Inhibition of tumor necrosis factor-alpha and inducible nitric oxide synthase correlates with the induction of IL-10 in septic rats undergoing laparotomy and laparoscopy.

Abstract

Proinflammatory mediators are implicated in the mediation of host response to surgical stress. Greater inflammatory response has been reported after open surgery than after laparoscopic surgery in animal models. This study investigated the inflammatory response of tumor necrosis factor alpha (TNF) and inducible nitric oxide synthase (iNOS) and the anti-inflammatory response of interleukin (IL)-10 after laparotomy and laparoscopy in a rat endotoxic shock model. Rats received lipopolysaccharide (LPS) intraperitoneally and underwent laparotomy (n = 5), laparoscopy (n = 5), or no surgical intervention (n = 5). A control group received anesthesia only (n = 5). Serum TNF levels peaked at 2 hours after LPS injection and were significantly suppressed in animals undergoing laparotomy and laparoscopy ( < 0.05). Serum IL-10 levels were higher at 2 hours in the laparotomy and laparoscopy groups but were higher only in the laparotomy group at 4 hours after LPS injection ( < 0.05). Hepatic iNOS mRNA and protein were significantly inhibited at 4 and 8 hours in the laparotomy and laparoscopy groups in comparison with the animals receiving LPS only ( < 0.05). The induction of IL-10 correlated with the suppression of TNF and iNOS suggests that IL-10 may play a role in downregulating TNF and iNOS in septic rats undergoing laparotomy and laparoscopy.