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首页> 外文期刊>Japanese Journal of Pharmacology >Effects of Apomorphine on Urinary Bladder Motility in Anesthetized Rats
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Effects of Apomorphine on Urinary Bladder Motility in Anesthetized Rats

机译:阿扑吗啡对麻醉大鼠尿膀胱动力的影响

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References(14) Cited-By(18) We studied the effects of apomorphine (AM) on bladder motility in anesthetized rats in which Tyrode's solution was continuously infused into the bladder at a constant rate, inducing an almost constant rate of bladder contraction accompanying micturition. AM at a dose of 1 mg/kg, i.v., caused a hyperactive bladder response, during which micturition disappeared. AM (12.5 μg) for intracerebroventricular (i.c.v.) injection or 50 μg for intrathecal (i.t.) injection also caused a hyperactive response in about half of the rats. Supersensitization to AM appeared in reserpine-treated rats (2.5 mg/kg, i.p., 48 and 24 hr before the experiment). Haloperidol (1 mg/kg; i.v.) or SCH 23390 (5 mg/kg, i.v.) completely suppressed the hyperactive bladder response induced by AM (5 mg/kg, i.v.), and then the bladder contraction accompanying micturition reappeared after administration of these drugs. Pretreatment with sulpiride (100 mg/kg, i.p.) for 60 min, which hardly affected the bladder contraction induced by infusion of Tyrode's solution, suppressed the hyperactive bladder response induced by AM. These results suggest that the hyperactive bladder response induced by i.v.-injected AM results from synchronous stimulation of the micturition reflex centers in the brain stem and sacral cord and that the hyperactive bladder response is elicited via both D1 and D2 receptors.
机译:参考文献(14)Cited-By(18)我们研究了阿扑吗啡(AM)对麻醉大鼠的膀胱运动的影响,在该大鼠中,将Tyrode's溶液以恒定速率连续注入膀胱,诱导了伴随排尿的几乎恒定的膀胱收缩速率。静脉内以1 mg / kg的剂量AM引起膀胱过度活动症,在此期间排尿消失。脑室内(i.c.v.)注射的AM(12.5μg)或鞘内(i.t.)注射的AM(12.5μg)也会在大约一半的大鼠中引起过度活跃的反应。在利血平治疗的大鼠中出现了对AM的超敏反应(2.5 mg / kg,在实验前48和24小时腹腔注射)。氟哌啶醇(1 mg / kg; iv)或SCH 23390(5 mg / kg,iv)完全抑制了AM(5 mg / kg,iv)引起的膀胱过度活动症,给药后又出现伴随排尿的膀胱收缩毒品。用舒必利(100 mg / kg,i.p.)预处理60分钟,几乎不影响输注Tyrode溶液引起的膀胱收缩,抑制了AM引起的膀胱过度活动症。这些结果表明,静脉注射AM引起的膀胱过度活动症是由同步刺激脑干和部的排尿反射中心引起的,并且膀胱过度活动症是通过D1和D2受体引起的。

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