Role of mesenteric lymph pathway in the effects of exogenous somatostatin against early intestinal injury after ischemia-reperfusion in rats

摘要

Intestinal ischemia-reperfusion (I/R)-induced gut injury remains a challenge for critically ill patients. This study aims to test whether mesenteric lymph pathway is involved in intestinal I/R injury and whether somatostatin (SST) affects mesenteric lymph pathway after mesenteric reperfusion. Intestinal I/R rats were treated with SST-14 by intravenous injection combined with intraperitoneal injection before occlusion of the SMA until the end of the experiment. When intestinal I/R injury treated with SST, the volumes of mesenteric lymph flow at the 6th h after reperfusion following intestinal ischemia were increased ([0.55±0.24] ml/h vs [0.25±0.09] ml/h, p0.05) and the number of intestinal lymphocytes per milliliter ([2.30±0.72]×107/ml vs [1.16±0.63]×107/ml, p0.05) was also increased, which caused the number of intestinal lymphocytes output at the same period of time was significantly increased compared with intestinal I/R group ([1.33±0.88]×107/h vs [0.28±0.15]×107/h, p0.05). Meanwhile, the number of 51Cr-lymphocytes migration from systemic circulation to the effector sites in GALT was significantly increased ([1.93±0.23]×105/h vs [0.90±0.25]×105/h, p0.05), although the percentage of 51Cr-lymphocytes in the effector sites ([1.45±0.26]% vs [3.23±1.69]%, p0.05) was sharply decreased compared with intestinal I/R group. The accompanying decreases of the endotoxin concentration ([0.038±0.017] EU/mL vs [0.110±0.028] EU/mL, compared with intestinal I/R group p0.05) and the TNF-α levels ([37.50±10.45] ρg/ml) vs ([74.93±14.77] ρg/ml), compared with intestinal I/R group p0.05) in mesenteric lymph and the improvement of vital organ dysfunction happened during the early intestinal I/R injury. Suppression of gut-derived toxic mediators reaching systemic circulation and increases of the number of lymphocytes homing to the effector sites in GALT to strengthen the effective immune responses in intestinal mucosa account for the protective effects of exogenous SST against early intestinal I/R injury.