reduces substrate availability for NO synthases, and thereby contributes to organ dysfunction following transplantation. NO deficiency after lung transplantation impacts on perfusion and ventilation of the donor organ. L-ornithine, the product of arginase activity, is precursor for polyamine and proline biosynthesis which are both involved in airway remodeling. The purpose of this review is to summarize the current knowledge on the role of alterations in the L-arginine metabolism in lung transplantation.

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Section: No/l-arginine Metabolismmentioning

confidence: 99%

Alterations in L-Arginine Metabolism After Lung Transplantation~!2009-11-12~!2010-03-25~!2010-05-04~!

Mehl¹,

Grasemann²

2010

TONOJ

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“…Administration of NO has been shown to inhibit neutrophil and platelet sequestration into the lung allograft. 22,23 (3) Increased endothelin-1 (ET-1) production-ET-1 is a potent vasoconstrictor peptide, with mitogenic as well as apoptotic effects on vessel wall cells. 24 NO is known to inhibit the synthesis of ET-1.…”

Section: Nitric Oxidementioning

confidence: 99%

Report of the ISHLT Working Group on Primary Lung Graft Dysfunction Part VI: Treatment

Shargall

Guenther

Ahya

et al. 2005

The Journal of Heart and Lung Transplantation

117

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“…Among the free radicals produced during IR, NO is also important 32 . Excessive production of NO through the activity of iNOS contributes to the pathophysiology of II/R 17 .…”

Section: Discussionmentioning

confidence: 99%

Panax notoginseng saponins attenuate acute lung injury induced by intestinal ischaemia/reperfusion in rats

Rong

Chen

et al. 2009

Respirology

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NO: More Than Just a Vasodilator in Lung Transplantation

Cited by 16 publications

References 48 publications

Alterations in L-Arginine Metabolism After Lung Transplantation~!2009-11-12~!2010-03-25~!2010-05-04~!

Alterations in L-Arginine Metabolism After Lung Transplantation~!2009-11-12~!2010-03-25~!2010-05-04~!

Report of the ISHLT Working Group on Primary Lung Graft Dysfunction Part VI: Treatment

Panax notoginseng saponins attenuate acute lung injury induced by intestinal ischaemia/reperfusion in rats

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