Yuan et al Figure 4. Development of Gruenhagen’s space at tip of a vil- lus in group III rats (Grade 2) (H&E, × 100). Kruskal-Wallis test and Tukey Post Hoc (nonparametric) test. The signiﬁcance level was established in P < 0.05 for all the tests. Results The levels of BT in different groups The levels of BT had a signiﬁcant increase in animals dis- tributed to the IR group, compared to animals in the IR+L- carnitine and S groups (P < 0.05). In the S group, there were few colony forming units in culture plates of MLN and por- tal vein blood (Table 2). Changes of intestinal mucosa under light microscope The villus and glands were normal and inﬂammatory cell inﬁltration was not observed in mucosal epithelial layer in the sham operated group (Fig. 2). Multiple erosions, inﬂam- matory cells and bleeding were observed in the IR group (Fig. 3). Lighter edema of mucosa villus and fewer inﬁltra- tion of necrotic epithelial inﬂammatory cells neutrophil leu- komonocyte were found in mucosa epithelial layer in IR+L group than the IR group (Fig. 4). Table 3. The Levels of Chiu’s Score in Small Intestinal Structure (Mean ± SD) Groups S IR IR+L n 10 10 10 Small intestinal structure 0 ± 0.00Δ 4.0 ± 0.41* 2.4 ± 0.46 Δ P < 0.05 compared to IR and IR+L groups * P < 0.05 compared to IR+L group J Clin Med Res • 2011;3(2):78-84 Chiu’s score of small intestinal structure In all of the three groups, the Chiu’s score was highest in the IR group, and it was lowest in the S group (P < 0.05). The score in the IR+L group was signiﬁcantly lower than that in the IR group (P < 0.05) (Table 3). Changes in TNF-α and interleukins in vena systemic se- rum The concentrations of pro-inﬂammatory factors including TNF-α, IL-1, and IL-6 in the experimental rats’ serum in the IR and IR+L group were higher than that in the S group (P < 0.05). And the levels of TNF-α, IL-1 and IL-6 in the IR group rats were higher than that in the IR+L group (P < 0.05). The levels of inhibitive inﬂammatory factor IL-10 in the IR+L group were lower than that in the IR group (P < 0.05) (Table 4). Discussion The primary functions of the intestine are to absorb nutri- ents and exclude food debris, bacteria and their products. The maintenance of these functions relies on the integrity of mucosal and barrier of intestine. However, under certain pathological circumstances such as intestinal IR injury, the intestine may lose its barrier function so that the systemic microbial infection, and even MODS could be induced [7]. Compared to other internal organs, the intestine is the organ that is most sensitive to IR injury in the body [15, 16]. There is increasing evidence from experimental and clinical stud- ies to support the ‘intestinal hypothesis of sepsis’, which is based on bacterial or endotoxin translocation from the intes- tinal lumen to the extra-intestinal sites [17]. Nevertheless, growing acceptance of the ‘intestinal hypothesis of sepsis’ was mainly triggered by indirect supports rather than con- crete scientiﬁc evidence. IR injury of the intestine is a complex, multifactorial, and pathophysiological process that involves the dysfunc- tion of absorption, BT, actions of oxygen-derived free radi- cals, cytokines, nitric oxide, and PMNs [18]. IR injury to the small intestine causes local production of the ROS, which is known to play an important role in gut epithelial damage [19]. Intestinal mucosal mast cells (IMMC) are particularly frequent in close proximity to epithelial surfaces, where they are strategically located for optimal interaction with the en- vironment and for their putative functions of host defense [20]. Previous studies have demonstrated that the degranula- tion of IMMC can be induced by oxidants generated in the post-ischemic gut, and the released inﬂammatory mediators such as histamine and tumor necrosis factor-α (TNF-α) could aggravate the injury to intestine after reperfusion [21, 22]. In line with general IR-induced cell damage, also in intestinal Articles © The authors | Journal compilation © J Clin Med Res and Elmer Press™ | www.jocmr.org 81