Preventive Influence of Inhaled Nitric Oxide on Lung Ischemia-Reperfusion Injury

Surgery Today ◽  
1999 ◽  
Vol 29 (9) ◽  
pp. 897-901 ◽  
Author(s):  
Hiroyuki Yamagishi ◽  
Chojiro Yamashita ◽  
Masayoshi Okada
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide

Protection of lung tissue against ischemia/reperfusion injury by preconditioning with inhaled nitric oxide in an in situ pig model of normothermic pulmonary ischemia

Nitric Oxide ◽  
2004 ◽  
Vol 10 (4) ◽  
pp. 195-201 ◽  
Author(s):  
Thomas Waldow ◽  
Konstantin Alexiou ◽  
Wolfgang Witt ◽  
Florian M Wagner ◽  
Utz Kappert ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Lung Tissue ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide ◽  
Pig Model ◽  
Pulmonary Ischemia

Preventive influence of inhaled nitric oxide on lung ischemia-reperfusion injury

Surgery Today ◽  
1999 ◽  
Vol 29 (9) ◽  
pp. 897-901 ◽  
Author(s):  
Hiroyuki Yamagishi ◽  
Chojiro Yamashita ◽  
Masayoshi Okada
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide

Inhaled nitric oxide attenuates apoptosis in ischemia-reperfusion injury of the rabbit lung

2004 ◽  
Vol 78 (1) ◽  
pp. 292-297 ◽  
Author(s):  
Hideki Yamashita ◽  
Shinji Akamine ◽  
Yorihisa Sumida ◽  
Masao Inoue ◽  
Takahiro Sawada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide ◽  
Rabbit Lung

A Randomized Trial of Inhaled Nitric Oxide to Prevent Ischemia–Reperfusion Injury after Lung Transplantation

2003 ◽  
Vol 167 (11) ◽  
pp. 1483-1489 ◽  
Author(s):  
Maureen O. Meade ◽  
John T. Granton ◽  
Andrea Matte-Martyn ◽  
Karen McRae ◽  
Bruce Weaver ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Transplantation ◽  
Randomized Trial ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide

Pulmonary Macrophage Inhibition and Inhaled Nitric Oxide Attenuate Lung Ischemia-Reperfusion Injury

2007 ◽  
Vol 84 (1) ◽  
pp. 247-253 ◽  
Author(s):  
Leo M. Gazoni ◽  
Curtis G. Tribble ◽  
Min Q. Zhao ◽  
Eric B. Unger ◽  
Robert A. Farrar ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide ◽  
Pulmonary Macrophage

scholarly journals No Signs of Inflammation during Knee Surgery with Ischemia: A Study Involving Inhaled Nitric Oxide

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Lars Hållström ◽  
Claes Frostell ◽  
Anders Herrlin ◽  
Eva Lindroos ◽  
Ingrid Lundberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Reperfusion Injury ◽  
Cell Activation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide ◽  
Endothelial Cell Activation ◽  
Soluble Adhesion Molecules ◽  
Group 2

Nitric oxide donors and inhaled nitric oxide (iNO) may decrease ischemia/reperfusion injury as reported in animal and human models. We investigated whether the attenuation of reperfusion injury, seen by others, in patients undergoing knee arthroplasty could be reproduced when patients had spinal anesthesia. 45 consecutive patients were randomized into three groups (n=15). Groups 1 and 3 were receiving iNO 80 ppm or placebo (nitrogen, N2) throughout the entire operation, and group 2 only received iNO in the beginning and at the end of the operation. Blood samples were collected before surgery, at the end of the surgery, and 2 hours postoperatively. Muscle biopsies were taken from quadriceps femoris muscle before and after ischemia. There were no increases in plasma levels of soluble adhesion molecules: ICAM, VCAM, P-selectin, E-selectin, or of HMGB1, in any of the groups. There were low numbers of CD68+ macrophages and of endothelial cells expression of ICAM, VCAM, and P-selectin in the muscle analyzed by immunohistochemistry, prior to and after ischemia. No signs of endothelial cell activation or inflammatory response neither systemically nor locally could be detected. The absence of inflammatory response questions this model of ischemia/reperfusion, but may also be related to the choice of anesthetic method EudraCTnr.

scholarly journals Medical Gases: A Novel Strategy for Attenuating Ischemia—Reperfusion Injury in Organ Transplantation?

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Arunotai Siriussawakul ◽  
Lucinda I. Chen ◽  
John D. Lang
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
Organ Transplantation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide ◽  
Clinical Consequence ◽  
Solid Organ

Ischemia reperfusion injury (IRI) is an inevitable clinical consequence in organ transplantation. It can lead to early graft nonfunction and contribute to acute and chronic graft rejection. Advanced molecular biology has revealed the highly complex nature of this phenomenon and few definitive therapies exist. This paper reviews factors involved in the pathophysiology of IRI and potential ways to attenuate it. In recent years, inhaled nitric oxide, carbon monoxide, and hydrogen sulfide have been increasingly explored as plausible novel medical gases that can attenuate IRI via multiple mechanisms, including microvascular vasorelaxation, reduced inflammation, and mitochondrial modulation. Here, we review recent advances in research utilizing inhaled nitric oxide, carbon monoxide, and hydrogen sulfide in animal and human studies of IRI and postulate on its future applications specific to solid organ transplantation.

PREVENTIVE EFFECT OF INHALED NITRIC OXIDE AND PENTOXIFYLLINE ON ISCHEMIA/REPERFUSION INJURY AFTER LUNG TRANSPLANTATION

2001 ◽  
Vol 71 (9) ◽  
pp. 1295-1300 ◽  
Author(s):  
Gabriel Thabut ◽  
Olivier Brugi??re ◽  
Guy Les??che ◽  
Jean Baptiste Stern ◽  
Karim Fradj ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide ◽  
Preventive Effect

Preconditioning by inhaled nitric oxide prevents hyperoxic and ischemia/reperfusion injury in rat lungs

2008 ◽  
Vol 21 (2) ◽  
pp. 418-429 ◽  
Author(s):  
Thomas Waldow ◽  
Wolfgang Witt ◽  
André Ulmer ◽  
Andreas Janke ◽  
Konstantin Alexiou ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide ◽  
Rat Lungs

scholarly journals Brief Periods of Nitric Oxide Inhalation Protect against Myocardial Ischemia–Reperfusion Injury

2008 ◽  
Vol 109 (4) ◽  
pp. 675-682 ◽  
Author(s):  
Yasuko Nagasaka ◽  
Bernadette O. Fernandez ◽  
Maria F. Garcia-Saura ◽  
Bodil Petersen ◽  
Fumito Ichinose ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide ◽  
Cardiac Ischemia ◽  
Nitric Oxide Inhalation ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Nitric Oxide Metabolites

Background Prolonged breathing of nitric oxide reduces myocardial ischemia-reperfusion injury, but the precise mechanisms responsible for the cardioprotective effects of inhaled nitric oxide are incompletely understood. Methods The authors investigated the fate of inhaled nitric oxide (80 parts per million) in mice and quantified the formation of nitric oxide metabolites in blood and tissues. The authors tested whether the accumulation of nitric oxide metabolites correlated with the ability of inhaled nitric oxide to protect against cardiac ischemia-reperfusion injury. Results Mice absorbed nitric oxide in a nearly linear fashion (0.19 +/- 0.02 micromol/g x h). Breathing nitric oxide rapidly increased a broad spectrum of nitric oxide metabolites. Levels of erythrocytic S-nitrosothiols, N-nitrosamines, and nitrosyl-hemes increased dramatically within 30 s of commencing nitric oxide inhalation. Marked increases of lung S-nitrosothiol and liver N-nitrosamine levels were measured, as well as elevated cardiac and brain nitric oxide metabolite levels. Breathing low oxygen concentrations potentiated the ability of inhaled nitric oxide to increase cardiac nitric oxide metabolite levels. Concentrations of each nitric oxide metabolite, except nitrate, rapidly reached a plateau and were similar after 5 and 60 min. In a murine cardiac ischemia-reperfusion injury model, breathing nitric oxide for either 5 or 60 min before reperfusion decreased myocardial infarction size as a fraction of myocardial area at risk by 31% or 32%, respectively. Conclusions Breathing nitric oxide leads to the rapid accumulation of a variety of nitric oxide metabolites in blood and tissues, contributing to the ability of brief periods of nitric oxide inhalation to provide cardioprotection against ischemia-reperfusion injury. The nitric oxide metabolite concentrations achieved in a target tissue may be more important than the absolute amounts of nitric oxide absorbed.

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