Nitric Oxide (Endothelium-Derived Relaxing Factor) Attenuates Revascularization-Induced Lung Injury

Abdih, H.; Kelly, C. J.; Bouchier‐Hayes, David; William, R.; Watson, Grace; Redmond, H. P.; Burke, P.

doi:10.1006/jsre.1994.1106

Cited by 52 publications

(27 citation statements)

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“…It has been recognized that NO inhibits neutrophil adherence and activation in different organs [17] and also prevents the production of oxygen free radicals by N-formyl-methionyl-leucyl-phenylalanine (FMLP) or phorbol myristate acetate (PMA)-stimulated neutrophils [34]. Thus, NO, released in response to cytokines produced by endothelial cells or macrophages at sites of inflammation, may protect against neutrophil-dependent tissue injury [35].…”

Section: Discussionmentioning

confidence: 99%

“…In isolated rabbit lungs perfused with the xanthine-xanthine oxidase superoxide generating system, inhaled NO prevented oedema formation [16]. It is also hypothesised that NO protects against cellular damage likely to occur during reperfusion following lung ischaemia [17]. It was recently demonstrated that an NO-precursor, Larginine [18] and inhaled NO [4] prevented ischaemiareperfusion lung injury.…”

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confidence: 99%

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L-NAME aggravates pulmonary oxygen toxicity in rats

Capellier¹,

Maupoil²,

Boillot³

et al. 1996

Eur Respir J

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L L--N NA AM ME E a ag gg gr ra av va at te es s p pu ul lm mo on na ar ry y o ox xy yg ge en n t to ox xi ic ci it ty y i in n r ra at ts s G. Capellier*, V. Maupoil**, A. Boillot + , J-P. Kantelip ++ , L. Rochette ‡ , J. Regnard ‡ ‡ , F. Barale* + L-NAME aggravates pulmonary oxygen toxicity in rats. G. Capellier, V. Maupoil, A. Boillot, J-P. Kantelip, L. Rochette, J. Regnard, F. Barale. ERS Journals Ltd 1996. ABSTRACT: Exposure to high oxygen concentration leads to acute lung injury and death in rats after 72 h. The pathophysiology of this phenomenon relies on several mechanisms, including alteration of vascular reactivity, recruitment and activation of neutrophils and alveolar macrophages, production of cytokines and excess production of free radicals. In addition to its potent vasodilating effect, nitric oxide (NO) has also been reported to prevent free radical-mediated damage. We wanted to determine whether N G -nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, might modulate oxygen toxicity. In rats exposed to continuous high oxygen concentration, we studied the effect of administration of 50 mg·kg -1 of intraperitoneal L-NAME twice a day on the first day of oxygen exposure.L-NAME resulted in earlier death, since 57% of the animals exposed to oxygen and injected with L-NAME died within 60 h as compared to 22% of the animals exposed to oxygen and treated with saline (p<0.01). Haematocrit and bronchoalveolar lavage fluid protein were also significantly increased in animals exposed to oxygen and receiving L-NAME. The lung water content was higher in the oxygen-exposed groups (p<0.01) and slightly decreased by L-NAME (p<0.05). Thiobarbituaric acid reactive substances (TBARS) were elevated in plasma (p<0.01) and decreased in lung (p<0.001) of oxygen-exposed animals, but no significant effect of L-NAME was observed.N G -nitro-L-arginine methyl ester had a deleterious effect in rats exposed to hyperoxia, which might suggest that endogenous nitric oxide has a protective role against hyperoxia-induced pulmonary lesions.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

L-NAME aggravates pulmonary oxygen toxicity in rats

Capellier¹,

Maupoil²,

Boillot³

et al. 1996

Eur Respir J

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“…NO donors and stimulation of endogenous NO production reduce pulmonary injury due to IRI (38,39), reduce PMN influx after pulmonary IRI, assessed by myeloperoxidase (MPO) assay (31,40). NO inhibits neutrophil activation, aggregation and migration (37,41), platelet activation (42), and reduces cytokine-induced CAM expression (43).…”

Section: No Reduces Iri In Lungs Transplanted From Nhbdsmentioning

confidence: 99%

Nitric Oxide Ventilation of Rat Lungs from Non-Heart-Beating Donors Improves Posttransplant Function

Dong

Abano

Egan

2009

American Journal of Transplantation

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Lungs from non-heart-beating donors (NHBDs) would enhance the donor pool. Ex vivo perfusion and ventilation of NHBD lungs allows functional assessment and treatment. Ventilation of rat NHBD lungs with nitric oxide (NO) during ischemia, ex vivo perfusion and after transplant reduced ischemia-reperfusion injury (IRI) and improved lung function posttransplant. One hour after death, Sprague-Dawley rats were ventilated for another hour with either 60% O2 or 60% O2/40 ppm NO. Lungs were then flushed with 20-mL cold Perfadex, stored cold for 1 h, perfused in an ex vivo circuit with Steen solution and warmed to 37• C, ventilated 15 min, perfusion-cooled to 20 • C, then flushed with cold Perfadex and stored cold. The left lung was transplanted and ventilated separately. Recipients were sacrificed after 1 h. NO-ventilation was associated with significantly reduced wet:dry weight ratio in the ex vivo circuit, better oxygenation, reduced pulmonary vascular resistance, increased lung tissue levels of cGMP, maintained endothelial NOS eNOS, and reduced increases in tumor necrosis factor alpha (TNF-a ) and inducible nitric oxide synthase (iNOS). NO-ventilation had no effect on MAP kinases or NFj B activation. NO administration to NHBDs before and after lung retrieval may improve function of lungs from NHBDs.

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“…NO has vasodilatory effects and inhibits platelet aggregation and neutrophil infiltration. In recent studies, the cytoprotective role of L-arginine/NO donors in the prevention of myocardial, lung and cerebral ischemia reperfusion injury is reported [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Effect of Nitric Oxide on Postoperative Adhesion Formation

Özden¹,

Bostancı²,

Sarioğlu

et al. 1999

Eur Surg Res

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Peritoneal adhesions continue to be a significant cause of postoperative complications. The purpose of the present study was to investigate the effect of nitric oxide in preventing postoperative adhesion formation in rats. Three randomized groups of Sprague-Dawley rats were subjected to a standardized lesion by cecal abrasion and parietal peritoneal defect. 0.9% NaCl (control, group 1), L-arginine (300 mg/kg, group 2) and Nω-nitro arginine methyl ester (L-NAME; 25 mg/kg, group 3) were administered intraperitoneally before abdominal closure and during 3 consecutive days after surgery. Two weeks after surgery, a relaparotomy was performed and the extent of adhesion formation was determined. In groups 1 and 3 heavy adhesions were detected. In the L-arginine group, adhesion formation was significantly less than in the other groups (p < 0.05). This study showed that L-arginine reduced adhesion formation.

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Nitric Oxide (Endothelium-Derived Relaxing Factor) Attenuates Revascularization-Induced Lung Injury

Cited by 52 publications

References 0 publications

L-NAME aggravates pulmonary oxygen toxicity in rats

L-NAME aggravates pulmonary oxygen toxicity in rats

Nitric Oxide Ventilation of Rat Lungs from Non-Heart-Beating Donors Improves Posttransplant Function

Effect of Nitric Oxide on Postoperative Adhesion Formation

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