Effect of inhaled nitric oxide on hemodynamics and VA/Q inequalities in patients with chronic obstructive pulmonary disease.

Moinard, J.; Manier, G.; Pillet, O.; Castaing, Y.

doi:10.1164/ajrccm.149.6.8004302

Cited by 84 publications

(42 citation statements)

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“…In biopsy lung specimens from patients with PPH, the greater the area of pulmonary artery media, the greater the changes in PAP induced by intravenous or oral vasodilator drugs [20]. The reduction of mPAP during NO inhalation was correlated with the level of mPAP without NO in ARDS [12,13,21], chronic obstructive pulmonary disease [22] and congenital heart disease [18], but not in PPH [3] and another group of ARDS [5]. The degree of response to inhaled NO was quite variable [1].…”

Section: Discussionmentioning

confidence: 99%

Correlation of inhaled nitric-oxide induced reduction of pulmonary artery pressure and vascular changes

Jiang

Maruyama²,

Yokochi³

et al. 2002

European Respiratory Journal

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The purpose of the present study was to determine the relationship between hypertensive pulmonary vascular remodelling and the changes in mean pulmonary artery pressure (mPAP) during low-dose nitric oxide (NO) inhalation.Rats were exposed to chronic hypobaric hypoxia (air at 50.5 kPa (380 mmHg), 10% oxygen, for 5-29 days) to induce chronic pulmonary hypertension (PH) with pulmonary vascular structural changes. After the chronic hypoxic exposure, the rats had an indwelling pulmonary artery catheter inserted and changes in mPAP with NO were correlated to morphometrical analysis of pulmonary vascular changes.All concentrations of inhaled NO (0.1-2.0 parts per million) reduced mPAP with a similar per cent reduction from baseline mPAP in PH rats, while no changes were observed in control rats. During NO inhalation in PH rats, the absolute value of the decrease in mPAP, but not per cent reduction in mPAP, significantly correlated with baseline mPAP, the percentage of muscularised arteries at the alveolar wall level and at the alveolar duct level, and the per cent medial wall thickness of muscularised arteries.In the chronic hypoxic pulmonary hypertension model, the severity of pulmonary vascular remodelling did not alter the reactivity of the pulmonary arteries to nitric oxide and might, in part, determine the magnitude of nitric-oxide induced absolute reduction in mean pulmonary artery pressure. In all conditions causing pulmonary hypertension (PH), vascular changes include new muscularisation of normally non-muscular peripheral pulmonary arteries and medial muscle hypertrophy of normally muscular arteries. Abnormal muscular pulmonary vasculature might have a heightened reactivity [1, 2], which may explain the effect of nitric oxide (NO) inhalation in hypertensive pulmonary disease, because NO dilates constricted pulmonary vasculature. Although inhaled NO can dilate these structurallyremodelled pulmonary arteries, the degree of response to inhaled NO was quite variable in patients with congenital heart disease [1], primary pulmonary hypertension (PPH) [3], limited scleroderma and isolated PH [4] and severe acute respiratory distress syndrome (ARDS) [5]. The differences in severity of pulmonary vascular structural changes might explain the differences in inhaled NO-induced reduction in pulmonary artery pressure (PAP) among patients.Chronic hypoxia induces PH and hypertensive pulmonary vascular changes in rats [6][7][8]. With increasing exposure to hypoxia, there is a progressive increase in the severity of the hypertensive pulmonary vascular changes [7]. These findings allowed the authors to make a rat model of experimentally different degrees of PH and hypertensive pulmonary vascular changes. To determine the relationship between the hypertensive pulmonary vascular changes and response to inhaled NO, NO inhalation was carried out in a rat model of chronic PH induced by chronic hypoxic exposure of varying durations. Quantitative morphometrical analysis was applied to determine the severity of hypertensive pu...

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Section: Discussionmentioning

confidence: 99%

Correlation of inhaled nitric-oxide induced reduction of pulmonary artery pressure and vascular changes

Jiang

Maruyama²,

Yokochi³

et al. 2002

European Respiratory Journal

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“…43 Inhalation of NO has no comparing NO and 100% oxygen, no significant overall effect was seen on Pa 2 or V /Q following inhaled NO effect on pulmonary or systemic haemodynamics, nor on gas exchange in awake lambs 44 or humans 45 breathing (15 ppm). 56 However, a follow up study from the group of Barberà air, but completely reversed HPV induced in the same studies by inspiring 12% oxygen. In mechanically ventiland colleagues using non-invasive measurements of arterial oxygenation and cardiac output confirmed worated sheep this response has been attributed to redistribution of blood flow to better ventilated lung sening gas exchange following inhalation of NO (40 ppm), not only in patients with severe COPD but units.…”

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confidence: 88%

“…Some hypertension. [55][56][57] Changes in haemodynamics and gas exchange were investigated in patients with advanced agents induce a worsening of peripheral oedema due to negative inotropy and a fall in cardiac output. 37 38 COPD in response to breathing room air, NO at 40 parts per million in air, and 100% oxygen.…”

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confidence: 99%

NO: COPD and beyond

Jones

Evans²

1997

Thorax

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“…Inhaled nitric oxide (NO) has been shown to selectively and acutely vasodilate pulmonary vessels in various hypertensive lung diseases [8][9][10][11]. Inhaled NO has been shown to be more effective than inhaled oxygen (O 2 ) in decreasing the mean pulmonary artery pressure (Ppa) in disorders associated with chronic pulmonary hypertension [12]. Moreover, inhaled NO improves arterial oxygenation in patients with the acute respiratory distress syndrome (ARDS) undergoing O 2 therapy [13].…”

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confidence: 99%

The effect of low-dose inhalation of nitric oxide in patients with pulmonary fibrosis

Yoshida¹,

Taguchi²,

Gabazza³

et al. 1997

Eur Respir J

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The aim of this study was to determine whether low-dose inhalation of nitric oxide (NO) improves pulmonary haemodynamics and gas exchange in patients with stable idiopathic pulmonary fibrosis (IPF).The investigation included 10 IPF patients breathing spontaneously. Haemodynamic and blood gas parameters were measured under the following conditions: 1) breathing room air; 2) during inhalation of 2 parts per million (ppm) NO with room air; 3) whilst breathing O 2 alone (1 L·min -1 ); and 4) during combined inhalation of 2 ppm NO and O 2 (1 L·min -1 ).During inhalation of 2 ppm NO with room air the mean pulmonary arterial pressure (Ppa 25±3 vs 30±4 mmHg) and the pulmonary vascular resistance (PVR 529±80 vs 699±110 dyn·s·cm -5 ) were significantly (p<0.01) lower than levels measured whilst breathing room air alone. These findings suggest that the combined use of nitric oxide and oxygen might constitute an alternative therapeutic approach for treating idiopathic pulmonary fibrosis patients with pulmonary hypertension. However, further studies must first be carried out to demonstrate the beneficial effect of oxygen therapy on pulmonary haemodynamics and prognosis in patients with idiopathic pulmonary fibrosis and to rule out the potential toxicity of inhaled nitric oxide, particularly when used in combination with oxygen. Eur Respir J 1997; 10: 2051-2054. Idiopathic pulmonary fibrosis (IPF) is characterized by progressive inflammatory and fibrotic processes of the lung [1][2][3]. The beneficial effect of long-term oxygen therapy (LTOT) has not been demonstrated in IPF patients: however, LTOT is commonly prescribed to patients with advanced IPF associated with hypoxaemia and pulmonary hypertension [4][5][6][7]. Inhaled nitric oxide (NO) has been shown to selectively and acutely vasodilate pulmonary vessels in various hypertensive lung diseases [8][9][10][11]. Inhaled NO has been shown to be more effective than inhaled oxygen (O 2 ) in decreasing the mean pulmonary artery pressure (Ppa) in disorders associated with chronic pulmonary hypertension [12]. Moreover, inhaled NO improves arterial oxygenation in patients with the acute respiratory distress syndrome (ARDS) undergoing O 2 therapy [13].This effect of inhaled NO has also been demonstrated in cases of pulmonary fibrosis during acute exacerbation undergoing O 2 therapy [14,15]. CHANNICK et al. [14] first reported that inhalation of 40 parts per million (ppm) NO is effective for improving pulmonary haemodynamics and arterial oxygenation. However, NO concentrations lower than 10 ppm have been shown to be sufficient for improving pulmonary hypertension and gas exchange in ARDS patients [16]. In fact, we have previously reported that 2 ppm NO improved pulmonary hypertension and arterial oxygenation in a patient with IPF undergoing acute exacerbation [15].However, the effect of inhaled NO in clinically stable IPF patients spontaneously breathing room air has not yet been reported. The combined inhalation of NO and O 2 has been reported to be effective for impro...

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Effect of inhaled nitric oxide on hemodynamics and VA/Q inequalities in patients with chronic obstructive pulmonary disease.

Cited by 84 publications

References 0 publications

Correlation of inhaled nitric-oxide induced reduction of pulmonary artery pressure and vascular changes

Correlation of inhaled nitric-oxide induced reduction of pulmonary artery pressure and vascular changes

NO: COPD and beyond

The effect of low-dose inhalation of nitric oxide in patients with pulmonary fibrosis

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