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    <title>Boere-van der Straat, S.</title>
    <link>http://repub.eur.nl/res/aut/4168/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>Influence of lung parenchymal destruction on the different indexes of the methacholine dose-response curve in COPD patients (Article)</title>
      <link>http://repub.eur.nl/res/pub/9317/</link>
      <pubDate>2000-01-01T00:00:00Z</pubDate>
      <description>STUDY OBJECTIVES: The interpretation of nonspecific bronchial provocation
          dose-response curves in COPD is still a matter of debate. Bronchial
          hyperresponsiveness (BHR) in patients with COPD could be influenced by the
          destruction of the parenchyma and the augmented mechanical behavior of the
          lung. Therefore, we studied the interrelationships between indexes of BHR,
          on the one hand, and markers of lung parenchymal destruction, on the
          other. PATIENTS AND METHODS: COPD patients were selected by clinical
          symptoms, evidence of chronic, nonreversible airways obstruction, and BHR,
          which was defined as a provocative dose of a substance (histamine) causing
          a 20% fall in FEV(1) (PC(20)) of &lt;/= 8 mg/mL. BHR was subsequently studied
          by methacholine dose-response curves to which a sigmoid model was fitted
          for the estimation of plateau values and reactivity. Model fits of
          quasi-static lung pressure-volume (PV) curves yielded static lung
          compliance (Cstat), the exponential factor (KE) and elastic recoil at 90%
          of total lung capacity (P90TLC). Carbon monoxide (CO) transfer was
          measured with the standard single-breath method. RESULTS: Twenty-four
          patients were included in the study, and reliable PV data could be
          obtained from 19. The following mean values ( +/- SD) were taken: FEV(1),
          65 +/- 12% of predicted; reversibility, 5.6 +/- 3.1% of predicted; the
          PC(20) for methacholine, 4.3 +/- 5.2 mg/mL; reactivity, 11.0 +/- 5.6%
          FEV(1)/doubling dose; plateau, 48.8 +/- 17.4% FEV(1); transfer factor,
          76.7 +/- 17.9% of predicted; transfer coefficient for carbon monoxide
          (KCO), 85.9 +/- 22.6% of predicted; Cstat, 4.28 +/- 2.8 kPa; shape factor
          (KE), 1.9 +/- 1.5 kPa; and P90TLC, 1.1 +/- 0.8 kPa. We confirmed earlier
          reported relationships between Cstat, on the one hand, and KE (p &lt;
          0.0001), P90TLC (p = 0.0012), and KCO percent predicted (p = 0.006), on
          the other hand. The indexes of the methacholine provocation test were not
          related to any parameter of lung elasticity and CO transfer. CONCLUSION:
          BHR in COPD patients who smoke most probably is determined by airways
          pathology rather than by the augmented mechanical behavior caused by lung
          parenchymal destruction.</description>
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