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大鼠中胆囊收缩素与阿片类物质在调节直肠结肠抑制性反射中的相互作用。

Interaction between CCK and opioids in the modulation of the rectocolonic inhibitory reflex in rats.

作者信息

Gué M, del Rio C, Junien J L, Buéno L

机构信息

Department of Pharmacology, Institute National de la Recherche Agronomique, Toulouse, France.

出版信息

Am J Physiol. 1995 Aug;269(2 Pt 1):G240-5. doi: 10.1152/ajpgi.1995.269.2.G240.

Abstract

The effects of cholecystokinin octapeptide (CCK-8) as well as the involvement of opioid system were evaluated in rectal distension (RD)-induced colonic motor inhibition in rats. Rats were surgically prepared with electrodes implanted on the proximal colon, and a catheter was implanted in lateral ventricle of the brain. RD was performed by inflation (0.0-1.6 ml) of a balloon rectally inserted. RD 1.6 ml of induced an inhibition of the colonic spike bursts (3.1 +/- 0.5 per 5 min vs. 8.1 +/- 0.4 before RD). Intracerebroventricular but not intravenous injection of CCK-8 and A-71623 (50 and 100 ng/kg) reduced the RD-induced colonic motor inhibition, whereas A-63387 was ineffective. PD-135,158 (10 micrograms/kg icv) suppressed the inhibitory reflex caused by RD. Devazepide (100 micrograms/kg icv) had no effect in this reflex function. Devazepide (1 microgram/kg), naloxone (0.1 mg/kg), and nor-binaltorphimine (nor-BNI; 10 mg/kg) reversed the blocking effect of CCK-8, whereas PD-135,158 (0.1 microgram/kg) and naltrindole (1 mg/kg) have no effect. In conclusion, CCK-8 acts on central alimentary cholecystokinin receptors to modulate the RD-induced inhibition of colonic motility through pathways involving activation of endogenous kappa-receptors.

摘要

评估了八肽胆囊收缩素(CCK - 8)的作用以及阿片样物质系统在大鼠直肠扩张(RD)诱导的结肠运动抑制中的参与情况。通过手术在大鼠近端结肠植入电极,并在脑侧脑室植入导管。通过向直肠插入的球囊充气(0.0 - 1.6 ml)来进行直肠扩张。1.6 ml的直肠扩张诱导了结肠峰电位爆发的抑制(每5分钟3.1±0.5次,而直肠扩张前为8.1±0.4次)。脑室内而非静脉注射CCK - 8和A - 71623(50和100 ng/kg)可减轻直肠扩张诱导的结肠运动抑制,而A - 63387无效。PD - 135,158(10微克/千克,脑室内注射)抑制了直肠扩张引起的抑制性反射。地伐西匹(100微克/千克,脑室内注射)对该反射功能无影响。地伐西匹(1微克/千克)、纳洛酮(0.1毫克/千克)和去甲双丙戊酰胺(nor - BNI;10毫克/千克)可逆转CCK - 8的阻断作用,而PD - 135,158(0.1微克/千克)和纳曲吲哚(1毫克/千克)则无作用。总之,CCK - 8作用于中枢消化胆囊收缩素受体,通过涉及内源性κ受体激活的途径来调节直肠扩张诱导的结肠运动抑制。

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