Objective: To examine whether surgical stress causes blood cells to lose their responsiveness to endotoxin during surgery.
Design: Prospective case series.
Setting: A university hospital.
Patients: Sixteen volunteers classified as American Society of Anesthesiologists physical status I-II who were scheduled for elective distal partial gastrectomy.
Interventions: We studied nine patients who underwent elective distal partial gastrectomy. Blood samples for tumor necrosis factor (TNF) and interleukin (IL)-10 assay were obtained before anesthesia, preincision, 2 hrs and 4 hrs postincision, postextubation, and 24 hrs postincision. The rest of each blood sample was diluted with 5 volumes of endotoxin-free saline, incubated for 4 hrs in the presence of lipopolysaccharide (LPS), centrifuged to remove cells, and assayed for TNF. In another seven patients, antihuman IL-10 antibody was added into the diluted whole blood sample before LPS stimulation.
Measurements and main results: TNF activity was not detected in the blood of any patient throughout the study. In contrast, plasma cortisol and IL-10 levels increased rapidly during surgery (p < .01, p < .05, respectively). LPS-induced TNF activity in whole blood decreased significantly during surgery (p < .01) and recovered to control levels by 24 hrs postincision. The peak suppression of LPS-induced TNF and the peak value of plasma IL-10 levels occurred postextubation. Treatment with anti-IL-10 antibody partially restored the ability of LPS to induce TNF activity postextubation (p < .05).
Conclusions: Surgical trauma rapidly induces a transient hyporesponsiveness of blood cells to endotoxin. Plasma IL-10, which increases during surgery, participates in this hyporesponsiveness.