Angiotensin-converting enzyme inhibitors attenuate propofol-induced pro-oxidative and antifibrinolytic effect in human endothelial cells

作者：Wojewodzka Zelezniakowicz Marzena; Gromotowicz Poplawska Anna; Kisiel Wioleta; Konarzewska Emilia; Szemraj Janusz; Ladny Jerzy Robert; Chabielska Ewa

来源：Journal of the Renin-Angiotensin-Aldosterone System, 2017, 18(1): UNSP 1470320316687197.

DOI：10.1177/1470320316687197

• Human umbilical vein cells
• quinaprilat
• enalaprilat
• propofol
• fibrinolysis
• nitric oxide
• oxidative stress

Introduction: 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.
Materials and methods: We examined the effects of propofol (50 mu M), quinaprilat and enalaprilat (10(-5) M) on fibrinolysis (t-PA, PAI-1, TAFI antigen levels), oxidative stress parameters (H2O2 and MDA antigen levels and SOD and NADPH oxidase mRNA levels) and nitric oxide bioavailability (NO2/NO3 concentration and NOS expression at the level of mRNA) in human umbilical vein endothelial cells (HUVECs).
Results: 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.
Conclusions: This observation suggests that the studied ACE-Is exerted protective effects against endothelial cell dysfunction caused by propofol, independently of hemodynamics.

• 出版日期2017-3