Xiao C G, de Groat W C, Godec C J, Dai C, Xiao Q
Department of Urology, the Long Island College Hospital, SUNY Health Science Center at Brooklyn, New York 11203, USA.
J Urol. 1999 Sep;162(3 Pt 1):936-42. doi: 10.1097/00005392-199909010-00094.
A "skin-CNS-bladder" reflex pathway for inducing micturition after spinal cord injury has been established in cat. This reflex pathway which is basically a somatic reflex arc with a modified efferent limb that passes somatic motor impulses to the bladder, has been designed to allow spinal cord injured patients to initiate voiding by scratching the skin.
The skin-CNS-bladder reflex was established in the cat by intradural microanastomosis of the left L7 ventral root (VR) to the S1 VR while leaving the L7 dorsal root (DR) intact to conduct cutaneous afferent signals that can trigger the new micturition reflex arc. After allowing 11 weeks for axonal regeneration, urodynamic, pharmacological and electrophysiological studies were conducted in pentobarbital or chloralose anesthetized animals.
A detrusor contraction was initiated at short latency by scratching the skin or by percutaneous electrical stimulation in the L7 dermatome. Maximal bladder pressures during this stimulation were similar to those activated by bladder distension in control animals. Electrophysiological recording revealed that single stimuli (0.3 to 3 mA, 0.02 to 0.2 msec duration) to the left L7 spinal nerve in which the efferent axons had degenerated evoked action potentials (0.5 to 1 mV) in the left S1 spinal nerve distal to the anastomosis. In addition, increases in bladder pressure were elicited by trains of the stimuli (5 to 20 Hz, 5 seconds) applied to the L7 spinal nerve. Urodynamic studies including external sphincter EMG recording demonstrated that the new reflex pathway could initiate voiding without detrusor-external urethral sphincter dyssynergia. Atropine (0.05 mg./kg., i.v.) or trimethaphan (5 mg./kg., i.v.), a ganglionic blocking agent, depressed the bladder contractions elicited by skin stimulation. The skin-CNS-bladder reflex could also be elicited after transecting the spinal cord at the L2-L3 or L7-S1 levels.
The cross-wired somato-autonomic bladder reflex is effective in initiating bladder contractions and coordinated voiding in cats with an intact neuraxis and can also induce bladder contractions after acute transection of the lumbar spinal cord. The new pathway is mediated by cholinergic transmission involving both nicotinic and muscarinic receptors. It is concluded that somatic motor axons can innervate bladder parasympathetic ganglion cells and thereby transfer somatic reflex activity to the bladder smooth muscle.
在猫身上已建立起一种“皮肤-中枢神经系统-膀胱”反射通路,用于脊髓损伤后诱导排尿。该反射通路本质上是一个躯体反射弧,其传出支经过改良,可将躯体运动冲动传递至膀胱,旨在让脊髓损伤患者通过搔抓皮肤来启动排尿。
通过将左侧L7腹根(VR)与S1腹根进行硬膜内显微吻合,同时保持L7背根(DR)完整以传导可触发新排尿反射弧的皮肤传入信号,从而在猫身上建立皮肤-中枢神经系统-膀胱反射。在给予11周时间让轴突再生后,对戊巴比妥或氯醛糖麻醉的动物进行尿动力学、药理学和电生理学研究。
搔抓皮肤或对L7皮节进行经皮电刺激可在短潜伏期内引发逼尿肌收缩。此刺激过程中的最大膀胱压力与对照动物膀胱扩张所激活的压力相似。电生理记录显示,对传出轴突已退化的左侧L7脊神经施加单次刺激(0.3至3毫安,持续时间0.02至0.2毫秒),可在吻合口远端的左侧S1脊神经中诱发动作电位(0.5至1毫伏)。此外,对L7脊神经施加一连串刺激(5至20赫兹,持续5秒)可引起膀胱压力升高。包括外括约肌肌电图记录在内的尿动力学研究表明,新的反射通路可启动排尿,且无逼尿肌-尿道外括约肌协同失调。静脉注射阿托品(0.05毫克/千克)或神经节阻断剂三甲噻方(5毫克/千克)可抑制皮肤刺激引起的膀胱收缩。在L2-L3或L7-S1水平横断脊髓后,也可引发皮肤-中枢神经系统-膀胱反射。
交叉连接的躯体-自主神经膀胱反射在具有完整神经轴的猫中可有效引发膀胱收缩并协调排尿,在腰段脊髓急性横断后也可诱导膀胱收缩。新通路由涉及烟碱样和毒蕈碱样受体的胆碱能传递介导。得出的结论是,躯体运动轴突可支配膀胱副交感神经节细胞,从而将躯体反射活动传递至膀胱平滑肌。