Abstract
AIM: To study how intestinal lymph after trauma-induced shock (TIS) interferes with expression of neutrophil adhesion factors (CD11b and CD18) and causes lung injury. METHODS: Thirty-two adult healthy Sprague-Dawley rats were randomly divided into four experimental groups. Groups 1 and 2 included rats with TIS caused by hitting the mid-upper part of both side femoral bones with a 2,500 kg raw- iron, and with or without ligation of mesenteric lymph duct. Groups 3 and 4 included rats with sham-TIS and with or without ligation of mesenteric lymph duct. Expression of neutrophil CD18 and CD11b in at 1 and 3 h after a 90-min TIS/sham-TIS was evaluated. These rats were killed at 3 h after TIS/sham-TIS, and lungs were taken immediately. The main lung injury indexes (the MPO activity and lung injury score) were measured. RESULTS: The expressions of CD18 and CD11b at 1 and 3 h after a 90-min TIS and the main lung injury indexes were significantly increased compared with those in the sham-TIS groups (P<0.05). Moreover, at 1 and 3 h after TIS, the expressions of CD18 (32.12+/-1.25 and 33.46+/-0.98) and CD11b (29.56+/-1.35 and 30.56+/-1.85) were significantly decreased in rats with ligation of mesenteric lymph duct, compared with those (52.3+/-1.12 and 50.21+/-1.25, and 42.24+/-1.24 and 42.81+/-1.12, respectively) in those without the ligation (all P<0.05). The main lung injury indexes in rats with TIS with ligation of mesenteric lymph duct (0.96+/-0.12 and 6.54+/-0.35) were also significantly decreased, compared with those (1.56+/-0.21 and 9.56+/-0.23) in rats with TIS without the ligation (both P<0.05). However, there was no significant difference in expressions of CD18 and CD11b and the main lung injury indexes between the two sham-TIS groups. CONCLUSION: Previous ligation of mesenteric lymph ducts prevents or alleviates the up-regulated expression of PMN CD18 and CD11b and the lung injury induced by TIS. Our findings also indicate that neutrophil adhesion molecule activation and lung injury during TIS appear to be caused by some factors that are released or produced by post-ischemic intestine through the mesenteric lymph pathway.