5-HT及电刺激对胃节律紊乱模型新西兰白兔胃电活动的影响  

Effect of 5-HT and electrical stimulating on gastric electric activity in rabbits with gastric dysrhythmia

作　　者：黄伟锋[1] 张慧[1] 欧阳守[1] 卢春敬 

机构地区：[1]厦门市医药研究所生理室,福建省厦门市361008 [2]厦门市妇幼保健院输血科,福建省厦门市361003

出　　处：《世界华人消化杂志》2011年第23期2486-2491,共6页World Chinese Journal of Digestology

基　　金：福建省科技厅重点基金资助项目;No.2009D026;福建省卫生厅青年科研课题基金资助项目;No.2009-2-89;No.2010-2-112~~

摘　　要：目的:观察5-HT及电刺激对胃节律紊乱模型新西兰白兔胃电活动的影响.方法:对以胰高血糖素造模的新西兰白兔胃节律紊乱模型采用外周注射5-HT、胃起步点起搏,电刺激室旁核和中缝大核(P7)的方法,四导胃浆膜电信号同步记录,分析胃体、及胃窦部胃电信号的平均频率,相位差,负相位比率,波形对应率,幅度等指标,考察5-HT及电刺激对胃节律紊乱模型新西兰白兔胃电活动的影响.结果:(1)胰高血糖素外周注射,胃体2频率加快(4.29±0.60→4.56±0.59,P=0.05),胃窦频率减慢(4.54±0.51→4.27±0.44,P=0.013),胃节律紊乱模型建立成功;(2)胃节律紊乱模型外周注射500μg5-HT后频率均加快(胃体1:4.06±0.45→4.25±0.37,P=0.031;胃体3:4.32±0.51→4.58±0.36,P=0.041;胃窦:4.54±0.47→4.73±0.44,P=0.017),波形对应率变好(胃体3:0.78±0.13→0.83±0.10,P=0.030);(3)胃节律紊乱模型胃起搏后频率均加快,胃体3(4.27±0.53→4.52±0.47,P=0.022);(4)胃节律紊乱模型室旁核电刺激能进一步减慢频率,胃体3(4.47±0.44→4.14±0.46,P=0.046)、胃窦(4.05±0.54→3.69±0.55,P=0.039)差异显著,胃窦负相位比率升高(0.32±0.19→0.40±0.19,P=0.046).单纯室旁核电刺激抑制胃电,进一步证实中枢存在"下行性抑制系统";(5)胃节律紊乱模型P7电刺激后胃窦频率减慢(4.31±0.44→3.86±0.47,P=0.012).结论:外周注射胰高血糖素后,胃节律紊乱模型建立成功.外周注射5-HT500μg或胃起步点起搏后节律趋向正常,浆膜胃电波形转好;室旁核和P7电刺激则进一步减慢胃电频率,可能是下行性抑制系统在发挥作用.AIM： To evaluate the effect of 5-hydroxytryptamine （5-HT） and electrical stimulation on gastric electric activity （GEA） in rabbits with gastric dysrhythmia （GD）. METHODS： GD was induced in rabbits by peripheral injection of glucagon. Peripheral injection of 5-HT, gastric pacemaking, and electrical stimulation of the paraventricular nucleus （PVN） and raphe magnus （RM, P7） were performed in GD rabbits. Four pairs of bipolar Ag-AgCl electrodes implanted on the serosa along the gastric greater curve were used for recording GEA. The stimulation of PVN and RM was carried out using brain stereotaxis apparatus （SN-2）. The analyzed parameters included frequency （F）, phase difference （PD）, ratio of negative PD （RNPD） and corresponding rate of waves （CRW）. RESULTS： The F of GEA in the gastric corpus 2 increased （from 4.29 ± 0.60 to 4.56 ± 0.59, P = 0.05） and that in the gastric antrum decreased （from 4.54 ± 0.51 to 4.27 ± 0.44, P = 0.013） in GD rabbits. Injection of 500 μg 5-HT accelerated the F of GEA in the gastric corpus 1 （from 4.06 ± 0.45 to 4.25 ± 0.37, P = 0.031）, corpus 3 （from 4.32 ± 0.51 to 4.58 ± 0.36, P = 0.041） and gastric antrum （from 4.54 ± 0.47 to 4.73 ± 0.44, P = 0.017） and im- proved the CRW in the gastric corpus 3 （from 0.78 ± 0.13 to 0.83 ± 0.10, P = 0.030） in GD rabbits. The F of GEA in the gastric corpus 3 was （from 4.27 ± 0.53 to 4.52 ± 0.47, P = 0.022） increased by gastric pacing. Electrical stimulation of PVN decreased the F of GEA in the gastric corpus 3 （from 4.47 ± 0.44 to 4.14 ± 0.46, P = 0.046） and gastric antrum （from 4.05 ± 0.54 to 3.69 ± 0.55, n = 12, P = 0.039）, increased the RNPD in the gastric antrum （from 0.32 ± 0.19 to 0.40 ± 0.19, P = 0.046）, and greatly inhibited GEA in GD rabbits. Electrical stimulation of P7 slowed the F of GEA in the gastric antrum （from 4.31 ± 0.44 to 3.86 ± 0.47, P = 0.012） in GD rabbits. CONCLUSION： A rabbit model of GD has been successfully develop

关 键 词：胃节律紊乱 五羟色胺 电刺激 浆膜胃电 活动 新西兰白兔 

分 类 号：R573[医药卫生—消化系统]