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Inhibitory effects of S-(-) and R-(+) bupivacaine on neutrophil function
I D Welters1, A Menzebach, T W Langefeld
1Department of Anaesthesiology and Intensive Care Medicine, Justus-Liebig-Universität, Rudolf-Buchheim-Str. 7, 35385 Giessen, Germany. Ingeborg.D.Welters@chiru.med.uni-giessen.de
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 Fcgamma receptors.
Methods:
Venous blood was pre-incubated with different concentrations of either racemic bupivacaine, R-(+) or S-(-) bupivacaine. Fluoresceine isothiocyanate (FITC)-labeled antibodies against Fcgamma 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.
Insights
Bupivacaine, a local anesthetic, was found to inhibit neutrophil functions like phagocytosis and oxidative burst. While enantiomers showed some differences, racemic bupivacaine
Area of Science:
- Immunology
- Pharmacology
- Cell Biology
Background:
- Polymorphonuclear leukocytes (PMN) are crucial for bacterial defense via phagocytosis.
- Local anesthetics are known to affect PMN functions, including migration and oxidative burst.
- This study investigates the impact of bupivacaine and its enantiomers on neutrophil immune functions.
Purpose of the Study:
- To determine the influence of racemic bupivacaine and its enantiomers (R-(+) and S-(-)) on neutrophil phagocytic activity.
- To assess the effects on oxidative burst and surface expression of complement and Fcgamma receptors.
- To elucidate potential enantiomer-specific effects on these leukocyte functions.
Main Methods:
- Neutrophil function assays were performed on venous blood pre-incubated with varying concentrations of bupivacaine enantiomers.
- Surface receptor expression (CD16, CD35, CD11b) was measured using FITC-labeled antibodies and flow cytometry.
- Phagocytic activity and oxidative burst were quantified by measuring the ingestion of Staphylococcus aureus and the conversion of dihydrorhodamine 123, respectively.
Main Results:
- Racemic bupivacaine demonstrated a time- and concentration-dependent inhibition of neutrophil surface receptor expression, phagocytosis, and oxidative burst.
- The S-(-) bupivacaine enantiomer exhibited less inhibitory action compared to R-(+) and racemic bupivacaine.
- However, the observed enantiomer-specific effects were minor in the context of the overall functional changes.
Conclusions:
- Bupivacaine impairs neutrophil surface receptor expression, potentially leading to reduced phagocytic activity and oxidative burst.
- These findings suggest a mechanism by which local anesthetics can modulate innate immune responses.
- Enantiomer-specific effects of bupivacaine on leukocyte functions appear to play a limited role.