@article{3157097,
    title = "Preclinical pulmonary capillary endothelial dysfunction is present in
brain dead subjects",
    author = "Glynos, Constantinos and Athanasiou, Chariclea and Kotanidou, Anastasia and and Korovesi, Ioanna and Kaziani, Katerina and Livaditi, Olga and and Dimopoulou, Ioanna and Maniatis, Nikolaos A. and Tsangaris, Iraklis and and Roussos, Charis and Armaganidis, Apostolos and Orfanos, Stylianos E.",
    journal = "Pulmonary Circulation",
    year = "2013",
    volume = "3",
    number = "2",
    pages = "419-425",
    publisher = "SAGE Publications Inc.",
    issn = "2045-8932, 2045-8940",
    doi = "10.4103/2045-8932.113189",
    keywords = "angiotensin converting enzyme; brain death; pulmonary endothelium",
    abstract = "Pulmonary endothelium is a major metabolic organ affecting pulmonary and
systemic vascular homeostasis. Brain death (BD)-induced physiologic and
metabolic derangements in donors’ lungs, in the absence of overt lung
pathology, may cause pulmonary dysfunction and compromise
post-transplant graft function. To explore the impact of BD on pulmonary
endothelium, we estimated pulmonary capillary endothelium-bound
(PCEB)-angiotensin converting enzyme (ACE) activity, a direct and
quantifiable index of pulmonary endothelial function, in eight
brain-dead patients and ten brain-injured mechanically ventilated
controls. No subject suffered from acute lung injury or any other overt
lung pathology. Applying indicator-dilution type techniques, we measured
single-pass transpulmonary percent metabolism (%M) and hydrolysis (v)
of the synthetic, biologically inactive, and highly specific for ACE
substrate H-3-benzoyl-Phe-Ala-Pro, under first order reaction
conditions, and calculated lung functional capillary surface area
(FCSA). Substrate % M (35 +/- 6.8%) and v (0.49 +/- 0.13) in BD
patients were decreased as compared to controls (55.9 +/- 4.9, P = 0.033
and 0.9 +/- 0.15, P = 0.033, respectively), denoting decreased pulmonary
endothelial enzyme activity at the capillary level; FCSA, a reflection
of endothelial enzyme activity per vascular bed, was also decreased (BD
patients: 1,563 +/- 562 mL/min vs 4,235 +/- 559 in controls; P = 0.003).
We conclude that BD is associated with subtle pulmonary endothelial
injury, expressed by decreased PCEB-ACE activity. The applied
indicator-dilution type technique provides direct and quantifiable
indices of pulmonary endothelial function at the bedside that may reveal
the existence of preclinical lung pathology in potential lung donors."
}