改良神经转位手术修复神经源性膀胱排尿障碍实验性研究

神经源性膀胱功能障碍所致并发症（肾积水、尿路感染、慢性肾功能衰竭）是长期生存者死亡的主要原因。神经转位手术通过将肋间或腰神经缝合于支配膀胱的骶神经，神经再生后改善膀胱排尿功能。传统神经转位手术存在临床效果不确切及膀胱逼尿肌-尿道外括约肌协同失调等问题。根据我们前期研究基础，进一步提出骶1神经部分束吻合骶3、4盆内脏神经分支的改良手术方式。理论上，新的改良手术神经再生错配率更低，距离短,恢复膀胱收缩排尿的有效性更高；同时骶1神经部分束支配膀胱逼尿肌，骶3、4神经发出阴部神经支配尿道外括约肌，能够解决膀胱逼尿肌-尿道外括约肌协同失调问题。本研究主要构建骶1神经部分束吻合骶3、4盆内脏神经分支的动物模型，验证改良手术治疗神经源性膀胱的有效性及能否解决传统神经转位手术存在的不足，从而为临床上使用改良神经转位手术治疗神经源性膀胱排尿障碍提供理论依据。

The complications, including hydronephrosis, urinary tract infection, chronic renal failure, have been the main causes of death in long-term survivors suffering from neurogenic bladder. Nerve transfer is the remedial measure for restoring continence and micturition in these survivors by suturing intercostal or lumbar nerves to the sacral nerves innervating the bladder. However，traditional method of nerve transfer exists some shortcomings such as inconsistent clinical differences and unsolvable detrusor–external sphincter dyssynergia. Based on our previous research, the operation method of nerve transfer can be modified by suturing the nerve fascicle using a part of the S1 nerve to the visceral branches arising from S3 and S4. Theoretically, the modified operation method of nerve transfer facilitates the process of bladder reinnervation with the advantages of lower mismatch rate and shorter regeneration distance and the effectiveness of restoring bladder continence and micturition is higher. After the modified operation, the nerve fascicle as a part of the S1 nerve innervates the bladder detrusor muscle and the pudendal nerve arising from the sacral 3 and 4 nerves controls the external sphincter of the urethra. This study aims to construct the animal model of nerve transfer by suturing the nerve fascicle using a part of the S1 nerve to the visceral branches arising from S3 and S4, and evaluate the effectiveness of modified operation method. Furthermore, we should figure out whether the modified operation method overcomes the shortcomings of traditional method of nerve transfer including inconsistent clinical differences and detrusor–external sphincter dyssynergia.