Ohmura M, Yokoi K, Kondo A, Miyake K, Saito M
Department of Urology, Nagoya University School of Medicine, Japan.
Hinyokika Kiyo. 1996 Feb;42(2):111-5.
Ischemia of vital organs causes various degrees of impairment. We studied the in vitro effects of ischemia on the function of the rat bladder. Ischemia was induced by ligation of the bilateral (bilateral ischemia) or right (unilateral ischemia) internal iliac arteries. Bladder weight increased significantly following 1 week of bilateral and unilateral ischemia. Passive tension was significantly higher in ischemic bladders than in control bladders at an increase in length between 6 and 12 mm. In both control and ischemic bladders, active tension was highest at a 16-mm increase in length. Bladders subjected to unilateral or bilateral ischemia for 1 or 2 weeks demonstrated impaired contractile responses to field stimulation, bethanechol, ATP and KCl. There were no differences in contractile strength between muscle specimens obtained from the ipsilateral or contralateral sides of unilateral ischemic bladders. Our findings showed that unilateral and bilateral ischemia inhibited the in vitro contractile strength of the detrusor muscle in response to intramural and pharmacologic stimulation.
重要器官的缺血会导致不同程度的损害。我们研究了缺血对大鼠膀胱功能的体外影响。通过结扎双侧(双侧缺血)或右侧(单侧缺血)髂内动脉诱导缺血。双侧和单侧缺血1周后膀胱重量显著增加。在长度增加6至12毫米时,缺血膀胱的被动张力明显高于对照膀胱。在对照膀胱和缺血膀胱中,主动张力在长度增加16毫米时最高。单侧或双侧缺血1或2周的膀胱对场刺激、氨甲酰甲胆碱、三磷酸腺苷和氯化钾的收缩反应受损。从单侧缺血膀胱的同侧或对侧获取的肌肉标本之间的收缩强度没有差异。我们的研究结果表明,单侧和双侧缺血抑制了逼尿肌对壁内和药理刺激的体外收缩强度。