PULMONARY VASODILATORY PROPERTIES OF PROSTAGLANDIN-E(1) ARE BLUNTED AFTER EXPERIMENTAL SINGLE-LUNG TRANSPLANTATION

Citation
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
Citations number
NO
Categorie Soggetti
Cardiac & Cardiovascular System",Transplantation
ISSN journal
10532498
Volume
14
Issue
2
Year of publication
1995
Pages
280 - 288
Database
ISI
SICI code
1053-2498(1995)14:2<280:PVPOPA>2.0.ZU;2-I
Abstract
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.