Radhakrishnan Ravi S, Xue Hasen, Moore-Olufemi Stacey D, 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. 2006 Jun;34(6):1713-8. doi: 10.1097/01.CCM.0000218811.39686.3D.
We have shown that acute edema induced by mesenteric venous hypertension (MV-HTN) impairs intestinal transit and reduces the standardized engineering measures of intestinal stiffness (elastic modulus) and residual stress (opening angle). We hypothesized that hypertonic saline (7.5%) would reverse these detrimental effects of acute edema.
Laboratory study.
University laboratory.
Male Sprague Dawley rats (270-330 g).
Rats were randomized to five groups: sham, MV-HTN alone, MV-HTN with 4 mL/kg normal saline resuscitation (equal volume), MV-HTN with 33 mL/kg normal saline resuscitation (equal salt), and MV-HTN with 4 mL/kg hypertonic saline. Intestinal edema was measured by wet to dry tissue weight ratio. A duodenal catheter was placed and, 30 mins before death, fluorescein isothiocyanate Dextran was injected. At death, dye concentrations were measured to determine intestinal transit. Segments of distal ileum were hung to a fixed point in a tissue bath and to a force displacement transducer and stretched in increments of 1 mm; we recorded the new length and the corresponding force from the force displacement transducer to determine elastic modulus. Next, two transverse cuts were made yielding a 1- to 2-mm thick ring-shaped segment of tissue which was then cut radially to open the ring. Then the opening angle was measured.
MV-HTN, MV-HTN with 4 mL/kg normal saline, and MV-HTN with 33 mL/kg normal saline caused a significant increase in tissue edema and a significant decrease in intestinal transit, stiffness, and residual stress compared with sham. Hypertonic saline significantly lessened the effect of edema on intestinal transit and prevented the changes in stiffness and residual stress.
Hypertonic saline prevented intestinal tissue edema. In addition, hypertonic saline improved intestinal transit, possibly through more efficient transmission of muscle force through stiffer intestinal tissue.
我们已经表明，肠系膜静脉高压（MV-HTN）诱导的急性水肿会损害肠道运输，并降低肠道硬度（弹性模量）和残余应力（开口角度）的标准化工程测量值。我们假设高渗盐水（7.5%）会逆转急性水肿的这些有害影响。
实验室研究。
大学实验室。
雄性Sprague Dawley大鼠（270 - 330克）。
将大鼠随机分为五组：假手术组、单纯MV-HTN组、MV-HTN伴4 mL/kg生理盐水复苏组（等体积）、MV-HTN伴33 mL/kg生理盐水复苏组（等盐量）和MV-HTN伴4 mL/kg高渗盐水组。通过湿重与干重组织重量比测量肠道水肿。放置十二指肠导管，并在死亡前30分钟注射异硫氰酸荧光素葡聚糖。在死亡时，测量染料浓度以确定肠道运输情况。将回肠远端段悬挂在组织浴中的固定点和力位移传感器上，并以1毫米的增量拉伸；我们记录新的长度和来自力位移传感器的相应力以确定弹性模量。接下来，进行两次横向切割，得到一个1至2毫米厚的环形组织段，然后径向切割该环以打开它。然后测量开口角度。
与假手术组相比，MV-HTN组、MV-HTN伴4 mL/kg生理盐水组和MV-HTN伴33 mL/kg生理盐水组导致组织水肿显著增加，肠道运输、硬度和残余应力显著降低。高渗盐水显著减轻了水肿对肠道运输的影响，并防止了硬度和残余应力的变化。
高渗盐水可预防肠道组织水肿。此外，高渗盐水可能通过更有效地通过更硬的肠道组织传递肌肉力量来改善肠道运输。
