Sillén U, Persson B, Rubenson A
Naunyn Schmiedebergs Arch Pharmacol. 1985 Sep;330(3):175-8. doi: 10.1007/BF00572430.
Cystometric recordings were performed in pentobarbitone anaesthetized rats and the effects of baclofen on urinary bladder function were evaluated as their influence on bladder hyperactivity induced by 1-dihydroxyphenylalanine (L-dopa) after peripheral decarboxylase inhibition. The bladder response was inhibited by intracerebroventricularly (i.c.v., 4th ventricle, 0.1 microgram) as well as by systemically administered (10 mg/kg i.v.) baclofen. Intravenous naloxone but not i.v. bicuculline i.c.v. substance P or i.c.v. glutamate antagonized the inhibitory actions of i.c.v. or/and i.v. baclofen. It is suggested that baclofen depresses the hyperactive bladder by a central action that is unrelated to bicuculline sensitive gamma aminobutyric acid mechanisms, substance P or glutamate neurotransmission but that is possibly related to interference with opioid mechanisms.
在戊巴比妥麻醉的大鼠中进行膀胱压力测定记录,并评估巴氯芬对膀胱功能的影响,即其对在外周脱羧酶抑制后由1-二羟基苯丙氨酸(L-多巴)诱导的膀胱活动亢进的影响。脑室内(第四脑室,0.1微克)以及全身给药(静脉注射10毫克/千克)巴氯芬均可抑制膀胱反应。静脉注射纳洛酮而非静脉注射荷包牡丹碱、脑室内注射P物质或脑室内注射谷氨酸可拮抗脑室内或/和静脉注射巴氯芬的抑制作用。提示巴氯芬通过一种与荷包牡丹碱敏感的γ-氨基丁酸机制、P物质或谷氨酸神经传递无关,但可能与干扰阿片类机制有关的中枢作用来抑制活动亢进的膀胱。