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Pulmonary hypertension in chronic obstructive pulmonary disease

J.A. Barberà, V.I. Peinado, S. Santos
European Respiratory Journal 2003 21: 892-905; DOI: 10.1183/09031936.03.00115402
J.A. Barberà
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V.I. Peinado
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S. Santos
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Figures

  • Fig. 1.—
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    Fig. 1.—

    Pulmonary muscular artery from a patient with chronic obstructive pulmonary disease. Note the prominent intimal thickening and the luminal narrowing. a) Immunostaining with monoclonal antibody against α–smooth muscle actin, showing abundant proliferation of smooth-muscle cells in the intima. b) Orcein stain disclosing abundant deposition of elastic fibres in the intimal layer. Internal scale bar=42.2 µm.

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    Fig. 2.—

    Changes in tension of pulmonary arteries, expressed as per cent reduction from precontraction with L‐phenylephrine (LP), in response to cumulative concentrations of adenosine diphosphate (ADP), in patients with chronic obstructive pulmonary disease (○) and nonsmokers (•). *: p<0.05 compared with nonsmokers.

  • Fig. 3.—
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    Fig. 3.—

    Photomicrograph of a pulmonary muscular artery from a patient with chronic obstructive pulmonary disease, immunostained with monoclonal antibody against CD8+. Positive cells (brown) are located in the adventitia. Internal scale bar=42.2 µm.

  • Fig. 4.—
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    Fig. 4.—

    Immunohistochemical expression of endothelial nitric oxide synthase in a smoker's lung. *: Note the negative signal in a small pulmonary artery, whereas positive staining is apparent in a portion of a larger artery (arrows). Internal scale bar=85.1 µm.

  • Fig. 5.—
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    Fig. 5.—

    Pathophysiology of pulmonary hypertension in chronic obstructive pulmonary disease where cigarette-smoke products play a central role in initiating the sequence of changes which results in pulmonary hypertension.

  • Fig. 6.—
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    Fig. 6.—

    Alveolar ventilation/perfusion ratio (V′A/Q′) distributions in a patient with chronic obstructive pulmonary disease, recovered while breathing a) room air and b) 100% oxygen. During 100% oxygen breathing the V′A/Q′ distribution became worse, as shown by increased perfusion in poorly ventilated alveolar units with low V′A/Q′. Such an increase in V′A/Q′ inequality is explained by the inhibition of hypoxic pulmonary vasoconstriction. •: Blood flow; ○: ventilation.

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    Fig. 7.—

    Ventilation/perfusion ratio (V′A/Q′) distributions in a patient with COPD, obtained a) before and b) after administering 20 mg of nifedipine. Note the increase in V′A/Q′ mismatch (increase in perfusion of lung units with low V′A/Q′) after nifedipine, which resembles that shown during 100% oxygen breathing (fig. 6⇑). •: Blood flow; ○: ventilation.

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Pulmonary hypertension in chronic obstructive pulmonary disease
J.A. Barberà, V.I. Peinado, S. Santos
European Respiratory Journal May 2003, 21 (5) 892-905; DOI: 10.1183/09031936.03.00115402

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Pulmonary hypertension in chronic obstructive pulmonary disease
J.A. Barberà, V.I. Peinado, S. Santos
European Respiratory Journal May 2003, 21 (5) 892-905; DOI: 10.1183/09031936.03.00115402
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  • Article
    • Abstract
    • Incidence
    • Clinical relevance
    • Natural history of pulmonary hypertension in chronic obstructive pulmonary disease
    • New concepts in pathogenesis
    • Physiopathology
    • Assessment of pulmonary hypertension in chronic obstructive pulmonary disease
    • Treatment
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    • References
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  • Non-CPAP therapy in obstructive sleep apnoea
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