| Co-Investigator(Kenkyū-buntansha) |
NOTO Hiromitsu Akita Univ., Dept.of Urology, Assistant Prof., 医学部, 助手 (60164711)
NISHIZAWA Osamu Akita Univ., Dept.of Urology, Assistant Prof., 医学部, 講師 (60091815)
HARADA Tadashi Akita Univ., Dept.of Urology, Assistant Prof., 医学部, 講師 (00108953)
OGAWA Tetsurou Akita Univ., 1st Dept.of Physiology, Professor, 医学部, 教授 (80004555)
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| Research Abstract |
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
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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
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