Gué M, del Rio C, Junien J L, Buéno L
Department of Pharmacology, Institute National de la Recherche Agronomique, Toulouse, France.
Am J Physiol. 1995 Aug;269(2 Pt 1):G240-5. doi: 10.1152/ajpgi.1995.269.2.G240.
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.
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。