Objective To explore the correlation between bladder compliance and nerve growth factor (NGF) expression in rats with spinal cord injury at different segments. Methods Included in this study were 180 female SD rats randomly divided into three groups:thoracolumbar injury group (n=60), sacral injury group (n=60) and the control group (n=60). Animal models of dorsal spinal cord injury were established by using standardized animal experimental apparatus. The site of spinal cord injury was T10-L1 for thoracolumbar injury, and S2-S4 for sacral injury. The control rats received removal of spinous process and vertebral lamina, and were free of injury to the spinal cord. Four weeks later, all rats underwent cystometry; then the bladders were harvested for preparation of tissue homogenate. The NGF expression level was determined by using ELISA. Results ①Thoracolumbar injury was characterized by low compli-ance bladder, while sacral injury resulted in high compliance bladder. ②ELISA showed that the NGF expression in bladder tissue homogenate was increased in thoracolumbar injury group and decreased in the sacral injury group. ③There was a negative correlation between bladder compliance and bladder tissue NGF expression in thoracolumbar in-jury (r=-0.655, P<0.05) and in sacral injury (r=-0.783, P<0.05). Conclusion High-level injury of spinal cord leads to reduced bladder compliance and increased NGF expression in bladder tissue. The opposite holds true with low-level injury of spinal cord. Bladder compliance is negatively correlated with NGF expression level in bladder tissue after spinal cord injury.
目的 应用生物素葡聚糖胺(BDA)示踪技术观察大鼠背侧胸腰段脊髓损伤(SCI)后不同时间段膀胱排尿神经通路改变的差异.方法 清洁级雌性SD大鼠90只,随机分为5组:1d组、3d组、7d组、14d组、21d组(每组分别设对照组8只,SCI组10只).使用标准化脊髓损伤动物模型实验装置制备背侧脊髓损伤动物模型,损伤部位定于T10~L1水平,对照组大鼠仅咬除棘突和椎板,不损伤脊髓.模型制备后分别于1d、3d、7d、14d、21 d给予对照组及SCI组大鼠膀胱壁注射BDA.注射2周后取材,免疫组化方法显示大鼠脊髓切片中BDA阳性神经元.结果 BDA阳性神经元经免疫组化学方法显色后呈棕褐色.SCI 1 d、3 d、7 d、14 d、21 d各组脊髓T10~L1平面的阳性神经细胞数与对照组相比均明显减少,SCI 14 d、21 d组较SCI 3 d、7d组阳性神经细胞数又有所增加.结论 大鼠背侧胸腰段脊髓损伤后支配排尿的神经通路受损,在损伤早期呈现出损伤进行性加重趋势,至损伤后1周左右脊髓神经细胞出现修复,神经通路可有部分修复.
人乳头瘤病毒(human papilloma virus,HPV)是目前已知唯一能引起人类上皮组织增生性病变的双链DNA病毒[1]。HPV的感染在宫颈癌、尖锐湿疣的病因中起着主要的作用。按与癌变发生的关系HPV可分为高危型、中危型和低危型,高危型(如16、18、45、56型)与子宫癌、喉癌、膀胱癌等密切相关,低危型(如6、11型)与尖锐湿疣、乳头状瘤等良性疾病相关,中危型(如31、33、35、51、58型)介于两者之间[2]。研究表明,持续的高危型HPV感染是浸润性宫颈癌发生的必须病因[3],故HPV分型检测对于各种宫颈病变的早期筛查、防治及预后判断具有重要的意义。本研究收集了山西医科大学第一医院就诊的289例太原市区居住的疑似HPV感染者的泌尿生殖道分泌物,并运用实时荧光定量PCR技术( FQ-PCR)技术对标本进行HPV分型检测,以了解太原市HPV感染状况和相关因素。
Objective To determine the changes in micturition nervous pathways induced by traumatic dorsal thoracolumbar spinal cord injury by using pseudorabies virus (PRV) tracer technique. Methods Twenty-four clean female SD rats were randomly assigned to sham operation group (n=12) and dorsal spinal cord injury group (group SCI, n=12), respectively. A standardized dorsal spinal cord injury animal model was constructed based on the T12 to L1 injury. In sham operation group, the spinal process and lamina were removed while sparing the spinal cord. Rats in group SCI were subjected to spinal process and lamina removal. This was followed by PRV injection to the cystic wall that entailed extraction of the spinal cord at 96 h for assessment of the PRV-positive neurons by immunohistochemistry assay. Results The PRV-positive neurons, labelled as browns-staining cells by immunohistochemistry assay, were noted above and below the injured planes of spinal cord injury. Compared with sham operation group, group SCI was associated with a significantly reduced and increased number of positive neurons in the plane above and below the injured spinal cord, respectively. Conclusion Traumatic spinal cord injury results in absence of micturition reflex conduction to the central nervous system yet augmented micturition reflex below the injured plane as a compensatory response.
神经源性膀胱(neurogenic bladder)是一类由神经病变导致膀胱和(或)尿道功能失常,因而产生一系列并发症的疾病的总称,在有些文献中称其为下尿路神经肌肉失调.其临床表现可以随病因的不同而变化.在长期的疾病作用下,患者既可以无任何症状或仅有轻微反应,也可以出现严重的肾功能损害,甚至死亡.神经源性膀胱病因十分复杂,但目前还没有大样本的神经源性膀胱的流行病学研究资料.本文从中枢神经系统、外周神经系统、感染及免疫性疾病、先天遗传以及医源性等方面对神经源性膀胱的病因进行了划分,并结合目前国内外最新的研究进展加以详细的阐述.