目的 探索大鼠脊髓损伤所致神经源性肠功能障碍的肠道功能动态改变。方法 24只雌性Sprague-Dawley大鼠分为对照组(n=12)和脊髓损伤组(n=12)。采用动脉瘤夹(标定力为70 g)钳夹60 s制作T10脊髓损伤模型;对照组只暴露硬脊膜。分别于造模前和造模后4周,X线造影观察肠道功能的动态改变,HE染色观察结肠病理改变。结果 与对照组相比,脊髓损伤组胃排空及肠道传输功能明显降低(P<0.05)。结论 采用动脉瘤夹能成功复制大鼠脊髓损伤模型。大鼠脊髓损伤后出现神经源性肠功能障碍,胃排空及肠道传输功能明显减弱。
蔡畅
,
李建军
,
高峰
,
杨明亮
,
杜良杰
,
杨德刚
,
刘长彬
,
李大鹏
,
张文豪
,
徐珮珮
. 大鼠脊髓损伤后胃肠动力的X线研究[J]. 中国康复理论与实践, 2018
, 24(6)
: 645
-649
.
DOI: 10.3969/j.issn.1006-9771.2018.06.005
Objective To study the dynamic changes of the intestinal function of neurogenic bowel dysfunction rats caused by spinal cord injury using X-ray radiography.Methods Twenty-four female Sprague-Dawley rats were divided into control group (n=12) and spinal cord injury group (n=12). The T10 spinal cord injury model was established using aneurysm clip (70 grams calibration force) for 60 seconds. The control group exposed the dura only. X-ray Barium was used to observe the dynamic changes of intestinal function, and HE staining was used to observe the pathology of the colon before and four weeks after modeling.Results Compared with the control group, gastric emptying and intestinal transit function significantly reduced in the spinal cord injury group (P<0.05).Conclusion The spinal cord injury model can be successfully duplicated with aneurysm clip in rats; neurogenic bowel dysfunction occurs after spinal cord injury, gastric emptying and intestinal transit function are weakened.
[1] 徐青,高飞,王磊,等. 脊髓损伤后肠道功能障碍:美国临床实践指南解读[J]. 中国康复理论与实践, 2010, 16(1): 83-86.
[2] Hocevar B, Gray M.Intestinal diversion (colostomy or ileostomy) in patients with severe bowel dysfunction following spinal cord injury[J]. J Wound Ostomy Continence Nurs, 2008, 35(2): 159-166.
[3] Liu CW, Huang CC, Chen CH, et al.Prediction of severe neuro-genic bowel dysfunction in persons with spinal cord injury[J]. Spinal Cord, 2010, 48(7): 554-559.
[4] Pan Y, Liu B, Li R, et al.Bowel dysfunction in spinal cord injury: current perspectives[J]. Cell Biochem Biophys, 2014, 69(3): 385-388.
[5] 张洁,杨德刚,李建军,等. 国际脊髓损伤肠道功能基础数据集最新修订及解读[J]. 中国康复理论与实践, 2017, 23(10): 1236-1240.
[6] Cabezos PA, Vera G, Castillo M, et al.Radiological study of gastrointestinal motor activity after acute cisplatin in the rat. Temporal relationship with pica[J]. Auton Neurosci, 2008, 141(1-2): 54-65.
[7] Vera G, Lópezpérez AE, Martínezvillaluenga M, et al.X-ray analysis of the effect of the 5-HT3 receptor antagonist granisetron on gastrointestinal motility in rats repeatedly treated with the antitumoral drug cisplatin[J]. Exp Brain Res, 2014, 232(8): 2601-2612.
[8] Cabezos PA, Vera G, Martín-Fontelles MI, et al.Cisplatin-induced gastrointestinal dysmotility is aggravated after chronic administration in the rat. Comparison with pica[J]. Neurogastroenterol Motil, 2010, 22(7): 797-805.
[9] 刘小康,徐建广,连小峰,等. 大鼠钳夹式急性脊髓损伤模型的制备与评价[J]. 中国矫形外科杂志, 2012, 20(14): 1318-1322.
[10] Preziosi G, Raptis DA, Raeburn A, et al.Autonomic rectal dysfunction in patients with multiple sclerosis and bowel symptoms is secondary to spinal cord disease[J]. Dis Colon Rectum, 2014, 57(4): 514-521.
[11] 逯晓蕾,李建军,杜良杰,等. 脊髓损伤后肠道功能的变化[J]. 中国康复理论与实践, 2010, 16(8): 758-760.
[12] Meshkinpour H, Harmon D, Thompson R, et al.Effects of thoracic spinal cord transection on colonic motor activity in rats[J]. Paraplegia, 1985, 23(5): 272-276.
[13] Gondim FA, Rodrigues CL, da Graca JR, et al. Neural mechanisms involved in the delay of gastric emptying and gastrointestinal transit of liquid after thoracic spinal cord transection in awake rats[J]. Auton Neurosci, 2001, 87(1): 52-58.
[14] 韩芸峰,王振宇,于涛. 大鼠脊髓损伤模型建立及神经源性肠功能障碍的初步评价[J]. 中国临床神经外科杂志, 2015, 20(10): 617-620.
[15] 朱黎婷,朱毅. 脊髓损伤神经源性肠道功能障碍的诊断、评价和康复治疗现况[J]. 中国康复医学杂志, 2013, 28(12): 1163-1167.
[16] Media S, Christensen P, Lauge I, et al.Reproducibility and validity of radiographically determined gastrointestinal and segmental colonic transit times in spinal cord-injured patients[J]. Spinal Cord, 2009, 47(1): 72-75.
[17] Liu GX, Yang YX, Yan J, et al.Glial-derived neurotrophic factor reduces inflammation and improves delayed colonic transit in rat models of dextran sulfate sodium-induced colitis[J]. Int Immunopharmacol, 2014, 19(1): 145-152.
