The influence of propofol on P-selectin expression and nitric oxide production in re-oxygenated human umbilical vein endothelial cells

T. B. Corcoran, A. O'Shea, A. Engel, G. D. Shorten

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19 Citations (Scopus)


Background: Reperfusion injury is characterized by free radical production and endothelial inflammation. Neutrophils mediate much of the end-organ injury that occurs, requiring P-selectin-mediated neutrophil-endothelial adhesion, and this is associated with decreased endothelial nitric oxide production. Propofol has antioxidant properties in vitro which might abrogate this inflammation. Methods: Cultured human umbilical vein endothelial cells were exposed to 20 h of hypoxia and then returned to normoxic conditions. Cells were treated with saline, Diprivan 5 μg/l or propofol 5 μg/l for 4 h after re-oxygenation and were then examined for P-selectin expression and supernatant nitric oxide concentrations for 24 h. P-selectin was determined by flow cytometry, and culture supernatant nitric oxide was measured as nitrite. Results: In saline-treated cells, a biphasic increase in P-selectin expression was demonstrated at 30 min (P = 0.01) and 4 h (P = 0.023) after re-oxygenation. Propofol and Diprivan prevented these increases in P-selectin expression (P < 0.05). Four hours after re-oxygenation, propofol decreased endothelial nitric oxide production (P = 0.035). Conclusion: This is the first study to demonstrate an effect of propofol upon endothelial P-selectin expression. Such an effect may be important in situations of reperfusion injury such as cardiac transplantation and coronary artery bypass surgery. We conclude that propofol attenuates re-oxygenation-induced endothelial inflammation in vitro.

Original languageEnglish
Pages (from-to)348-354
Number of pages7
JournalActa Anaesthesiologica Scandinavica
Issue number3
Publication statusPublished - Mar 2006
Externally publishedYes


  • Endothelium
  • Leukocytes
  • Nitric oxide
  • P-selectin
  • Reactive oxygen species
  • Reperfusion injury

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