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出 处:《中华消化杂志》2011年第3期178-181,共4页Chinese Journal of Digestion
基 金:国家自然科学基金资助项目(30871148)
摘 要:目的 通过记录胆囊收缩素(CCK)对近端结肠平滑肌条和平滑肌细胞膜离子通道电流的影响,研究其对结肠动力的影响及其在肠易激综合征(IBS)发病中可能存在的病理机制.方法 成年豚鼠(200~250 g)实验前禁食12 h,不禁水.处死动物取近端结肠约6 cm,记录离体近端结肠肌条在浓度为1×10-7、5×10-7、1×10-6mol/L的胆囊收缩素八肽(CCK-8)作用下的张力和收缩频率变化;用EPC-10膜片钳和图像分析软件系统检测1×10-7、5×10-7、1×10-6 mol/L CCK-8及经尼非地平预处理的1×10-6mol/L CCK-8对近端结肠平滑肌细胞钙依赖钾通道电流(1BKca)的影响.结果 结肠平滑肌肌条实验中,分别加入1×10-7、5×10-7、1×10-6mol/L CCK-8后正常的收缩活动明显增强,与加药前[(0.68±0.12)g]相比,收缩幅度分别增加(15.0±1.5)%、(28.0±1.4)%和(36.0±1.6)%(n=7,P值分别=0.023、0.005和0.001),但频率变化不明显.膜片钳实验中,当越阶刺激为+60 mV时加入1×10-7、5×10-7、1×10-6mol/LCCK-8,此时IBKCa电流分别为对照组的(117.45±3.60)%、(125.42±5.30)%和(136.98±6.80)%(n=7,P值均<0.01).预先加入尼非地平后,1×10-6mol/L CCK-8组+60 mV时IBKca为对照组的(102.23±5.60)%(n=7,P=1.491).结论 CCK通过促进Ca2+内流,增加Ibkca,进而增强结肠平滑肌的运动,主要表现为收缩幅度的加快.Objective To investigate the effect of cholecystokinin (CCK) on colon motility and its mechanism in development of irritable bowel syndrome via recording ionic channels currents and contraction of guinea-pig proximal colon. Methods The guinea-pigs (body weight ranged from 200 g to 250 g) were deprived of food, but not water, for 12 hours before experiment. The animal was sacrificed and 6 cm of proximal colon was obtained. The contractile activity of isolated proximal colon in 1 × 10-7 ,5 × 10-7 or 1 × 10-6 mol/L of CCK-8 solution was recorded. The impact of 1 × 10-7 , 5 × 10-7 and 1 × 10-6 mol/L of CCK-8 and 1 × 10-6 mol/L CCK-8 nifidipin on current of calcium activated potassium channel (IBKac) was detected with an EPC-10 amplifier and an image analysis software.Results In comparison with blank [(0. 68 ±0. 12) g], the amplitude of colon contraction in 1 × 10-7 ,5×10-7 and 1×10-6 mol/L of CCK-8 was increased by (15. 0±1.5)%,(28. 0±1.4)%, and (36.0±1.6) %, respectively ( n = 7, P = 0. 023,0. 005 and 0. 01 ), but there was no significant change of frequency. When exogenous stimulation at +60 mV, the current of IBKac was enhanced to (117. 45 ± 3.60)%, (125.42± 5. 30)% or (136. 98±6. 80)% in 10-7 ,5 × 10-7 or 10-6 mol/L of CCK-8,respectively, compared with controls (n= 7, P<0.01 ). However, after adding nifidipin, the current of IBKca was reduced to (102.23±5.60)% in 10-6mol/L of CCK-8 at +60 mV when compared with controls (n=7, P= 1. 491 ). Conclusion CCK enhances proximal colonic motility by increasing Ca2+ influx and IBKac current, which is characterized by enhancement of amplitude of contraction.
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