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新生儿肠道血管系统:坏死性小肠结肠炎的促成因素

The neonatal intestinal vasculature: contributing factors to necrotizing enterocolitis.

作者信息

Nankervis Craig A, Giannone Peter J, Reber Kristina M

机构信息

Center for Perinatal Research, Nationwide Children's Hospital, Columbus, OH, USA.

出版信息

Semin Perinatol. 2008 Apr;32(2):83-91. doi: 10.1053/j.semperi.2008.01.003.

Abstract

Based on the demonstration of coagulation necrosis, it is clear that intestinal ischemia plays a role in the pathogenesis of necrotizing enterocolitis (NEC). Intestinal vascular resistance is determined by a dynamic balance between vasoconstrictive and vasodilatory inputs. In the newborn, this balance heavily favors vasodilation secondary to the copious production of endothelium-derived nitric oxide (NO), a circumstance which serves to ensure adequate blood flow and thus oxygen delivery to the rapidly growing intestine. Endothelial cell injury could shift this balance in favor of endothelin (ET)-1-mediated vasoconstriction, leading to intestinal ischemia and tissue injury. Evidence obtained from animal models and from human tissue collected from infants with NEC implicates NO and ET-1 dysregulation in the pathogenesis of NEC. Strategies focused on maintaining the delicate balance favoring vasodilation in the newborn intestinal circulation may prove to be useful in the prevention and treatment of NEC.

摘要

基于凝固性坏死的表现,很明显肠道缺血在坏死性小肠结肠炎(NEC)的发病机制中起作用。肠道血管阻力由血管收缩和血管舒张输入之间的动态平衡决定。在新生儿中,这种平衡严重倾向于血管舒张,这是由于大量产生内皮源性一氧化氮(NO)所致,这种情况有助于确保充足的血流,从而为快速生长的肠道提供氧气。内皮细胞损伤可能会使这种平衡转向有利于内皮素(ET)-1介导的血管收缩,导致肠道缺血和组织损伤。从动物模型以及从患有NEC的婴儿收集的人体组织中获得的证据表明,NO和ET-1失调与NEC的发病机制有关。专注于维持新生儿肠道循环中有利于血管舒张的微妙平衡的策略可能被证明对NEC的预防和治疗有用。

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