Laval K U, Lutzeyer W
Urol Int. 1980;35(3):182-7. doi: 10.1159/000280321.
Uninhibited detrusor contractions of neurogenic origin have been described repeatedly. Since a spontaneous myogenic activity of the detrusor has been demonstrated in isolated muscle strips, it seems reasonable that an increase of this spontaneous contraction activity may induce bladder instability of pure myogenic origin. 30 patients separated into two groups were investigated. All patients suffered from involuntary contractions of the detrusor, accompanied by loss of urine. Nifedipin was applied as a selective Ca-antagonistic drug to block the phasic detrusor activity. In our experiment, involuntary detrusor contractions could not be suppressed, and also bladder capacity could not be increased by this drug. This result leads to the assumption that the spontaneous phasic activity of the detrusor does not induce any involuntary bladder contraction.
神经源性无抑制逼尿肌收缩已被多次描述。由于在分离的肌条中已证明逼尿肌存在自发肌源性活动,因此这种自发收缩活动的增加可能诱发纯肌源性膀胱不稳定似乎是合理的。对30例患者进行了分组研究。所有患者均有逼尿肌不自主收缩,并伴有尿失禁。应用硝苯地平作为选择性钙拮抗剂来阻断逼尿肌的阶段性活动。在我们的实验中,该药物无法抑制逼尿肌的不自主收缩,也无法增加膀胱容量。这一结果导致这样一种假设,即逼尿肌的自发阶段性活动不会诱发任何膀胱不自主收缩。