不同迷走神经阻滞方法的大鼠模型对外源性CCK诱导的胰腺外分泌的影响

The effects of different rat models of vagal afferent pathway blockade on the exogenous CCK-induced pancreatic protein secretion

目的探讨不同迷走神经阻滞方法的大鼠模型对外源性胆囊收缩素(CCK)诱导的胰腺外分泌的影响。方法利用成年SD大鼠构建急性迷走神经切除和慢性迷走神经辣椒素阻滞的动物模型,比较不同剂量外源性CCK诱导下的胰腺外分泌的状况,根据结果评价动物模型的作用和效果。结果急性迷走神经切除可以阻断生理剂量CCK(40 pmol.kg-1.h-1)诱发的胰蛋白分泌74.8%,可以抑制超生理剂量CCK(80 pmol.kg-1.h-1)诱发的胰蛋白分泌61.4%。慢性迷走神经辣椒素阻滞并不能抑制生理剂量CCK所诱发的胰蛋白分泌,而超生理剂量CCK所诱发的胰蛋白分泌不仅不能被抑制,相反还有升高的趋势。结论 2种模型均不能完全阻滞生理剂量CCK诱发的胰蛋白分泌。由于器官功能的代偿,慢性迷走神经辣椒素阻滞的动物模型不适用于胰蛋白分泌机制神经调节的评估。

Objective To investigate the effects of exogenous cholecystokinin（CCK） on pancreatic protein secretion in different rat modes of vagal afferent pathway blockade.Methods The animal models of acute vagotomy and chronic vagal blockade with capsaicin were established using adult male SD rats.The actions and effects of different doses of exogenous CCK on pancreatic protein secretion were compared in the rats.Results The pancreatic protein output induced by CCK at a physiological dose（40 pmol·kg-1·h-1） was blocked by 74.8% and 61.4% of the output induced by dose CCK at a supraphysiological dose（80 pmol·kg-1·h-1） was inhibited in acute vagotomy model.In contrast,chronic vagal blockade with capsaicin could not inhibit the pancreatic protein secretion induced by a physiologic dose of CCK,while the pancreatic protein secretion induced by CCK at a supraphysiologic dose CCK could not be inhibited but increased,compared with the control rats.Conclusion Neither a physiologic nor a supraphysiological dose of CCK could completely block the pancreatic protein secretion.Due to functional compensation,the animal model of chronic vagal blockade with capsaicin is not applicable in the evaluation of the mechanisms by which CCK mediates pancreatic protein secretion via the vagal afferent pathway.