title: About mechanisms of prostaglandin E1 induced deterioration of pulmonary gas exchange in COPD patients.
abstract: Prostaglandin E1 (PGE1) has been reported to attenuate COPD-related pulmonary hypertension and to slightly lower the arterial oxygen tension (PaO2). In order to infer the involved mechanisms, the effects of intravenous infusion of PGE1 on pulmonary haemodynamics, diffusing lung capacity for CO (DLCO), membrane diffusing capacity (Dm), pulmonary capillary blood volume (Vc), physiological shunt (Qps/Qt), arterial blood gases and other lung functional indices were evaluated in 20 COPD patients with pulmonary hypertension and, excluding right catheterization, in 14 control subjects. The examines were studied at baseline and during infusion of 20-30 ng kg-1 min PGE1 or placebo. In control subjects PGE1 only caused systemic arterial pressure decrease (-17.8%). In COPD patients, as expected, PGE1 increased cardiac index (16.2%), but decreased systemic arterial pressure (-21.2%), pulmonary arterial pressure (-27.9%), pulmonary vascular resistance (-45.4%) and PaO2 (-10.4%), worsening their hypoxaemia. However, the effect of PGE1 on DLCO was an increase (11.9%), due to an increase in Vc (15.2%) and less markedly in Dm (4.9%). Physiological and anatomical shunts were increased with PGE1 (20.2% and 14.8%) and the overall ventilation/perfusion ratio decreased from 0.89 to 0.79. Decrements in PaO2 correlated with increments in Qps/Qt (r = 0.86). In conclusion, in COPD patients studied, PGE1 increased DLCO, which compensated for the deleterious effect of increased cardiac output on alveolar-capillary gas equilibration. Therefore, worsening of hypoxaemia during PGE1 infusion was related with increased right-to-left shunt and deterioration of ventilation-perfusion relationship.
authors.affiliation: Department of Clinical Physiology, Zagreb University School of Medicine in Split, Republic of Croatia.
authors.forename: Z
authors.initials: Z
authors.lastname: Dujić
authors.forename: D
authors.initials: D
authors.lastname: Eterović
authors.forename: J
authors.initials: J
authors.lastname: Tocilj
authors.forename: Z
authors.initials: Z
authors.lastname: Kusić
authors.forename: V
authors.initials: V
authors.lastname: Capkun
mesh_terms: D000527:Alprostadil / Q000494:pharmacology*; D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology; D008168:Lung / Q000187:drug effects / Q000502:physiology; D008173:Lung Diseases, Obstructive / Q000503:physiopathology*; D008875:Middle Aged; D010100:Oxygen / Q000494:pharmacology; D010313:Partial Pressure; D011653:Pulmonary Diffusing Capacity / Q000502:physiology; D011659:Pulmonary Gas Exchange / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors; D014655:Vascular Resistance / Q000502:physiology; D014692:Ventilation-Perfusion Ratio / Q000502:physiology
chemical_list: D000527:Alprostadil; D010100:Oxygen