期刊文献+

膀胱缺血对膀胱出口部分梗阻兔膀胱组织形态及功能影响的初步研究 被引量:2

Effect of ischemia on the structure of bladder in rabbits with partial bladder outlet obstruction
原文传递
导出
摘要 目的观察膀胱缺血情况下膀胱出口部分梗阻兔膀胱组织形态及酶学变化情况,探讨膀胱缺血对膀胱出口部分梗阻后膀胱病变的影响。方法64只成年新西兰兔电脑随机分为4组,每组16只。采用半缝扎腹主动脉制造膀胱缺血动物模型,采用部分结扎膀胱出口制造膀胱出12]部分梗阻动物模型。每组中随机选择4只行膀胱缺血手术(缺血组),4只行膀胱出口部分梗阻手术(梗阻组),4只行膀胱缺血及膀胱出口部分梗阻手术(联合组),4只为假手术对照组。于术后第1、2、4、8周各取1组测量膀胱湿重,然后膀胱全层石蜡切片MASSON染色观察黏膜层、黏膜下层、肌层及浆膜层厚度并分析膀胱间质平滑肌与胶原成分含量变化,S-100染色分析组织内神经元变化情况。检测膀胱肌层组织中肌浆网钙ATP酶与柠檬酸盐合酶活性。结果梗阻组与联合组兔膀胱重量自术后1周开始增加,分别为(5.10±0.29)、(4.80±0.37)g,均高于对照组[(1.93±0.17)g,均P〈0.05];在术后第4周达到最大值分别为(18.48±2.03)与(12.35±0.39)g,同期梗阻组膀胱重量大于联合组(P〈0.05)。梗阻组在处置前4周主要表现为肌层组织代偿性增厚,4周后出现纤维组织及胶原成分增加,而联合组处置后即出现肌层和纤维组织及胶原成分增加,2周后主要为纤维组织及胶原成分增加。S-100染色分析显示,与对照组相比,所有处理组兔膀胱组织内均出现了不同程度的神经缺失,以联合组尤为明显。梗阻组兔膀胱平滑肌肌浆网钙ATP酶与柠檬酸盐合酶活性在术后第4周达最大值,术后第8周降至低于术后第1周水平;联合组术后第1周两种酶活性开始持续下降;同期对照组两种酶活性均高于梗阻组和联合组(均P〈0.05)。结论膀胱缺血可降低膀胱对梗阻的耐受力,加重膀胱功能的损害。 Objective To compare the structures and functions of rabbit bladder after partial bladder outlet obstruction versus without ischemia so as to explore the effects of ischemia on bladder pathogenesis in rabbits with partial bladder outlet obstruction. Methods A total of 64 mature male rabbits were divided into 4 groups (n : 16 each). Four of each group underwent operation to establish an ischemic animal model (ischemia group ), another 4 underwent operation to establish a partial bladder outlet obstruction animal model ( obstruct group), the other 4 underwent operation to establish an ischemic and partial bladder outlet obstruction animal model ( combination group) and the remaining 4 underwent a sham operation as control. The rabbits in 4 groups were evaluated at Week 1, 2, 4 and 8 post-operation respectively. The weight of bladder, the thickness of mucosal, submucosa, muscular layer and placenta percreta and the activities of sarco/endoplasmic reticulum Ca2~ ATPase citrate synthase of cystic smooth muscle were detected respectively. MASSON staining was used to observe the smooth muscle and collagen in stroma of bladder and S-100 staining for observing the neurons in bladder. Results In obstruct and combination groups, the weights of bladder at week 1 were ( 5.10 ±0. 29 ) g and ( 4. 80± 0. 37 ) g respectively. They were both significantly higher than control group [ ( 1.93 ±0. 17 ) g, all P 〈 0. 05 ]. The weights of bladder in obstruct and combination groups peaked at Week 4 and they were ( 18.48 ± 2. 03) g and (12. 35±0. 39) g respectively. The weight of bladder in obstruct group was significantly heavier than combination group in the same terms. And they were both significantly heavier than control and ischemia groups(all P 〈 0. 05 ). Muscular tissue vicariously thickened during the first 4 weeks, and collagen and stroma increased at Week 4 in obstruct group. Muscular tissue, collagen and stroma all increased initially. But at Week 2 only collagen and stroma increased in combination group. Compare with control group, the other groups all have deletion of neurons, especially in combination group. The activities of sarco/ endoplasmic reticulum Ca2+ ATPase and citrate synthase of cystic smooth muscle of obstruct group peaked at Week 4. In combination group , the activities of sarco/endoplasmic reticulum Ca2+ ATPase and citrate synthase of cystic smooth muscle were decreased over 2 - 8 weeks. In the same terms, the activities of sarco/ endoplasmic reticulum Ca2+ ATPase and citrate synthase of cystic smooth muscle in control group were significantly higher than those in obstruct and combination groups ( all P 〈 0. 05 ). Conclusion Ischemia can reduce the tolerance of bladder and aggravate the impairment of bladder to partial outlet obstruction.
出处 《中华医学杂志》 CAS CSCD 北大核心 2011年第42期3007-3011,共5页 National Medical Journal of China
基金 广东省自然科学基金(8251001002000001)
关键词 膀胱颈梗阻 缺血 动物实验 Urinary bladder neck obstruction Ischemia Animal experimentation
  • 相关文献

参考文献2

二级参考文献32

  • 1那彦群.我国良性前列腺增生临床治疗现状及思考[J].中华外科杂志,2007,45(14):937-938. 被引量:23
  • 2Ghafar MA, Puchner PJ, Anastasiadis AG, et al. Does the prostatic vascular system contribute to the development of benign prostatic hyperplasia? Curr Urol Rep,2002,3: 292-296.
  • 3Berger AP, Bartsch G, Deibl M, et al. Atherosclerosis as a risk factor for benign prostatic hyperplaisa. BJU Int,2006, 98: 1035- 1042.
  • 4Kozlowski R, Kershen RT, Siroky MB, et al. Chronic ischemia alters prostate structure and reactivity in rabbits. J Urol, 2001, 165 : 1019-1026.
  • 5Soulitzis N, Karyotis I, Delakas D, et al. Expression analysis of peptide growth factors VEGF, FGF2, TGFB1, EGF and IGF1 in prostate cancer and benign prostatic hyperplasia. Int J Oncol, 2006, 29 : 305-314.
  • 6Pich A, Ponti R. MIB-1, Ki67 and PCNA scores and flowcytometry in intermediate grade malignant lymphomas. J Clin Pathol, 1994, 47 : 18-22.
  • 7Berger AP, Kofler K, Bektic J, et al. Increased growth factor production in a human prostatic stromal cell culture model caused by hypoxia. Prostate ,2003,57 : 57-65.
  • 8Wendy W, Barclay, Ralph D, et al. A system for studying epithelial-stromal interactions reveals distinct inductive abilities of stromal cells from benign prostatic hyperplasia and prostate cancer. Endocrinology,2005, 146: 13-18.
  • 9Emberton M, Fitzpatrick JM, Garcia-Losa M, et al. Progression of benign prostatic hyperplasia : systematic review of the placebo arms of clinical trials. BJU Int, 2008, 102: 981-956.
  • 10胡建新,何坚,罗战利,孙兆林,梁文通,潭宗建,刘军,张孝斌,刘修恒.相对缺血缺氧促进前列腺增生作用的研究[J].临床泌尿外科杂志,2007,22(8):630-632. 被引量:4

共引文献10

同被引文献15

  • 1吴士良,肖云翔,段继宏,杨勇,那彦群.膀胱出口部分梗阻后膀胱功能和组织学变化的相关性研究[J].中华泌尿外科杂志,2006,27(5):308-310. 被引量:12
  • 2Pampinella F, Roelofs M, Castellucci E, et al. Time-dependentremodeling of the bladder wall in growing rabbits after partial outletobstruction. J Urol, 1997,157: 677-682.
  • 3徐叔.药理实验方法学.第3版.北京:人民卫生出版社,2002.
  • 4Quasie 0, Martey ON, Nyarko AK, et al. Modulation of penileerection in rabbits by Mondia whitei : possible mechanism ofaction. Afr J Tradit Complement Altem Med,2010, 7 : 241-252.
  • 5Gosling JA, Kung LS, Dixon JS, et al. Correlation between thestructure and function of the rabbit urinary bladder following partialoutlet obstruction. J Urol, 2000, 163 : 1349-1356.
  • 6Broderick GA, Brock GB, Roehrbom CG, et al. Effects oftadalafil on lower urinary tract symptoms secondary to benignprostatic hyperplasia in men with or without erectile dysfunction.Urology, 2010,75: 1452-1458.
  • 7Kang YJ, Jin LH, Park CS, et al. Early sequential changes inbladder function after partial bladder outlet obstruction in awakesprague-dawley rats : focus on the decompensated bladder. KoreanJ Urol, 2011,52:835-841.
  • 8Khan MA, Shukla N,Thompson CS, et al. Endothelin-1 andurinary bladder hyperplasia following partial bladder outletobstruction. J Cardiovasc Pharmacol, 2000, 36 ( 5 Suppl 1):S262-S263.
  • 9Khan MA, Shukla N, Auld J, et al. Possible role of endothelin-1in the rabbit urinary bladder hyperplasia secondary to partialbladder outlet obstruction. Scand J Urol Nephrol,2000, 34: 15-20.
  • 10Theobald RJ Jr. Differing effects of N ( G) -monomethyl L-arginineand 7-nitroindazole on detrusor activity. Neurourol Urodyn, 2003 ,22: 62-69.

引证文献2

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部