Gotoh M, Kato K, Saito M, Kondo A
Department of Urology, Nagoya University School of Medicine, Japan.
Urol Int. 1987;42(6):450-5. doi: 10.1159/000282014.
Three cases of disopyramide-induced urinary retention were reported and effects of disopyramide on agonist-induced contraction of detrusor muscle were studied in vitro. Muscle strips were obtained from rabbit bladder body and changes in isometric contraction of the strips were monitored. Acetylcholine, prostaglandin F2-alpha, potassium chloride, barium chloride, adenosine triphosphate and Ca2+ were used as agonists for detrusor muscle contraction. Disopyramide relaxed the contraction elicited by acetylcholine in normal Krebs solution, but exhibited no relaxing effect on contractions induced by prostaglandin F2-alpha, potassium chloride, barium chloride and adenosine triphosphate. In Ca2+-free Krebs solution, basal tension of the strips declined and spontaneous contractile activity was eliminated. Replenishment of 3 mM Ca2+ induced a slow contraction and redevelopment of spontaneous contraction of the strips. Pretreatment of the strips with disopyramide had no inhibitory effect on the Ca2+-induced contraction or on the spontaneous contractile activity in Ca2+-free solution. In normal Krebs solution, acetylcholine (10(-9)-10(-2)M) caused dose-dependent contractions of the detrusor muscle strips. Pretreatment of the strips with disopyramide (10(-5)-10(-3)M) dose-dependently inhibited the acetylcholine-induced contraction in a competitive way. The inhibitory effect of disopyramide on acetylcholine-induced contraction was less potent than that of atropine. We conclude that disopyramide may inhibit detrusor contractile activity mostly by its anticholinergic effect, resulting clinically in micturition disturbance.
报告了3例丙吡胺引起的尿潴留病例，并在体外研究了丙吡胺对激动剂诱导的逼尿肌收缩的影响。从兔膀胱体获取肌条，监测肌条等长收缩的变化。乙酰胆碱、前列腺素F2-α、氯化钾、氯化钡、三磷酸腺苷和Ca2+用作逼尿肌收缩的激动剂。丙吡胺在正常 Krebs 溶液中可松弛乙酰胆碱引起的收缩，但对前列腺素F2-α、氯化钾、氯化钡和三磷酸腺苷诱导的收缩无松弛作用。在无Ca2+的Krebs溶液中，肌条的基础张力下降，自发收缩活动消失。补充3 mM Ca2+可诱导肌条缓慢收缩并重新出现自发收缩。用丙吡胺预处理肌条对Ca2+诱导的收缩或无Ca2+溶液中的自发收缩活动无抑制作用。在正常Krebs溶液中，乙酰胆碱（10(-9)-10(-2)M）引起逼尿肌条剂量依赖性收缩。用丙吡胺（10(-5)-10(-3)M）预处理肌条以竞争性方式剂量依赖性抑制乙酰胆碱诱导的收缩。丙吡胺对乙酰胆碱诱导收缩的抑制作用比阿托品弱。我们得出结论，丙吡胺可能主要通过其抗胆碱能作用抑制逼尿肌收缩活动，临床上导致排尿障碍。
