Fujimura M
Nihon Geka Hokan. 1989 Sep 1;58(5):405-13.
Effects of neurotensin (NT) on gallbladder contraction were examined both in vivo and in vitro. Cholecystokinin-octapeptide (CCK-8) was used to evaluate the methods used in this study and to compare the action of NT on the gallbladder. In In vivo studies, gallbladder contraction was monitored by strain-gauge force transducers implanted on the surface of the dog gallbladder. Bolus intravenous (IV) injection of NT at doses of 20 and 40 ng/kg caused gallbladder contraction of similar of magnitudes in terms of contractile force, while CCK-8 caused contraction dose-dependently. Continuous IV infusion of NT at doses of 250 and 500 ng/kg/hr, which resulted in an elevation of blood levels of NT comparable with those achieved by endogenous release, induced a transient gallbladder contraction. Both maximum contractile force and onset time of contraction were similar to both does of NT. In contrast, CCK-8 induced gallbladder contraction was sustained during infusion of CCK-8 and was dose-dependent for both maximum contractile force and onset time of contraction. NT-induced gallbladder contraction was completely abolished by atropine treatment. In In vitro studies of longitudinal rabbit gallbladder muscle strips, NT was ineffective, while CCK-8 caused a dose-dependent contraction. The present study shows that NT can stimulate gallbladder contraction in the dog via cholinergic pathways.
在体内和体外研究了神经降压素（NT）对胆囊收缩的影响。使用胆囊收缩素八肽（CCK-8）来评估本研究中使用的方法，并比较NT对胆囊的作用。在体内研究中，通过植入狗胆囊表面的应变片力传感器监测胆囊收缩。静脉推注剂量为20和40 ng/kg的NT引起的胆囊收缩在收缩力方面幅度相似，而CCK-8引起的收缩呈剂量依赖性。以250和500 ng/kg/hr的剂量持续静脉输注NT，导致血液中NT水平升高至与内源性释放所达到的水平相当，引起短暂的胆囊收缩。最大收缩力和收缩起始时间在两种NT剂量下均相似。相比之下，CCK-8诱导的胆囊收缩在输注CCK-8期间持续存在，并且在最大收缩力和收缩起始时间方面均呈剂量依赖性。阿托品处理可完全消除NT诱导的胆囊收缩。在兔胆囊纵行肌条的体外研究中，NT无效，而CCK-8引起剂量依赖性收缩。本研究表明，NT可通过胆碱能途径刺激狗的胆囊收缩。
