Hypertonic saline reverses stiffness in a Sprague-Dawley rat model of acute intestinal edema, leading to improved intestinal function
Hypertonic saline reverses stiffness in a Sprague-Dawley rat model of acute intestinal edema, leading to improved intestinal function
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DOI：
10.1097/01.ccm.0000254330.39804.9c
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发表时间：
2007-02-01
影响因子：
8.8
通讯作者：
Cox, Charles S., Jr.
中科院分区：
文献类型：
--
作者：
Radhakrishnan, Ravi S.;Radhakrishnan, Hari R.;Cox, Charles S., Jr.
介绍。复苏引起的急性水肿和肠系膜静脉高压损害肠道。运输和收缩性并减少肠道僵硬。用高渗盐水 (HS) 预处理可以防止这些变化。组织硬度的变化已被证明可以通过应力纤维的形成触发信号级联。我们提出，急性肠水肿导致肠道运输减少，这可能是由硬度变化介导的，导致应力纤维形成和肠道运输减少。此外，HS给药将消除水肿的这些有害影响。结果：与假手术相比，肠水肿导致组织水分显着增加，肠道运输和硬度显着降低。 HS 将这些变化逆转至假水平。此外，组织水肿导致显着的应力纤维形成和焦点接触数量减少。 HS 保留了组织硬度，防止应力纤维形成，并与改善肠道功能相关。结论。 HS 消除肠道组织水肿形成并改善肠道运输。此外，HS 的作用可能是通过其保持组织硬度来介导的，这导致通过应力纤维形成阻止信号传导，从而保留肠道功能。最后，肠水肿可能为检查硬度和应力纤维信号提供一种新的生理模型。
Introduction. Acute edema induced by resuscitation and mesenteric venous hypertension impairs intestinal. transit and contractility and reduces intestinal stiffness. Pretreatment with hypertonic saline (HS) can prevent these changes. Changes in tissue stiffness have been shown to trigger signaling cascades via stress fiber formation. We proposed that acute intestinal edema leads to a decrease in intestinal transit that may be mediated by changes in stiffness, leading to stress fiber formation and decreased intestinal transit. Furthermore, HS administration will abolish these detrimental effects of edema.Results: Intestinal edema causes a significant increase in tissue water and a significant decrease in intestinal transit and stiffness compared with sham. HS reversed these changes to sham levels. In addition, tissue edema led to significant stress fiber formation and decreased numbers of focal contacts. HS preserved tissue stiffness, prevented stress fiber formation, and was associated with improved intestinal function.Conclusion. HS eliminates intestinal tissue edema formation and improves intestinal transit. In addition, the action of HS may be mediated through its preservation of tissue stiffness, which leads to prevention of signaling via stress fiber formation, leading to preserved intestinal function. Finally, intestinal edema may provide a novel physiologic model for examining stiffness and stress fiber signaling.