Whang E E, Dunn J C, Mahanty H, McFadden D W, Zinner M J, Ashley S W
Department of Surgery, UCLA School of Medicine, USA.
Am J Surg. 1996 Oct;172(4):341-4. doi: 10.1016/S0002-9610(96)00189-4.
The intestine is a target of septic insult. The aims of this study were to characterize sepsis-induced alterations in intestinal ion transport and to determine the role endotoxin plays in mediating these changes.
Rats underwent cecal manipulation alone (control), cecal ligation and puncture (CLP), or CLP plus intraperitoneal injection of 0.2 mg of a recently synthesized endotoxin inhibitor. At 24 hours, distal ileum was harvested, and transport parameters were determined.
Cecal ligation and puncture produced a significant increase in short-circuit current (Isc) that was attributable to the induction of chloride secretion. There were no alterations in transepithelial resistance or fluxes of mannitol and sodium. The sepsis-induced increase in Isc was prevented by administration of the endotoxin inhibitor.
In this model of sepsis, the primary alteration in ileal ion transport is an induction of electrogenic chloride secretion. Endotoxin inhibition may represent a strategy for prophylaxis against the intestinal effects of sepsis.
肠道是脓毒症攻击的靶器官。本研究的目的是描述脓毒症诱导的肠道离子转运变化,并确定内毒素在介导这些变化中所起的作用。
将大鼠分为仅行盲肠操作(对照组)、盲肠结扎穿刺术(CLP)或CLP加腹腔注射0.2mg最近合成的内毒素抑制剂三组。24小时后,采集远端回肠并测定转运参数。
盲肠结扎穿刺术使短路电流(Isc)显著增加,这归因于氯化物分泌的诱导。跨上皮电阻以及甘露醇和钠的通量没有改变。给予内毒素抑制剂可防止脓毒症诱导的Isc增加。
在这个脓毒症模型中,回肠离子转运的主要改变是诱导了电中性氯化物分泌。抑制内毒素可能是预防脓毒症肠道效应的一种策略。