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Changes of bladder activity and glycine levels in the lumbosacral cord after partial bladder outlet obstruction in rats
Author(s) -
Miyazato Minoru,
Sugaya Kimio,
Nishijima Saori,
Kadekawa Katsumi,
Oshiro Yoshinori,
Hokama Sanehiro,
Uchida Atsushi,
Ogawa Yoshihide
Publication year - 2008
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/j.1442-2042.2008.02079.x
Subject(s) - medicine , bladder outlet obstruction , cystometry , urology , glycine receptor , urinary bladder , spinal cord , urinary bladder neck obstruction , anesthesia , glycine , prostate , amino acid , cancer , psychiatry , biochemistry , chemistry
Objectives: We investigated the time course of changes in bladder activity as well as in spinal and serum levels of glutamate and glycine after partial bladder outlet obstruction (BOO) in rats. Methods: A total of 36 female rats were divided into six groups: sham operation (control); 3 days, 14 days, and 28 days after BOO; 3 days and 28 days after relief of BOO. Under urethane anesthesia, isovolumetric cystometry was carried out in each group. Then, spinal and serum levels of glutamate and glycine were measured. Results: The interval between bladder contractions was shorter in all of the groups compared with the control group. The amplitude and duration of bladder contractions was decreased at 3 days, 14 days, and 28 days after BOO, and at 3 days after relief of BOO. Spinal and serum glutamate levels showed no changes. However, the spinal glycine level was decreased at 14 days and 28 days after BOO, and at 28 days after relief of BOO. Serum glycine level was also decreased at 28 days after BOO and 28 days after relief of BOO. Conclusions: Detrusor overactivity during the chronic phase of partial BOO is partly caused by a decrease of glycinergic neuronal activity in the lumbosacral cord. A 3‐day period of BOO produces detrusor overactivity, which might be due to an irreversible decrease of spinal glycinergic neuronal activity.