Upregulation of IFN-γ and soluble interleukin-2 receptor release and altered serum cortisol and prolactin concentration during general anesthesia

The effects of surgery, surgical stress, and anesthesia compromise the optimal function of the immune system. Recent studies demonstrate the influence of anesthesia on the immune response by modulation of neural-immune interactions. To evaluate the immunologic effects of general anesthesia with the hypnotic agent propofol and the opioid fentanyl, two drugs used frequently in anesthesia, we studied 30 patients undergoing elective orthopedic surgery before and during narcosis. We found a significant enhancement of interferon-gamma (IFN-gamma) and soluble interleukin-2 receptor (sIL-2R) release in lipopolysaccharide (LPS)-stimulated whole blood cultures after induction of anesthesia. Similar results were observed in cultures stimulated with polyclonal T cell activators, such as staphylococcal enterotoxin B (SEB) and phytohemagglutinin (PHA). IL-1 beta and IL-8 release was not affected, but the anti-inflammatory cytokine IL-10 decreased after skin incision. Serum prolactin significantly increased immediately after induction of anesthesia, whereas serum cortisol levels declined. Our results point to enhanced proinflammatory T lymphocyte and natural killer (NK) cell activity, probably caused by prolactin and cortisol modulation in the serum. This may disturb the balance of human proinflammatory and anti-inflammatory pathways during surgery and general anesthesia.