Mixed agonistic-antagonistic cytokine response in whole blood from patients undergoing abdominal aortic aneurysm repair

Objective:To characterize the impact of abdominal aortic aneurysm repair (A AAR) on spontaneous as well as lipopolysaccharide (LPS)-induced gene expres sion of pro- and anti-inflammatory cytokines. Design: Prospective, controlled in vivo / ex vivo study. Setting: University hospital. Patients and interventions: Whole blood from 14 consecutive patients undergoing AAAR withdrawn prior to surgery (T1), at the end of ischemia (T2), 90 min after declamping (T3) and on the first po stoperative day (T4) was cultured in the absence or presence of LPS. Five p atients undergoing elective inguinal hernia repair served as controls. Measurements and results: While tumor necrosis factor (TNF), Interleukin (I L)-1 and IL-10 plasma concentrations did not increase significantly, IL-6 w as elevated at each time point, as compared with T1. Despite the spontaneou s release of trace amounts of IL-6, the ability of cultured whole blood to mount a cytokine response in vitro to LPS was impaired for all cytokines st udied at T2 (TNF -62 %, IL-1-51 %, IL-6 -20 %, IL-10-51%). The stimulated I L-6 response was restored early after declamping (T3: + 56%) and enhanced 1 day after operation (T4: + 144 %). In contrast, stimulated TNF and IL-1 re sponses remained depressed at T3 (TNF -48 %, IL-1-64 %) and T4 (TNF -40 %, IL-1-24 %). A biphasic pat tern was observed far IL-10 with initial depress ion at T3 (-51%) and restoration at T4 ( + 40 %). Among the different cytok ines monitored, only impaired TNF responsiveness at early reperfusion (T3) correlated with the postoperative course, as reflected by APACHE II. Cytoki ne response to LPS was maintained or even increased during and after surger y in the whole blood from patients undergoing hernia repair. Conclusions: Despite consistent development of clinical signs of systemic i nflammatory response syndrome (SIRS) and spontaneous release of IL-6 abdomi nal aortic aneurysm repair produces a state of impaired pro-inflammatory cy tokine response upon a subsequent in vitro Gram-negative stimulus. This ear ly impairment of TNF responsiveness seems to correlate with an unfavorable postoperative course.