Flow-mediated release of nitric oxide in isolated, perfused rabbit lungs

Ogasa, Toshiyuki; Nakano, Hitoo; Ide, Hiroshi; Yamämoto, Yasushi; Sasaki, Norihiko; Osanai, Shinobu; Akiba, Yuji; Kikuchi, Kenjiro; Iwamoto, Jun

doi:10.1152/jappl.2001.91.1.363

Cited by 11 publications

(12 citation statements)

References 24 publications

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“…This finding is consistent with studies from other laboratories (19,26,(35)(36)(37). Conversely, we recently found that in younger pigs (age 3-4 d), exNO production was decreased by chronic hypoxia but perfusate NOx (nitrites/nitrates) production was unaffected, and chronic hypoxia decreased only eNOS and nNOS protein levels in the airways (34).…”

supporting

confidence: 92%

l-Lysine Decreases Nitric Oxide Production and Increases Vascular Resistance in Lungs Isolated from Lipopolysaccharide-Treated Neonatal Pigs

2004

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Nitric oxide (NO) production may depend on the uptake of L-arginine (L-arg), the substrate for NO synthase in inflammatory lung diseases. The cellular transport of L-arg occurs via the cationic amino acid transporters (CAT), and L-lysine (L-lys) competitively inhibits CAT. Neonatal pigs were treated with lipopolysaccharide (LPS) or vehicle for 4 h. LPS increased exhaled NO (exNO; 0.026 Ϯ 0.003 to 0.046 Ϯ 0.003 nmol · kg Ϫ1 · minϪ1 ; p Ͻ 0.005) and decreased mean systemic arterial blood pressure (89 Ϯ 4 to 67 Ϯ 4 mm Hg; p Ͻ 0.05), whereas vehicle did not affect exNO or mean systemic arterial blood pressure. The lungs were then isolated and perfused; exNO was greater in lungs from LPS-treated animals (0.08 Ϯ 0.01 nmol/kg/min) than in lungs from vehicle-treated animals (0.05 Ϯ 0.01 nmol · kg Increased nitric oxide (NO) production is associated with diseases characterized by an inflammatory response, for example, acute respiratory distress syndrome and septic shock (1-4). Activation of inflammatory cells during infection causes the release of cytokines such as tumor necrosis factor-␣ (TNF-␣), IL-1␤, and interferon-␥, and these cytokines have been found to increase NO synthase (NOS) expression, resulting in increased NO production (5-7). The inflammation-induced increase in NO production potentiates vascular complications and participates in the pathogenesis of lung injury (1, 2, 4).NO is produced by the oxidation of L-arginine (L-arg) to L-citrulline and NO, which is catalyzed by NOS. There are three well-characterized isoforms of NOS: endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS). eNOS and nNOS are for the most part constitutively expressed, and iNOS expression is largely induced by various stimuli, Received October 8, 2003; accepted February 5, 2004

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confidence: 92%

l-Lysine Decreases Nitric Oxide Production and Increases Vascular Resistance in Lungs Isolated from Lipopolysaccharide-Treated Neonatal Pigs

2004

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“…Shear stress response elements have been identified in the sequence of genes encoding important vascular growth factors (Ballermann et al 1998). Furthermore, there is evidence that increased shear stress alters endothelial cell membrane potential and increases NO production in the isolated intact lung and in the whole organism (Nakache & Gaub, 1988;Hakim, 1994;Storme et al 1999;Tworetzky et al 2000;Ogasa et al 2001).…”

Section: Altered Endothelial Function and Vascular Remodellingmentioning

confidence: 99%

The structural basis of pulmonary hypertension in chronic lung disease: remodelling, rarefaction or angiogenesis?

Hopkins¹,

McLoughlin²

2002

Journal of Anatomy

128

105

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Chronic lung disease in humans is frequently complicated by the development of secondary pulmonary hypertension, which is associated with increased morbidity and mortality. Hypoxia, inflammation and increased shear stress are the primary stimuli although the exact pathways through which these initiating events lead to pulmonary hypertension remain to be completely elucidated. The increase in pulmonary vascular resistance is attributed, in part, to remodelling of the walls of resistance vessels. This consists of intimal, medial and adventitial hypertrophy, which can lead to encroachment into and reduction of the vascular lumen. In addition, it has been reported that there is a reduction in the number of blood vessels in the hypertensive lung, which could also contribute to increased vascular resistance. The pulmonary endothelium plays a key role in mediating and modulating these changes. These structural alterations in the pulmonary vasculature contrast sharply with the responses of the systemic vasculature to the same stimuli. In systemic organs, both hypoxia and inflammation cause angiogenesis.Furthermore, remodelling of the walls of resistance vessels is not observed in these conditions. Thus it has been generally stated that, in the adult pulmonary circulation, angiogenesis does not occur. Prompted by previous observations that chronic airway inflammation can lead to pulmonary vascular remodelling without hypertension, we have recently shown, using quantitative stereological techniques, that angiogenesis can occur in the adult pulmonary circulation. Pulmonary angiogenesis has also been reported in some other conditions including postpneumonectomy lung growth, metastatic disease of the lung and in biliary cirrhosis. Such angiogenesis may serve to prevent or attenuate increased vascular resistance in lung disease. In view of these more recent data, the role of structural alterations in the pulmonary vasculature in the development of pulmonary hypertension should be carefully reconsidered.

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“…In the literature, a large number of studies dealt with both ex vivo or in vivo analysis of the endothelial NO release (6)(7)(8)(9)(10). In the majority, different perfusion modes are given to the same subject following one another, but this change in perfusion modality affects other mechanisms involved in NO release (11)(12)(13), and consequently alters NO release measurement.…”

mentioning

confidence: 99%

Preservation of Endothelium Nitric Oxide Release by Pulsatile Flow Cardiopulmonary Bypass When Compared With Continuous Flow

et al. 2009

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The aim of this work is to analyze endothelium nitric oxide (NO) release in patients undergoing continuous or pulsatile flow cardiopulmonary bypass (CPB). Nine patients operated under continuous flow CPB, and nine patients on pulsatile flow CPB were enrolled. Plasma samples were withdrawn for the chemiluminescence detection of nitrite and nitrate. Moreover the cellular component was withdrawn for the detection of nitric oxide synthase (NOS) activity in the erythrocytes, and an estimation of systemic inflammatory response was carried out. Significant reduction in the intraoperative concentration with respect to the preoperative was observed only under continuous flow CPB for both nitrite and NO(x) (nitrite + nitrate) concentration (P = 0.010 and P = 0.016, respectively). Significant difference in intraoperative nitrite concentration was also observed between the groups (P = 0.012). Finally, erythrocytes showed a certain endothelial NOS activity, which did not differ between the groups, and no differences in the inflammatory response were pointed out. The significant reduction of NO(2)(-) concentration under continuous perfusion revealed the strong connection among perfusion modality, endothelial NO release, and plasmatic nitrite concentration. The similar erythrocyte eNOS activity between the groups revealed that the differences in blood NO metabolites are mainly ascribable to the endothelium release.

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Flow-mediated release of nitric oxide in isolated, perfused rabbit lungs

Cited by 11 publications

References 24 publications

l-Lysine Decreases Nitric Oxide Production and Increases Vascular Resistance in Lungs Isolated from Lipopolysaccharide-Treated Neonatal Pigs

l-Lysine Decreases Nitric Oxide Production and Increases Vascular Resistance in Lungs Isolated from Lipopolysaccharide-Treated Neonatal Pigs

The structural basis of pulmonary hypertension in chronic lung disease: remodelling, rarefaction or angiogenesis?

Preservation of Endothelium Nitric Oxide Release by Pulsatile Flow Cardiopulmonary Bypass When Compared With Continuous Flow

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