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Inhibitory effects of S‐(−) and R‐(+) bupivacaine on neutrophil function
Author(s) -
Welters I. D.,
Menzebach A.,
Langefeld T. W.,
Menzebach M.,
Hempelmann G.
Publication year - 2001
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1034/j.1399-6576.2001.045005570.x
Subject(s) - respiratory burst , receptor , phagocytosis , superoxide , bupivacaine , pharmacology , nop , medicine , chemotaxis , receptor expression , biochemistry , microbiology and biotechnology , immunology , biology , enzyme
Background: Local anesthetics inhibit migration, enzyme release and superoxide anion generation of polymorphonuclear leukocytes (PMN). Due to their ability to phagocytose and kill bacteria PMN represent a major defense mechanism in the circulating blood. In this study we determined the influence of racemic bupivacaine and its enantiomers on neutrophil phagocytic activity, oxidative burst as well as surface expression of complement and Fcγ receptors. Methods: Venous blood was pre‐incubated with different concentrations of either racemic bupivacaine, R‐(+) or S‐(−) bupivacaine. Fluoresceine isothiocyanate (FITC)‐labeled antibodies against Fcγ receptor III (CD16), complement receptor 1 (CD35) and complement receptor 3 (CD11b) were used to determine surface receptor expression. Phagocytic activity was measured by ingestion of FITC‐labeled vital Staphylococcus aureus . Oxidative burst was determined by conversion of nonfluorescent dihydrorhodamine 123 into fluorescent rhodamine 123. Fluorescent intensity of each sample was determined by flow cytometry. Results: Racemic bupivacaine inhibited surface receptor expression, phagocytosis, and oxidative burst in a time‐ and concentration‐dependent manner. Although the S‐(−) enantiomer exerted significantly less inhibitory action on neutrophil function compared to R‐(+) and racemic bupivacaine, these effects were small compared to the overall changes. Conclusion: These findings suggest that bupivacaine impairs surface receptor expression and may thereby contribute to reduced phagocytic activity and oxidative burst. Enantiomer‐specific effects of bupivacaine may play a minor role in the inhibition of these leukocyte functions.