Hypertonic saline modulation of intestinal tissue stress and fluid balance
Hypertonic saline modulation of intestinal tissue stress and fluid balance
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DOI：
10.1097/shk.0b013e318157eba7
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发表时间：
2008-05-01
期刊：
影响因子：
3.1
通讯作者：
Laine, Glen A.
中科院分区：
文献类型：
--
作者：
Cox, Charles S., Jr.;Radhakrishnan, Ravi;Laine, Glen A.
对严重受伤的创伤患者进行基于晶体的复苏会导致肠水肿。肠水肿引起的肠梗阻的潜在机制是肠平滑肌中肌球蛋白轻链磷酸化的减少。我们试图确定水肿的发作是否引发了可测量的早期机械传导信号，以及高渗盐水 (HS) 是否可以通过改变肠液平衡来调节这种早期信号。使用急性间质性肠水肿的麻醉大鼠模型。在剖腹术中，将插管插入肠系膜淋巴管以测量淋巴流量和压力，并将充满液体的微量移液器置于肠粘膜下层以测量间质压力。大鼠被随机分为四组（每组 n = 6）：假手术组、肠系膜静脉高压 + 80 mL/kg 0.9% 等渗氯化钠溶液 (ISCS 80)、肠系膜静脉高压 + 80 mL/kg 0.9% ISCS + 4 mL/kg 7.5% 盐水（ISCS 80 + HS）或 4 mL/kg 7.5% 盐水（仅 HS）接受上述静脉输液5分钟以上。准备完成后30分钟进行测量。测量组织水、淋巴流量和间质压力。计算所产生的施加在平滑肌上的体积诱导的应力(sigma(ravi-muscularis))。肠系膜静脉高压和晶体复苏引起肠水肿，但 HS 可以预防肠水肿。肠水肿导致肠间质压力早期升高，而 HS 可以防止这种情况。高渗盐水不能增强淋巴管对肠水肿的清除作用。 sigma(ravi-muscularis) 随着水肿的发生而增加，并被 HS 阻止，与间质压力数据平行。肠水肿会导致间质压力早期升高，而 HS 可以预防这种情况。预防水肿引起的间质压力增加可以减弱西格玛（拉维肌层）的机械传导信号。
Crystalloid-based resuscitation of severely injured trauma patients leads to intestinal edema. A potential mechanism of intestinal edema-induced ileus is a reduction of myosin light chain phosphorylation in intestinal smooth muscle. We sought to determine if the onset of edema initiated a measurable, early mechanotransductive signal and if hypertonic saline (HS) can modulate this early signal by changing intestinal fluid balance. An anesthetized rat model of acute interstitial intestinal edema was used. At laparotomy, the mesenteric lymphatic was cannulated to measure lymph flow and pressure, and a fluid-filled micropipette was placed in the intestinal submucosa to measure interstitial pressure. Rats were randomized into four groups (n = 6 per group): sham, mesenteric venous hypertension + 80 mL/kg 0.9% isotonic sodium chloride solution (ISCS 80), mesenteric venous hypertension + 80 mL/kg 0.9% ISCS + 4 mL/kg 7.5% saline (ISCS 80 + HS), or 4 mL/kg 7.5% saline (HS alone) to receive the aforementioned intravenous fluid administered over 5 min. Measurements were made 30 min after completion of the preparation. Tissue water, lymph flow, and interstitial pressure were measured. Resultant applied volume induced stress on the smooth muscle (sigma(ravi-muscularis)) was calculated. Mesenteric venous hypertension and crystalloid resuscitation caused intestinal edema that was prevented by HS. Intestinal edema caused an early increase in intestinal interstitial pressure that was prevented by HS. Hypertonic saline did not augment lymphatic removal of intestinal edema. sigma(ravi-muscularis) was increased with onset of edema and prevented by HS, paralleling the interstitial pressure data. Intestinal edema causes an early increase in interstitial pressure that is prevented by HS. Prevention of the edema-induced increase in interstitial pressure serves to blunt the mechanotransductive signal Of sigma(ravi-muscularis).