脊髄損傷・脳卒中モデルと排尿

Animal model with detrusor overactivity caused by cerebral infarction or spinal cord in jury

　脳血管障害のような脳幹部橋より上位の障害や脊髄損傷は，膀胱の蓄尿障害を引き起こす．筆者らは脳梗塞や脊髄損傷の動物モデルを用いて，蓄尿障害に対する薬剤の作用メカニズムについて検討してきた．抗コリン薬とα₁遮断薬は排尿筋過活動の主な治療薬であるが，これらの薬剤は，下部尿路の知覚C線維を遮断することで蓄尿障害を改善すると考えられた．

Suprapontine lesions such as those resulting from cerebrovascular disease, and spinal cord injury cause bladder storage dysfunction. We developed a rat model with DO (detrusor overactivity) caused by cerebral infarction or spinal cord injury. Antimuscarinic drugs and α₁-blockers are the main treatments for DO, a condition caused by neurologic lesions including cerebrovascular disease and spinal cord injury. These drugs affect sensory bladder storage symptoms, suggesting an action on bladder and urethral afferent pathways. Using animal models of DO, we demonstrated that these drugs improved bladder storage function via suppression of C-fiber afferent nerves from the lower urinary tract.