[Variable hemodynamic response to nifedipine in pulmonary hypertension secondary to chronic obstructive bronchopathy and pulmonary fibrosis].
The hemodynamic effects of nifedipine s.l. (20 mg) on pulmonary hypertension following chronic obstructive pulmonary disease (COPD) and advanced pulmonary fibrosis (PF) have been studied in 6 patients under stable conditions (3 patients with COPD and 3 patients with PF). Nifedipine induced a significant reduction in mean arterial pressure, right atrial pressure and systemic vascular resistances, with a significant increase in heart rate, right ventricular stroke work index and cardiac index. There was no significant change in mean pulmonary artery pressure, pulmonary arteriolar resistances and oxygen delivery. Individual analysis showed that in 2 patients with COPD there was a real direct vasodilating effect of nifedipine on the pulmonary circulation. In 2 patients with PF, the drug induced an increase in mean pulmonary artery pressure and pulmonary arteriolar resistances. In the last 2 patients, the effect of the drug on the pulmonary circulation was associated with an increase in driving pressure concomitantly with a rise in cardiac output, suggesting recruitment of the pulmonary vessels. In conclusion, nifedipine can dilate pulmonary vessels constricted by hypoxia in patients with COPD, but deleterious effects are observed in patients with pulmonary hypertension following PF.
D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D008173:Lung Diseases, Obstructive / Q000150:complications*; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000494:pharmacology / Q000627:therapeutic use*; D011658:Pulmonary Fibrosis / Q000150:complications*; D014655:Vascular Resistance / Q000187:drug effects
D009543:Nifedipine
Réponse hémodynamique variable à la nifédipine dans l'hypertension pulmonaire secondaire à la bronchopathie obstructive chronique et à la fibrose pulmonaire.