The aim of this study was to assess the influence of preservation solution type and extra- or intracellular composition on the occurrence of early graft dysfunction after clinical lung transplantation. For 170 patients who underwent a single (n = 124) or bilateral (n = 46) lung transplantation in two centers in Paris between 1988 and 1999, the preservation technique applied to the donor lung was single-flush perfusion of the pulmonary artery with one of several solutions of intracellular (Euro-Collins, n = 61; University of Wisconsin, n = 24) or extracellular composition (Cambridge, n = 64; Celsior, n = 21). The early postoperative outcome of these patients was reviewed. Reimplantation edema occurred in 48% of all patients, and the overall 1-mo survival rate was 84%. No significant difference in the incidence of edema, duration of mechanical ventilation, and 1-mo survival rate was observed between the four groups or between intra- and extracellular groups. After adjustment for graft ischemic time by means of multivariate analysis, the use of extracellular preservation fluid was associated with a lower incidence of reimplantation edema without effect on 1-mo mortality. Graft ischemic time was associated with both edema occurrence and 1-mo survival rate (p = 0.02 and p = 0.01, respectively). We conclude that extracellular-type solutions are associated with better lung preservation than intracellular-type solutions in clinical transplantation.
1 The purpose of this work was to investigate whether endothelin-1 (ET-1) was able to induce the release of an inhibitory factor from the airway epithelium in isolated human bronchi and to identify this mediator as well as the endothelin receptor involved in this phenomenon. 2 In intact bronchi, ET-1 induced a concentration-dependent contraction (7logEC 50 =7.92+0.09, n=18) which was potentiated by epithelium removal (7logEC 50 =8.65+0.11, n=17). BQ-123 , an ET A receptor antagonist, induced a signi®cant leftward shift of the ET-1 concentration-response curve (CRC). This leftward shift was abolished after epithelium removal. 3 L-NAME (3610 73 M), an inhibitor of nitric oxide (NO) synthase, induced a signi®cant leftward shift of the ET-1 CRC, and abolished the potentiation by BQ-123 (10 78 M) of ET-1-induced contraction. 4 In intact preparations, the ET B receptor antagonist BQ-788 induced only at 10 75 M a slight rightward shift of the ET-1 CRC. In contrast, in epithelium-denuded bronchi or in intact preparations in the presence of L-NAME, BQ-788 displayed a non-competitive antagonism toward ET-1-induced contraction. 5 IRL 1620, a selective ET B receptor agonist, induced a contraction of the isolated bronchus (7logEC 50 =7.94+0.11, n=19). This e ect was not modi®ed by epithelium removal or by BQ-123. BQ-788 exerted a competitive antagonism against IRL 1620 which was similar in the presence or absence of epithelium. 6 These results show that ET-1 exerts two opposite e ects on the human airway smooth muscle. One is contractile via ET B -receptor activation, the other is inhibitory and responsible of NO release which counteracts via ET A -receptor activation the contraction.
Between November 1989 and April 1991, 14 bilateral single lung transplantations (BSLT) were performed at our institution using the technique we have described without omentoplasty and rarely cardiopulmonary bypass. The indications included emphysema (8), cystic fibrosis (3), infected fibrosis (1), alveolar microlithiasis (1) and lymphocytic interstitial pneumonitis (1). Maximum mean pulmonary artery pressure was 53 mmHg and minimal right ventricular ejection fraction was 15%. Two patients experienced bronchial complications: 1 complete left bronchial dehiscence, 1 late partial stenosis which required a temporary insertion of a stent. One patient had a posterior dehiscence which healed spontaneously. Five patients died postoperatively (3 of infection, 1 after a volume mismatch and 1 after a circulating anticoagulant). BSLT is the technique of choice for double lung transplantation in adults and heart lung transplantation has very few indications in infected end-stage pulmonary disease. We hope that modification of our immunosuppressive regimen will decrease postoperative mortality.
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