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CRITICAL CARE AND TRAUMA

Hydroxyethyl Starch Exhibits Antiinflammatory Effects in the Intestines of Endotoxemic Rats

From the Department of Anesthesiology, Department of Cardiosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China; Department of General Surgery, the Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Address correspondence and reprint requests to Prof Jian-Guo Xu, MD, Department of Anesthesiology, Jinling Hospital, 305 East Zhongshan Road, Nanjing 210002, P.R. China. Address e-mail to nulvran{at}yahoo.com.cn.

We performed the present in vivo study to investigate the effect of hydroxyethyl starch (HES) on intestinal production of inflammatory mediators and activation of transcription factors during endotoxemia. Rats with endotoxemia induced by lipopolysaccharide (LPS) (5 mg/kg, IV) were treated with HES (16 mL/kg, IV) or saline (64 mL/kg, IV). At 2, 3, or 6 h after the LPS challenge, the rat ileal tissues were collected. Various ileal inflammatory mediator levels (tumor necrosis factor-, interleukin [IL]-6, cytokine-induced neutrophil chemoattractant-1, and IL-10), inflammatory mediator messenger RNAs (mRNAs), activities of nuclear factor (NF)-B and activator protein (AP)-1, and ileal myeloperoxidase-positive cells were determined in each group. HES significantly reduced the increased intestinal levels of tumor necrosis factor-, IL-6, cytokine-induced neutrophil chemoattractant-1, and the mRNAs in the endotoxemic rats. Similarly, HES could decrease the myeloperoxidase-positive cells induced by LPS and also inhibit ileal NF-B and AP-1 activations. Our results suggest that during endotoxemia HES may down-regulate intestinal inflammatory mediator production, and this antiinflammatory effect of HES may act through suppression of NF-B and AP-1 activations.

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