hypoxia research::blog

Abstract
Purpose  Leukocyte recruitment from blood vessels to inflamed tissues is the central step in the process of inflammation. This may cause damage of the inflamed tissues in the case of severe inflammatory conditions such as ischemia reperfusion or graft rejection. Adhesion molecules, such as E-selectin, are induced on activated endothelium and play an important role in this process. Volatile anesthetics protect tissues or organs in such conditions, and inhibition of leukocyte adhesion by anesthetics has been implicated. However, little is known about how the anesthetics act on individual adhesion molecules. We examined the effects of volatile anesthetics on E-selectin mediated leukocyte adhesion in a static condition using HL-60 cells, a granulocyte cell line, and E-selectin-coated plates as well as cytokine-activated human umbilical vein endothelial cells (HUVEC).
Methods  The adhesion assay was carried out by overlaying fluorescence-labeled HL-60 cells on E-selectin-coated plates or cytokine-activated HUVEC. E-selectin in the coated plates or activated HUVEC were quantified by enzyme-linked immunosorbent assay. E-selectin in the activated HUVEC was analyzed by immunoblot.
Results  Isoflurane and sevoflurane concentration-dependently suppressed adhesion of HL-60 cells to E-selectin-coated plates. Although isoflurane did not change the amount of expression, or the molecular weight of E-selectin in the activated HUVEC, it significantly suppressed HL-60 cell adhesion to activated HUVEC.
Conclusion  Volatile anesthetics suppress E-selectin-mediated cell adhesion in a static condition without changing the expression of E-selectin. A role for E-selectin in the organ protection by volatile anesthetics is suggested.

Key words  Anesthetic - HL-60 - HUVEC - Inflammation - Cytokine