Περίληψη:
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.
Συγγραφείς:
Glynos, Constantinos
Athanasiou, Chariclea
Kotanidou, Anastasia
and Korovesi, Ioanna
Kaziani, Katerina
Livaditi, Olga and
Dimopoulou, Ioanna
Maniatis, Nikolaos A.
Tsangaris, Iraklis and
Roussos, Charis
Armaganidis, Apostolos
Orfanos, Stylianos E.
