Thoracic epidural bupivacaine attenuates inflammatory response, intestinal lipid peroxidation, oxidative injury, and mucosal apoptosis induced by mesenteric ischemia/reperfusion.

Abstract

We conducted this study to evaluate the effects of thoracic epidural anesthesia (TEA) on inflammatory response, lipid peroxidation, and oxidative stress in a rat model of mesenteric ischemia/reperfusion (I/R). Rats were divided into 4 groups: sham group (n=6; sham laparotomy), control group (n=6; I/R), bupivacaine group (n=6; mesenteric I/R and 20 μL/h 0.5% bupivacaine), and saline group (n=6, mesenteric I/R and 20 μL/h 0.9% saline). I/R injury was established by occluding the superior mesenteric artery for 1 hour followed by 12 hours reperfusion. Blood gas, tumor necrosis factor-α, interleukin-6, interleukin-1β, glutathione peroxidise, superoxide dismutase, catalese, myeloperoxidase concentrations, immunohistochemical examinations (intracellular adhesion molecule-1), apoptosis determination, and wet/dry ratio of intestinal edema were determined. Bupivacaine significantly decreased the cytokine, malondialdehyde, and myeloperoxidase levels and increased the antioxidant enzyme levels. Wet/dry ratio comparison showed a significant decrease in the bupivacaine (2.88±0.17) group in comparison with control (5.45±0.67) and saline (5.87±0.17) groups. The intestinal injury score was significantly decreased in rats in the epidural bupivacaine (2 [1-2]) infusion group in comparison with rats in the control (3 [2-3]) and saline (3 [2-4]) groups. Bupivacaine (63%) caused a significant decrease in the percentage of apoptotic cells in comparison with control (85%) only. ICAM-1 levels in the bupivacaine (27.4±7.1) group decreased in comparison with control (12.3±7.4) and saline (24.9±3.2) groups. This study demonstrated that epidural bupivacaine attenuates the mesenteric I/R-related inflammatory response and intestinal damage.