Enhanced cyclooxygenase-2 activity leads to intestinal dysmotility following hemorrhagic shock

Abstract

PURPOSE:To test whether hemorrhagic shock (HS) increases the Cyclooxygenase-2 (COX-2) expression in the intestine and whether this enhanced COX-2 expression mediates the intestinal dysmotility after HS. METHODS: Male Wistar rats were randomly divided into HS sham group and HS group. At 180 min following HS establishment, the duodenum samples were harvested to assess the motility function, protein expression of COX-2 and the downstream products of COX-2, prostaglandins . RESULTS: Examination of motility function ex vivo showed that the contractile response to acetylcholine of smooth muscle strips of rats subjected to HS was significantly suppressed. A COX-2 inhibitor, NS-398, abolished this depressed contractile response after HS. Western blotting revealed an increased protein expression of COX-2 in intestinal tissues of HS rats. Immunohistochemical examination indicated that intestine tissues of HS rats were manifested by part of villous expansion and disruption, a large amount of COX-2 positive cells appearance in lamina propria and submucosa. Furthermore, the contents of prostaglandin E 2 was significantly increased in intestinal tissues of HS rats. CONCLUSION: The enhanced COX-2/ prostaglandin E 2 involves in the hemorrhagic shock induced intestinal dysmotility.

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“…Yu-Ping Zhang et al . previously observed a high level of COX-2 at the site of hemorrhagic injury35. Other research groups demonstrated that the inhibition of COX-2 expression and PGE 2 production could alleviate hemorrhagic gastrointestinal36, brain37, and bladder-related injury to improve survival in vivo 38.…”

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“…Other studies have also suggested that both COX-1 and COX-2 are important in the formation of collagen during wound healing, and that their deficiency may lead to alterations in the development of granulation tissue and re-epithelialization by inhibiting the proliferation of keratinocytes 12,19,20,23 .…”