{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T10:30:57Z","timestamp":1781001057703,"version":"3.54.1"},"reference-count":47,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,4,1]],"date-time":"2013-04-01T00:00:00Z","timestamp":1364774400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2013,4,1]],"date-time":"2013-04-01T00:00:00Z","timestamp":1364774400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Pulm. circ."],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:p>Pulmonary endothelium is a major metabolic organ affecting pulmonary and systemic vascular homeostasis. Brain death (BD)\u2010induced physiologic and metabolic derangements in donors' lungs, in the absence of overt lung pathology, may cause pulmonary dysfunction and compromise post\u2010transplant graft function. To explore the impact of BD on pulmonary endothelium, we estimated pulmonary capillary endothelium\u2010bound (PCEB)\u2010angiotensin converting enzyme (ACE) activity, a direct and quantifiable index of pulmonary endothelial function, in eight brain\u2010dead patients and ten brain\u2010injured mechanically ventilated controls. No subject suffered from acute lung injury or any other overt lung pathology. Applying indicator\u2010dilution type techniques, we measured single\u2010pass transpulmonary percent metabolism (%M) and hydrolysis (v) of the synthetic, biologically inactive, and highly specific for ACE substrate <jats:sup>3<\/jats:sup>H\u2010benzoyl\u2010Phe\u2010Ala\u2010Pro, under first order reaction conditions, and calculated lung functional capillary surface area (FCSA). Substrate %M (35 \u00b1 6.8%) and v (0.49 \u00b1 0.13) in BD patients were decreased as compared to controls (55.9 \u00b1 4.9, <jats:italic>P<\/jats:italic> = 0.033 and 0.9 \u00b1 0.15, <jats:italic>P<\/jats:italic> = 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 \u00b1 562\u00a0mL\/min vs 4,235 \u00b1 559\u00a0in controls; <jats:italic>P<\/jats:italic> = 0.003). We conclude that BD is associated with subtle pulmonary endothelial injury, expressed by decreased PCEB\u2010ACE activity. The applied indicator\u2010dilution 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.<\/jats:p>","DOI":"10.4103\/2045-8932.113189","type":"journal-article","created":{"date-parts":[[2013,7,8]],"date-time":"2013-07-08T09:01:27Z","timestamp":1373274087000},"page":"419-425","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":8,"title":["Preclinical Pulmonary Capillary Endothelial Dysfunction is Present in Brain Dead Subjects"],"prefix":"10.1002","volume":"3","author":[{"given":"Constantinos","family":"Glynos","sequence":"first","affiliation":[{"name":"First Department of Critical Care and Pulmonary Services Evangelismos Hospital Athens Greece"},{"name":"G. P. 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