Effects of Nifedipine on Gas Exchange in Patients with Chronic Lung Diseases

Abstract

Pulmonary function, blood gases and carbon monoxide diffusing capacity (DL_CO) were investigated in 10 patients with chronic pulmonary emphysema, 10 cases of chronic bronchitis, 10 cases of chronic interstitial lung deseases (ILD) and 10 healthy men, before and 20 minutes after 10mg sublingual administration of nifedipine.
1) Nifedipine did not modify the bronchial smooth muscle tone in the evaluation of maximal expiratory flowvolume curve.
2) Nifedipine induced a decrease in arterial Po₂ and an increase in alveolar-arterial Po₂ difference in all the patients, but no significant changes were observed in healthy volunteers. Patients with both chronic pulmonary emphysema and chronic bronchitis had the same degree of increase in alveolar-arterial Po₂ difference, while patients with ILD had smaller changes compared to patients with chronic obstructive pulmonary disease (COPD). This suggests that there was a difference of responsiveness of pulmonary vessels to nifedipine between ILD and COPD. It may be said that the responsiveness is affected by fixed vascular lesions in patients with ILD.
3) The changes in alveolar-arterial Po₂ difference was correlated with initial arterial Po₂ before administration of nifedipine in 20 patients with COPD. This finding could be explained by the following two hypotheses. (1) There are more pulmonary vessels manifesting hypoxic pulmonary vasoconstriction (HPV) which can be reactive to nifedipine and nifedipine dilates more pulmonary vessels constricted by hypoxia to induce the larger changes in alveolar-arterial Po₂ difference in patients with higher arterial Po₂. (2) A greater decrease in arterial Po₂ may occur in patients whose initial arterial Po₂ is located on the gentle portion of the hemoglobin oxygen-dissociation curve even if the increased volume of venous admixture due to rilief of HPV is the same degree.
4) Reduction in DL_CO was observed in all patients after administration of nifedipine. It may be partially explained by the fact that the effect of nifedipine on redistribution of blood flow to the units with low V/Q without changes in alveolar ventilation is greater than the effect of increased cardiac output on DL_CO.