机构地区:[1]南京医科大学第二附属医院泌尿外科,210011
出 处:《中华实验外科杂志》2014年第6期1178-1180,共3页Chinese Journal of Experimental Surgery
基 金:国家自然科学基金资助项目(81300572);江苏省自然科学基金资助项目(BK2011860);南京医科大学面上基金资助项目(2011NJMNU153)
摘 要:目的观察膀胱梗阻后不同时间点的逼尿肌功能、逼尿肌血管新生和增殖的变化,探讨梗阻后逼尿肌功能发生发展的机制。方法将成年雌性SD大鼠75只随机分为对照组、假手术组、梗阻1周组、梗阻2周组、梗阻6周组,每组各15只。采用尿动力学评估逼尿肌功能,通过免疫组织化学检测膀胱逼尿肌中的血管性假性血友病因子(vWF)和细胞核增殖抗原(Ki-67),分析血管新生及增殖变化。结果对照组、假手术组、梗阻1周组、梗阻2周组、梗阻6周组平均膀胱重量分别为(103.23±4.35)、(110.95±5.51)、(228.02±32.88)、(392.35±39.90)、(616.50±86.41)mg,梗阻组与对照组、假手术组比较差异有统计学意义(P〈0.05);膀胱逼尿肌收缩功能分别为(24.28±0.91)、(22.10±2.35)、(23.17±1.10)、(36.98±1.95)、(29.72±1.79)kPa,梗阻2周及6周组与对照组、假手术组、1周组比较差异有统计学意义(P〈0.05);逼尿肌层微血管密度分别为10.60±2.10、11.30±1.77、47.90±4.38、28.50±3.95、7.55±1.21,梗阻1周及2周组与对照组、假手术组、6周组比较差异有统计学意义(P〈0.01),Ki-67阳性指数分别为(19.10±8.18)%、(19.84±5.45)%、(53.08±7.25)%、(49.28±5.99)%、(13.66±4.42)%,梗阻组与对照组、假手术组比较差异有统计学意义(P〈0.05)。结论膀胱逼尿肌肌层细胞血流量减少引起细胞增殖下降可能是膀胱功能失代偿的重要原因。Objective To investigate the changes of morphology, angiogenesis, proliferation, and its correlation and mechanism of bladder contractile function during different phases. Methods Seventyfive female SD rats were divided into Control, sham group, 1 week obstruction group, 2 week obstruction group, 6 week obstruction group. Urodynamic were performed to evaluate bladder function, the changes of neovaseularization and proliferation realted factor vwf and Ki-67 in detrusor were evaluated with immunohistochemistry method. Results Control, sham group, 1 week, 2 week and 6 week obstruction group, the average weight of bladder was (103.23 ± 4.35), (110.95 ± 5.51), (228.02±32.88), (392.35 ± 39. 90), (616. 50 ± 86. 41 )mg respectively. Bladder weight in obstruction group was significantly greater compared with control and sham group (P 〈 0. 05). The average weight of bladder detrusor contractile function was ( 24. 28 ± 0. 91 ), ( 22. 10 ± 2. 35 ), ( 23.17 ± 1.10 ), ( 36. 98 ± 1.95 ), ( 29. 72 ± 1.79 ) kPa respectively. The detrusor contractile pressure in 2 week and 6 week obstruction group was significantly greater than others ( P 〈 0. 05 ). The expression of microvessle density was in the layer of detrusor was 10. 60 ± 2. 10, 11.30 ± 1.77, 47.90 ± 4. 38, 28.50 ± 3.95, 7.55 ± 1.21 respectively. The detrusor microvessie density in 1 week and 2 week obstruction group was significantly greater than others (P 〈 0. 01 ). The percentage of Ki-67 positive was (19.10±8.18)%, (19.84±5.45)%, (53.08±7.25)%, (49. 28 ± 5.99 ) % , ( 13.66 ± 4.42) % respectively. Bladder weight in obstruction group was significantly greater compared with control and sham group (P 〈 0. 05 ). Conclusion Partial bladder outlet obstruction (PBOO) mediated significant morphological changes in bladder wall relatively limited to some extent and was also time dependent. The inhibited proliferation of bladder detrusor layer cells owing to reduction of detru
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...