ABOUT MECHANISMS OF PROSTAGLANDIN-E(1) INDUCED DETERIORATION OF PULMONARY GAS-EXCHANGE IN COPD PATIENTS

Prostaglandin E1 (PGE1) has been reported to attenuate COPD-related pu lmonary hypertension and to slightly lower the arterial oxygen tension (PaO2). In order to infer the involved mechanisms, the effects of int ravenous infusion of PGE1 on pulmonary haemodynamics, diffusing lung c apacity for CO (DLCO), membrane diffusing capacity (Dm), pulmonary cap illary blood volume (Vc), physiological shunt (Q(ps)/Q(t)), arterial b lood gases and other lung functional indices were evaluated in 20 COPD patients with pulmonary hypertension and, excluding right catheteriza tion, in 14 control subjects. The examines were studied at baseline an d during infusion of 20-30 ng kg-1 min PGE1 or placebo. In control sub jects PGE1 only caused systemic arterial pressure decrease (-17.8%). I n COPD patients, as expected, PGE1 increased cardiac index (16.2%), bu t decreased systemic arterial pressure (-21.2%), pulmonary arterial pr essure (-27.9%), pulmonary vascular resistance (-45.4%) and PaO2 (-10. 4%), worsening their hypoxaemia. However, the effect of PGE1 on DLCO w as an increase (11.9%), due to an increase in Vc (15.2%) and less mark edly in Dm (4.9%). Physiological and anatomical shunts were increased with PGE1 (20.2% and 14.8%) and the overall ventilation/perfusion rati o decreased from 0.89 to 0-79. Decrements in PaO2 correlated with incr ements in Q(ps)/Q(t) (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. The refore, worsening of hypoxaemia during PGE1 infusion was related with increased right-to-left shunt and deterioration of ventilation-perfusi on relationship.