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REGIONAL ANESTHESIA

Epidural Analgesia Prevents Endotoxin-Induced Gut Mucosal Injury in Rabbits

Shizuko Kosugi, MD^*, Hiroshi Morisaki, MD^*, Tomoyuki Satoh, MD^*, Kimiaki Ai, MD^*, Michiko Yamamoto, BA^*, Junko Soejima, MD, Ryohei Serita, MD^*, Yoshifumi Kotake, MD^*, Akitoshi Ishizaka, MD, and Junzo Takeda, MD^*

Departments of *Anesthesiology and Medicine, Keio University School of Medicine, Tokyo, Japan

Address correspondence and reprint requests to H. Morisaki, MD, Department of Anesthesiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Address e-mail to anesmrsk{at}sc.itc.keio.ac.jp.

In the present study, we evaluated the effect of epidural analgesia on the alterations of gut barrier function elicited by endotoxin in rabbits. After the placement of an epidural catheter, 28 male rabbits were randomized into either 0.5% lidocaine (group E) or saline (group C) group. The solutions (0.4 mL/kg) were epidurally injected, followed by continuous infusion (0.1 mL · kg^–1 · h^–1) throughout the study period. Under a continuous infusion of lipopolysaccharide (15 µg · kg^–1 · h^–1), mean arterial blood pressure, intramucosal pH, and plasma thrombomodulin concentrations were measured. At 4 h, mean arterial blood pressure was lower (P < 0.05), intramucosal pH was higher (P < 0.01), and the progression of hemodilution more profound (P < 0.05) in group E versus group C, whereas plasma thrombomodulin levels were increased to a similar extent between the groups. With less wet-to-dry weight ratio of ileum, histopathological injury scores of gut mucosa were significantly less in group E versus group C (P < 0.01). In a separate series of experiments (n = 10 each group), mucosal permeability in group E was significantly less compared with group C (P < 0.05). Collectively, these studies showed that despite a significant decrease of perfusion pressure and arterial oxygen content, epidural analgesia minimized endotoxin-induced functional and structural injury of gut mucosa possibly through endothelium-independent mechanisms.