CAJ | 학술논문

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.
목적 관찰방광경조후불동시간점적핍뇨기공능、핍뇨기혈관신생화증식적변화,탐토경조후핍뇨기공능발생발전적궤제.방법 장성년자성SD대서75지수궤분위대조조、가수술조、경조1주조、경조2주조、경조6주조,매조각15지.채용뇨동역학평고핍뇨기공능,통과면역조직화학검측방광핍뇨기중적혈관성가성혈우병인자(vWF)화세포핵증식항원(Ki-67),분석혈관신생급증식변화.결과 대조조、가수술조、경조1주조、경조2주조、경조6주조평균방광중량분별위(103.23 ±4.35)、(110.95±5.51)、(228.02±32.88)、(392.35±39.90)、(616.50±86.41) mg,경조조여대조조、가수술조비교차이유통계학의의(P＜0.05);방광핍뇨기수축공능분별위(24.28±0.91)、(22.10±2.35)、(23.17±1.10)、(36.98±1.95)、(29.72±1.79) kPa,경조2주급6주조여대조조、가수술조、1주조비교차이유통계학의의(P＜0.05);핍뇨기층미혈관밀도분별위10.60±2.10、11.30±1.77、47.90±4.38、28.50±3.95、7.55±1.21,경조1주급2주조여대조조、가수술조、6주조비교차이유통계학의의(P＜0.01),Ki-67양성지수분별위(19.10±8.18)％、(19.84±5.45)％、(53.08±7.25)％、(49.28±5.99)％、(13.66±4.42)％,경조조여대조조、가수술조비교차이유통계학의의(P＜0.05).결론 방광핍뇨기기층세포혈류량감소인기세포증식하강가능시방광공능실대상적중요원인.
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 neovascularization 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 microvessle 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 detrusor blood flow,and it is the important explanation of bladder decompensation after partial bladder outlet ohstruction.