S. Kukkonen et al., PULMONARY VASODILATORY PROPERTIES OF PROSTAGLANDIN-E(1) ARE BLUNTED AFTER EXPERIMENTAL SINGLE-LUNG TRANSPLANTATION, The Journal of heart and lung transplantation, 14(2), 1995, pp. 280-288
Background: Pulmonary dysfunction and right heart failure are still a
common clinical problem after single lung transplantation. Methods: In
this study we investigated the pulmonary vasodilatory properties of p
rostaglandin E1 in pigs during the first 4 hours after left lung allot
ransplantation. With the use of extracorporeal circulation and total r
ight heart bypass, the right and left pulmonary arteries could be indi
vidually perfused and the drug effect in each lung separately analyzed
either at equal blood pressures or at equal blood flows in the pulmon
ary arteries. Twelve animals received in a randomized double-blind fas
hion either saline solution or an increasing prostagladin E1 infusion
(10, 25, 50, and 100 ng/kg/min; 15 minutes each). After a drug-free pe
riod of 75 minutes, the infusion schedule with 25, 50, and 100 ng/kg/m
in was repeated. Results: During the first part of the study the highe
st dose of prostaglandin E1 decreased the mean systemic arterial press
ure by 25%, but an almost similar decrease occurred in the control ani
mals. During the second infusion period a 28% decrease was observed on
ly in the animals treated with prostaglandin E1. None of the infusions
was able to decrease pulmonary vascular resistance. Instead prostagla
ndin E1 diverted two thirds of the pulmonary blood flow toward the nat
ive lung, and this diversion manifested itself as an earlier improveme
nt of the arterial oxygen tension in the drug-treated animals. The end
-tidal carbon dioxide values measured from each lung corresponded to t
hose from the common expiratory limb of the system, but there was a di
stinct gradient in the range of 14 to 20 mm Hg between the arterial an
d end-tidal carbon dioxide values. Conclusions: We conclude that prost
aglandin E1, in doses tolerated by the systemic circulation, is ineffe
ctive in the treatment of the increased pulmonary vascular resistance
after single lung transplantation.