Effects of in vivo Ischemia on the infusion cystometry and in vitro whole bladder contractility of the rat

Abstract

ラットの両側内腸骨動脈を結紮し虚血ラット膀胱を作成し, この虚血膀胱におけるurethane麻酔下の膀胱内圧測定及び摘出膀胱の電気刺激, bethanechol, ATP, KClに対する収縮力を検討した.次いで一定速度で生理食塩水を膀胱内に注入しながら電気刺激を繰り返しvolume-pressure studyを実施した.膀胱の重量は虚血により有意に増大した.膀胱内圧曲線を分析した結果, 膀胱容量, 残尿量は増大し, 排尿筋収縮圧は減少した.この結果, 虚血に伴い排尿効率(排尿量/膀胱容量)は有意に減少した.摘出膀胱における排尿収縮力は, 全ての刺激に対して虚血後に低下した.volume-pressure studyの結果からin vitroの膀胱complianceは7日後減少し14日後は逆に増大した

Ischemia induced by atherosclerosis is a common cause of organ failure in the elderly. We investigated the effects of in vivo ischemia created by ligation of the internal iliac arteries on the parameters of in vivo infusion cystometry under urethane anesthesia and on in vitro whole bladder contractility of the rat. Bladder weight significantly increased after ischemia for 14 days. Infusion cystometry demonstrated that in the ischemic bladders the capacity increased, the voiding pressure decreased, and the volume of residual urine increased, which resulted in deteriorated voiding efficacy. The in vitro whole bladder contractility to field stimulation, bethanechol, ATP, and KCl was reduced by ischemia. The passive pressure increased as the bladder volume enlarged and the bladder compliance once decreased by ischemia on the 7th day, but increased on the 14th day. In an active volume-pressure relationship study the peak response was decreased by ischemia. The volume at which response reached a peak value shifted to a larger volume 14 days after surgery. In conclusion, ischemia impaired in vivo rat detrusor power to empty. Since detrusor contractility in vitro decreased in response to various kinds of stimulation, this deteriorated bladder function was supposed to be caused by muscle degeneration.