{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T01:57:56Z","timestamp":1777859876398,"version":"3.51.4"},"reference-count":49,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Renin Angiotensin Aldosterone Syst"],"published-print":{"date-parts":[[2017,1]]},"abstract":"<jats:sec>\n                    <jats:title>Introduction:<\/jats:title>\n                    <jats:p>The aim of this study was to investigate the effects of plasma and tissue angiotensin-converting enzyme inhibitors (ACE-Is) against propofol-induced endothelial dysfunction and to elucidate the involved mechanisms in vitro.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods:<\/jats:title>\n                    <jats:p>\n                      We examined the effects of propofol (50 \u03bcM), quinaprilat and enalaprilat (10\n                      <jats:sup>\u22125<\/jats:sup>\n                      M) on fibrinolysis (t-PA, PAI-1, TAFI antigen levels), oxidative stress parameters (H\n                      <jats:sub>2<\/jats:sub>\n                      O\n                      <jats:sub>2<\/jats:sub>\n                      and MDA antigen levels and SOD and NADPH oxidase mRNA levels) and nitric oxide bioavailability (NO\n                      <jats:sub>2<\/jats:sub>\n                      \/NO\n                      <jats:sub>3<\/jats:sub>\n                      concentration and NOS expression at the level of mRNA) in human umbilical vein endothelial cells (HUVECs).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>We found that both ACE-Is promoted similar endothelial fibrinolytic properties and decreased oxidative stress in vitro. Propofol alone increased the release of antifibrinolytic and pro-oxidative factors from the endothelium and increased mRNA iNOS expression. We also found that the incubation of HUVECs in the presence of propofol following ACE-Is pre-incubation caused weakness of the antifibrinolytic and pro-oxidative potential of propofol and this effect was similar after both ACE-Is.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>This observation suggests that the studied ACE-Is exerted protective effects against endothelial cell dysfunction caused by propofol, independently of hemodynamics.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1470320316687197","type":"journal-article","created":{"date-parts":[[2017,1,18]],"date-time":"2017-01-18T04:01:40Z","timestamp":1484712100000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":7,"title":["Angiotensin-converting enzyme inhibitors attenuate propofol-induced pro-oxidative and antifibrinolytic effect 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