REMIFENTANIL, FENTANYL, AND ALFENTANIL HAVE NO INFLUENCE ON THE RESPIRATORY BURST OF HUMAN NEUTROPHILS IN-VITRO

Background: Anaesthetic agents inhibit certain functions of human neut rophils. The respiratory burst (RB) enzyme in the plasma membrane of n eutrophils leads to the production of superoxide anion. The oxygen rad icals are responsible for killing phagocytised micro-organisms. We inv estigated the in vitro influence of remifentanil, fentanyl, and alfent anil on the respiratory burst of human neutrophils. Methods: For the n ow-cytometric evaluation, leukocytes were obtained as supernatant foll owing sedimentation and were incubated with the tested drugs. The conc entrations in vitro were adjusted to conform to the plasma concentrati ons reported for anaesthesia and also to 10-fold higher concentrations . The RE was measured by intracellular oxidation of dihydrorhodamine t o fluorescent rhodamine after induction of phorbol-myristate-acetate ( PMA), Escherichia coli (E, coli) or priming by tumour necrosis factor alpha followed by stimulation of n-formyl-methionyl-leucyl-phenylalani ne (TNF-alpha/FMLP). In order to exclude prestimulation of the neutrop hil granulocytes, negative controls were carried out. Propidium iodide (PI) was added for viability discrimination immediately prior to flow cytometry measurement. Results: Regardless of the triggering agents c hosen (PMA, E. coli, TNF-alpha/FMLP), remifentanil, fentanyl, and alfe ntanil had no significant effect on the neutrophils' respiratory burst even in concentrations which were higher than those encountered durin g in vivo conditions. Conclusion: With respect to peri- and postoperat ive risk of infection, anaesthetics and analgetics with no inhibiting effect on neutrophil function should be used. These results show that remifentanil, fentanyl, and alfentanil do not influence the neutrophil s' respiratory burst in vitro.