BACKGROUND: @entity5721 ( @entity5721 ) is a major cause of mortality and morbidity among lung transplant recipients. We sought to determine if prophylactic administration of inhaled @entity842 (NO) to lung transplant recipients at reperfusion would prevent @entity5721 . We also hypothesized that if prophylactic NO proves ineffective in preventing @entity5721 then it may improve pulmonary hemodynamics and gas exchange in the subset of @entity1 who develop @entity5721 . METHODS: After informed consent, 28 consecutive, adult lung transplant recipients received NO at 20 ppm at reperfusion. NO was withdrawn for 15 min at 6 and 12 hr after reperfusion, and gas exchange and hemodynamics were measured. RESULTS: Five of the 28 lung transplant recipients (18%) developed @entity5721 . Withdrawal of NO for 15 min in this subset of @entity1 resulted in a significant rise in mean pulmonary artery pressure and a reduction in oxygenation index. All five @entity1 with @entity5721 were kept on inhaled NO until full functional recovery of the allograft and were then weaned from mechanical ventilation. None required extracorporeal membrane oxygenation support; the early mortality in this group was 20% (1/5). The remaining 23 @entity1 without @entity5721 had uneventful early postoperative course and were weaned from NO and mechanical ventilation within 36 hr of transplantation. CONCLUSIONS: Prophylactic-inhaled NO does not prevent @entity5721 in @entity1 lung transplantation. However, inhaled NO, started at reperfusion, improves gas exchange and reduces pulmonary artery pressure in those @entity1 who develop @entity5721 .

A prospective trial of inhaled XXXX in clinical lung transplantation.

@entity1 :: ('9606', 'Species') :: ['human', 'patients'] @entity842 :: ('MESH:D009569', 'Chemical') :: ['nitric oxide'] @entity5721 :: ('MESH:D015427', 'Disease') :: ['Reperfusion injury', 'RI']
@entity842 :: (MESH:D009569,Chemical) :: ['nitric oxide']
