EFFECTS OF INTRAVENOUS ANESTHETICS ON BACTERIAL ELIMINATION IN HUMAN BLOOD IN-VITRO

Background: Since anesthetics are widely used in critically ill patien ts, this study investigates anesthetic effects on neutrophil and monoc yte function concerning bacterial elimination in human whole blood. Me thods: The effects of thiopental (20 and 200 mu g/ml), propofol (5 and 50 mu g/ml), midazolam (0.15 and 1.5 mu g/ml) and ketamine (3 and 30 mu g/ml) on elimination of Escherichia (E.) coli from whole blood were investigated in vitro after incubation for 1 h in both clinical (1) ( n=10) and 10-fold higher (h) (n=11) concentrations. These data were co mpared to neutrophil and monocyte phagocytosis (1; n=6) and burst acti vity (1; n=10, h; n=11), measured by flow cytometry To enable quantifi cation of the clearance process, a defined number of 10(5) colony form ing units of E. coli were added to the blood assays and bacterial grow th was determined. Results: All anesthetics delayed bacterial clearanc e from the blood in the 10-fold concentration (P<0.05). Thiopental (1h) and propofol (h) suppressed neutrophil (59+/-3% and 38+/-6%) and mo nocytic (45+/-6% and 30+/-11%) oxidative burst (P<0.01). Phagocytosis was reduced even after propofol (1) in polymorphonuclear leukocytes (P MN) (34+/-9%; P<0.05) and monocytes (35+/-11%). Ketamine (h) prolonged bacterial elimination (P<0.01), which did correlate with inhibition o f monocytic phagocytosis, by 26+/-14%. Midazolam application (h) resul ted in an inhibition of PMN-respiratory burst by 19+/-6% (P<0.05) and impaired bacterial clearance (P<0.05). Conclusion: Thiopental, propofo l, midazolam and ketamine affect E. coli clearance and neutrophil and monocyte oxidative burst and phagocytosis in vitro only in high concen trations, while thiopental inhibited monocytic hurst and propofol impa ired PMN phagocytosis even in clinically used concentrations. These da ta suggest that i.v. anesthetics in concentrations recommended for gen eral anesthesia seem to have minor influence on the investigated host defense mechanisms.