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Inhaled nitric oxide (NO) has been shown to reduce the mean pulmonary artery pressure (mPAP) and to improve PaO2 in patients with acute respiratory failure undergoing oxygen (O2) therapy. However, inhaled NO reduced pulmonary hypertension without improving PaO2 in patients with chronic obstructive pulmonary disease (COPD). This study was intended to compare the hemodynamic and gas exchange responses during inhalation of NO or O2 with those observed during the combined inhalation of NO and O2 in 10 spontaneously breathing COPD patients. Hemodynamic and blood gas parameters were measured after breathing: (1) room air; (2) NO added to room air; (3) O2 (1 L/min); or (4) NO and O2. During inhalation of 2 ppm NO added to room air, the mPAP (23.1 +/- 2.5 versus 20.6 +/- 2.2 mm Hg) and the pulmonary vascular resistance (PVR) (434 +/- 70 versus 378 +/- 50 dyne s/cm5) were significantly (p < 0.05) lower than those measured with room air. However, the values of PaO2 did not improve. The combined inhalation of NO and O2 was associated not only with a significant (p < 0.05) decrease of mPAP (21.4 +/- 2.3 versus 19.7 +/- 1.8 mm Hg) and PVR (431 +/- 72 versus 370 +/- 44 dyne s/cm5), but also with a remarkable improvement (p < 0.05) in the values of PaO2 (91.4 +/- 6.6 versus 111.5 +/- 7.8 mm Hg) as compared with values obtained during the inhalation of O2 alone. These findings suggest that combined therapy with NO and O2 may constitute an alternative approach to treating patients with COPD and pulmonary hypertension.

Arterial endothelin-1 level in pulmonary emphysema and interstitial lung disease. Relation with pulmonary hypertension during exercise. T. Yamakami, O. Taguchi, E.C. Gabazza, M. Yoshida, T. Kobayashi, H. Kobayashi, H. Yasui, H. Ibata, Y Adachi. ERS Journals Ltd 1997. ABSTRACT: This study was undertaken to assess the arterial plasma levels of endothelin-1 (ET-1) and their relationship with pulmonary haemodynamic and gas exchange variables during exercise in patients with emphysema and interstitial lung disease (ILD).Incremental cycle ergometry was performed in all patients up to maximal capacity. At rest, arterial ET-1 levels were higher in emphysema (1.86±0.35 pg·mL -1 ; p<0.02) and ILD (1.75±0.25 pg·mL -1 ; p<0.03) patients than in controls (1.35±0.18 pg·mL -1 ). Emphysema (2.08±0.26 versus 1.70±0.40 pg·mL -1 ) and ILD (1.98±0.21 versus 1.67±0.02 pg·mL -1 ) patients with pulmonary hypertension (PH) presented significantly (p<0.05) higher arterial ET-1 levels than those without. At rest, arterial ET-1 levels were significantly correlated with mean pulmonary arterial pressure (Ppa) in both ILD (r=0.8, p=0.01) and emphysema (r=0.5, p=0.03) patients. During exercise, the arterial ET-1 levels were significantly correlated with arterial oxygen (Pa,O 2 ) (r=-0.6, p=0.04), alveolar-arterial oxygen difference (r=0.8, p=0.01), and Ppa (r=0.6, p=0.04) in ILD patients, but not in those with emphysema.In brief, the results of this study suggest that arterial endothelin-1 is markedly increased in interstitial lung disease and emphysema patients, and that, it is related to the exercise-induced exacerbation of pulmonary hypertension in patients with interstitial lung disease, but not in those with emphysema. Eur Respir J 1997; 10: 2055-2060. Pulmonary artery hypertension is the major cardiovascular complication of emphysema and advanced interstitial lung disease (ILD) [1]. Pulmonary hypertension (PH) is important, not only because it is associated with right ventricular hypertrophy (or cor pulmonale) but also because it adversely affects prognosis in these patients [2]. The mechanisms responsible for PH include thrombotic obstruction of pulmonary blood vessels, reduced distensibility of the pulmonary vascular bed, pulmonary vascular obstruction produced by medial hypertrophy or intimal proliferation, and pulmonary vasoconstriction elicited by acute or chronic alveolar hypoxia [3,4]. Of these, hypoxic vasoconstriction has been considered one of the major factors involved in the pathogenesis of sustained PH or in the development of acute exacerbation of PH in patients with emphysema or advanced ILD [5]. However, the precise mechanism by which hypoxia induces pulmonary vasoconstriction and the structural changes that ensue from chronic hypoxia have not been fully elucidated. Endothelin-1 (ET-1), a vasoconstricting peptide originally isolated from cultured human endothelial cells, may play a relevant role in the pathogenesis of PH during hypoxia [6][7][8]. This assumption is supported by previous findings that showed that the e...

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