Radhakrishnan Ravi S, Radhakrishnan Hari R, Xue Hasen, Moore-Olufemi Stacey D, Mathur Anshu B, Weisbrodt Norman W, Moore Frederick A, Allen Steven J, Laine Glen A, Cox Charles S
Department of Surgery, University of Texas-Houston Medical School, Houston, TX, USA.
Crit Care Med. 2007 Feb;35(2):538-43. doi: 10.1097/01.CCM.0000254330.39804.9C.
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.
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.
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.
复苏和肠系膜静脉高压引起的急性水肿会损害肠道运输和收缩能力,并降低肠道硬度。用高渗盐水(HS)预处理可预防这些变化。组织硬度的改变已被证明可通过应力纤维形成触发信号级联反应。我们提出,急性肠道水肿会导致肠道运输减少,这可能是由硬度变化介导的,进而导致应力纤维形成和肠道运输减少。此外,给予HS将消除水肿的这些有害影响。
与假手术组相比,肠道水肿导致组织水分显著增加,肠道运输和硬度显著降低。HS将这些变化逆转至假手术组水平。此外,组织水肿导致应力纤维显著形成,粘着斑数量减少。HS维持组织硬度,防止应力纤维形成,并与改善肠道功能相关。
HS可消除肠道组织水肿形成并改善肠道运输。此外,HS的作用可能是通过维持组织硬度介导的,这导致通过应力纤维形成的信号传导得到预防,从而维持肠道功能。最后,肠道水肿可能为研究硬度和应力纤维信号传导提供一种新的生理模型。