A sphingosine 1-phosphate 1 receptor agonist modulates brain death-induced neurogenic pulmonary injury.

ABSTRACT: Lung transplantation remains the only viable therapy for patients with end-stage lung disease. However, the full utilization of this strategy is severely compromised by a lack of donor lung availability. The vast majority of donor lungs available for transplantation are from individuals after brain death (BD). Unfortunately, the early autonomic storm that accompanies BD often results in neurogenic pulmonary edema (NPE), producing varying degrees of lung injury or leading to primary graft dysfunction after transplantation. We demonstrated that sphingosine 1-phosphate (S1P)/analogues, which are major barrier-enhancing agents, reduce vascular permeability via the S1P1 receptor, S1PR1. Because primary lung graft dysfunction is induced by lung vascular endothelial cell barrier dysfunction, we h

SUBMITTER: Sammani S 

PROVIDER: S-EPMC3262681 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature