Z. Dujic et al., ABOUT MECHANISMS OF PROSTAGLANDIN-E(1) INDUCED DETERIORATION OF PULMONARY GAS-EXCHANGE IN COPD PATIENTS, Clinical physiology, 13(5), 1993, pp. 497-506
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.