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ELECTRICAL AND CHEMICAL STIMULATION OF SPINAL CORD FOR TREATMENT OF URINARY DISTURBANCE

脊髓电刺激和化学刺激治疗排尿障碍

基本信息

批准号：
03557068
负责人：
TSUCHIDA Seigi
金额：
$ 10.11万
依托单位：
DEPT.OF UROLOGY, AKITA UNIVERSITY SCHOOL OF MEDICINE
依托单位国家：
日本
项目类别：
Grant-in-Aid for Developmental Scientific Research (B)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1993
项目状态：
已结题

项目摘要

For the purpose of evaluation of the chemical stimulation of sacral spinal cord to modulate the micturition reflex, intrathecal administration of various drugs was performed using decerebrate dogs. GABA (0.1-0.3 mg), muscimol (0.01-0.2 mg), bacrofen (0.01-0.3 mg) increased bladder capacity 65%, 142%, 95% respectively. Phaclofen did not have a significant effect. Picrotoxin (0.05-0.3 mg) inhibited the effect of muscimol, and picrotoxin alone decreased bladder capacity 28%. These results indicate that there are both GABA-A and -B receptors in the sacral spinal cord, and that intrinsic GABA acts though GABA-A receptor. Intrathecal administration of phenylephrine (0.01-0.43 mg) increased bladder capacity and external urethral sphincter activity. Prazocin (0.01-0.3 mg) did not change bladder activity but decreased external urethral sphincter activity. Clonidine (0.07-0.32 mg) did not change bladder activity but decreased external urethral sphincter activity. Yohimbine (0.07-0.45 mg) decreas … More ed bladder contraction pressure. These results suggest that alpha-adrenergic mechanism in the sacral spinal cord increases bladder capacity and increases the external urethral sphincter activity through alpha-1 receptor, and increases bladder contractility and decreases external urethral sphincter activity through alpha-2 receptor.Electrical stimulation of the sacral cord as well as sacral roots induced both bladder and urethral sphincter contractions. Bladder contraction was dominant when S-2 was stimulated while external urethral sphincter contraction was dominant when S-1 was stimulated. Potable stimulator (2.5 x 6 x 9 cm, 10-50 Hz, 0.2-1.0 msec duration, 0-50 V) was made for functional electrical stimulation. Electrical stimulation in the pontine micturition center (PMC) induced urethral relaxation as well as bladder contraction. Internal urethral sphincter relaxation was not inhibited by propranolol or atropine, but was abolished by hexamethonium or methylene blue. L-arginine increased bladder capacity and decreased bladder contraction pressure. These responses were partially reversed by methylene blue. Methylene blue enhanced bladder contraction evoked by PMC stimulation and induced spontaneous bladder contraction. These results indicate that internal urethral sphincter relaxations in mediated by non-adrenergic and non-cholinergic mechanism, and that L-arginine - NO pathway has a role in controlling the micturition reflex. Less

为了评估化学刺激骶脊髓对排尿反射的调节作用，我们用无脑狗进行鞘内给药。GABA （0.1 ~ 0.3 mg）、muscimol （0.01 ~ 0.2 mg）、baacrofen （0.01 ~ 0.3 mg）分别使膀胱容量增加65%、142%、95%。苯氯芬没有明显的效果。微微毒素（0.05 ~ 0.3 mg）可抑制木西莫的作用，单独微微毒素可使膀胱容量下降28%。这些结果表明，骶脊髓中同时存在GABA- a和-B受体，并且内源性GABA通过GABA- a受体起作用。鞘内注射苯肾上腺素（0.01 ~ 0.43 mg）可增加膀胱容量和外尿道括约肌活动。普唑嗪（0.01 ~ 0.3 mg）不改变膀胱活动，但使尿道外括约肌活动降低。可乐定（0.07 ~ 0.32 mg）不改变膀胱活动，但降低尿道外括约肌活动。育亨宾（0.07-0.45 mg）可降低膀胱收缩压力。提示骶脊髓α -肾上腺素能机制通过α -1受体增加膀胱容量，增加外尿道括约肌活动，通过α -2受体增加膀胱收缩力，降低外尿道括约肌活动。电刺激骶束和骶根引起膀胱和尿道括约肌收缩。刺激S-2时以膀胱收缩为主，刺激S-1时以外尿道括约肌收缩为主。制作便携式刺激器（2.5 x 6 x 9 cm, 10-50 Hz, 0.2-1.0 msec持续时间，0-50 V）用于功能性电刺激。电刺激脑桥排尿中心（PMC）可引起尿道松弛和膀胱收缩。普萘洛尔和阿托品对内尿道括约肌松弛无抑制作用，但六甲溴铵和亚甲基蓝可使内尿道括约肌松弛消失。l -精氨酸增加膀胱容量，降低膀胱收缩压力。这些反应被亚甲基蓝部分逆转。亚甲基蓝增强PMC刺激引起的膀胱收缩，诱导自发性膀胱收缩。上述结果提示，尿道内括约肌舒张是由非肾上腺素能和非胆碱能机制介导的，l -精氨酸- NO通路在控制排尿反射中具有一定的作用。少