大黄素对兔胃电的影响及其作用机制

Effect of emodin on rabbit gastric electric activity and mechanisms involved

目的:观察外周及延脑内侧网状结构注射大黄素、胃电起搏对新西兰白兔胃电的影响,探讨大黄素对胃肠运动的作用机制.方法:采用外周注射及延脑内侧网状结构(P7、P8.5、P9.5、P11)脑立体定位微量注射大黄素、电刺激胃起步点,胃浆膜双极四导联同步记录的方法,分析胃体及胃窦部胃电的平均频率、相位差、负相位比率、波形对应率、幅度等指标.结果:外周注射大黄素胃体1(P=0.031)、胃体2(P=0.047)频率减慢,胃体4(P=0.035)波形对应率降低.胃起搏可有效驱动胃电频率:胃体1(P=0.001)、胃体2(P=0.021)频率明显加快,胃体3相位差减小(P=0.037),胃体2负相位比率升高(P=0.007),胃体3(P=0.001)、胃窦(P=0.046)波形对应率降低.大黄素对于胃起搏引起的效应并无作用,但胃起搏可部分抑制大黄素引起的频率减慢.中枢不同部位微量注射大黄素的作用:P7:胃体2(P=0.026)频率明显减慢;P8.5:胃体1(P=0.045)频率明显减慢,阿托品可"翻转"大黄素引起的频率变慢效应;P9.5:胃窦(P=0.029)频率减慢;而P11:胃体1(P=0.011)频率明显加快.对照组中枢注射生理盐水,P7:胃体2的频率加快(pH8.5),其余部位胃电没有变化.结论:胃起步点起搏对胃电的驱动效应明显.外周注射大黄素对兔胃电主要起抑制作用,而中枢注射大黄素在不同的部位表现出不同的效应.

AIM：To observe the effect of emodin on rabbit gastric electric activity （GEA） by microinjecting emodin in the medial reticular formation （MRF） of the medulla oblongata （MO） and injecting emodin in external system, and to discuss the possible mechanisms responsible for the effect of emodin on gastrointestinal movement. METHODS：Rabbits were treated by intravenously injecting emodin in external system and microinjecting emodin in the MRF of MO, and giving electrical stimulation with a gastric pacemaker. Four pairs of bipolar Ag-AgCl electrodes were positioned under the serosa along the gastric greater curve to record GEA synchronously, and one pair of Pt stimulating electrodes were used for gastric pacing. The microinjection and stimulation of MRF were carried out using a brain stereo-localizer. Tested parameters included frequency （F）, phase difference （PD）, ratio of negative PD （RNPD） and corresponding rate of waves （CRW）. RESULTS：The normal frequency of GEA ranged from 3.48 to 3.77 cycles per minute （cpm） two hours after surgery, which could be driven by gastric pacing. The frequency of GEA at corpus 1 （P = 0.001） and corpus 2 （P = 0.021） and the RNPD of corpus 2 （P =0 .007） were increased, and the PD of corpus 3 （P = 0.037） and the CRW of corpus 3 （P = 0.001） and corpus 4 （P = 0.046） were decreased after pacing. Intravenous injection of emodin could decrease the frequency of corpus 1 （P = 0.031） and corpus 2 （P = 0.047） and the CRW of corpus 4 （P = 0.035）, but had no effect on gastric electrical stimulation-driven GEA. The effects of emodin could be partly reversed by gastric pacing. Microinjection of 7 μL emodin could decrease the frequency of corpus 2 in P7 （P = 0.026）, the frequency of corpus 1 in P8.5 （P = 0.045）, which could be reversed by atropine, the frequency of antrum in P9.5 （P = 0.029）, and greatly increased the frequency of corpus 1 in P11 （P = 0.011）. In the control group, microinjection of 0.9% saline in P8.5, P9.5 and P11 had no effect on the GEA, except the frequency of corpus 2 in P7, which was increased （pH 8.5）. CONCLUSION：Gastric pacing had notable ＂driven effects＂ on the GEA. The GEA could be greatly inhibited by intravenous injection of emodin. The frequency and PD of the GEA were decreased by microinjection of emodin in MRF of nuclei raphe magnus （P7-P9.5）. But in the P11, the frequency of the GEA was increased.