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

为了评价骶脊髓的化学刺激以调节排尿反射的目的，使用去大脑的狗进行各种药物的鞘内给药。GABA（0.1- 0.3mg）、蝇蕈醇（0.01- 0.2mg）、巴克罗芬（0.01- 0.3mg）分别增加膀胱容量65%、142%、95%。法氯芬没有显著的效果。印防己毒素（0.05-0.3 mg）抑制蝇蕈醇的作用，单独印防己毒素使膀胱容量降低28%。上述结果表明，骶髓内同时存在GABA-A和-B受体，内源性GABA通过GABA-A受体起作用。鞘内注射苯乙哌啶（0.01-0.43 mg）可增加膀胱容量和尿道外括约肌活动。吡唑酮（0.01-0.3毫克）没有改变膀胱活动，但减少外尿道括约肌的活动。可乐定（0.07-0.32毫克）没有改变膀胱活动，但减少尿道外括约肌的活动。育亨宾（0.07-0.45 mg）减量 ...更多信息 艾德膀胱收缩压。上述结果提示，骶髓α-肾上腺素能机制通过α 1受体增加膀胱容量和尿道外括约肌活动，通过α 2受体增加膀胱收缩力和尿道外括约肌活动，电刺激骶髓和骶神经根可引起膀胱和尿道外括约肌的收缩。刺激S-2时膀胱收缩占优势，刺激S-1时尿道外括约肌收缩占优势。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。电刺激脑桥排尿中枢（PMC）引起尿道松弛以及膀胱收缩。内尿道括约肌松弛不受普萘洛尔或阿托品的抑制，但被六烃季铵或亚甲蓝废除。L-精氨酸增加膀胱容量，降低膀胱收缩压。这些反应被亚甲蓝部分逆转。美蓝可增强刺激PMC引起的膀胱收缩和诱发自发性膀胱收缩。上述结果表明，内尿道括约肌的松弛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起作用。少

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