| ObjectiveThis study is based on the the innervation of gastric motility.Taking Zhongwan(CV12),Tianshu(ST25),Neiguan(PC6),Zusanli(ST36)as examples,taking gastric movement as an observation index,using vagus/visceral nerve resection,gene knockout technology(M2M3 receptor knock and β1β2 receptor knockout),DMV nucleus injection of L-glutamic acid(L-Glu)and GABA,the effects of different acupoints on gastric motility and its possible neurobiological mechanisms were explored to provide a scientific basis for clinical application.Methods(1)Thirty-six healthy adult SPF Sprague-Dawley(SD)male rats were randomly divided into normal group,vagus nerve resection group and visceral large nerve resection group,with 12 rats in each group.The balloon catheter was placed in the antrum of the animal through the duodenal incision,and the intra-arterial pressure was recorded by connecting the baroreceptor and the multi-conducting physiological recording system.The appropriate amount of warm water was injected into the balloon through the syringe to maintain the balloon pressure at about 0.8 Kp.The effects of electroacupunctxure(EA)at CV12,ST25,PC6 and ST36(2/15 Hz,3 mA,2 min)on gastric motility in rats were observed during different course of EA.(2)A total of 30 SPF mice,included wild-type mice(C57BL/6,n=10),M2&3 receptor knockout mice(M2&3_-,,n=10),and P1&2 receptor knockout mice((β1&2-/-,n=10).The experimental procedure of intragastric pressure recording was the same as that of the rats.The balloon pressure was maintained at about 0.4 Kp.The effects of EA at CV12,and left ST36(2/15 Hz,2 mA,1 min)on gastric motility in mice were observed during different course of EA.(3)Thirty-six healthy male SPF rats were randomly divided into artificial cerebrospinal fluid injection group,L-Glu injection group and GABA injection group,with 12 rats in each group.Surgical suture was performed by embedding a stainless steel catheter in the DMV nucleus.Five-days of recovery after the operation,a balloon was placed in the antrum of the stomach to record the intragastric pressure(the balloon pressure was maintained at about 0.8 Kp),and the artificial cerebrospinal fluid was injected into the DMV(0.2 μ1),L-glutamic acid(0.1 mol/L,0.2 μl)or GABA(0.1 mol/L,0.2 μl).The effects of EA at CV12,ST25,PC6 and ST36(2/15 Hz,3 mA,2 min)on gastric motility in rats were observed during different course of EA.Results1.For normal rats,the EA at the acupoints CV12 and ST25 located at the abdomen had an inhibitory effect on the gastric motility,while the acupoints of PC6 and ST36 located at limb had an excitatory effect.The responsing time of different acupoints toward gastric pressure was different:the abdominal acupoints could be effective within 30s,with a shorter responsing time,while the acupoints of the extremities were effective after 30s,with a longer responsing time,and the difference between left and right acupoints had no statistical significant.After vagus nerve resection,CV12 and ST25 still showed significant inhibitory effects on gastric motility;the excitatory effects of ST36 and PC6 on gastric motility disappeared.After the left visceral major nerve resection,the effect of the right ST25 and CV12 points on gastric motility inhibition was reduced,and the left Tianshu point was ineffective;ST36 and PC6 points still showed excitatory effects,but performing an fast acting characteristics.These results suggest that EA at CV12 and ST25 located at abdomen,which have a fast onset toward gastric motility,can inhibit gastric motility through sympathetic nerve;EA at ST36 and PC5 located at the extremities,which have longer responsing time,can promote gastric motility through vagus nerve.Sympathetic nerves may be one of the key factor for the delayed onset of ST36.2.In C57BL/6 mice,EA at CV12 showed an immediate inhibitory effect and a fast onset on the gastric motility,while ST36 showed an excitatory effect after 30 s.In fp 1&2-/-mice,the effect of CV12 on gastric motility regulation was significantly reduced,but there was still some inhibitory effect,suggesting that in addition to β1 β2 receptor,other receptor mechanisms for CV12 regulation of gastric motility may exist.The excitatory effects of ST36 on gastric motility showed rapid onset of action,suggesting that β1 and β2 receptors may be one of the receptor mechanisms for ST36 to regulate the delayed onset of gastric motility.In M2&3-/-mice,the inhibitory effect of CV12 on gastric motility was significantly reduced showing a slight inhibition or ineffectiveness,suggesting that M receptor may play a more important role in CV12 regullating gastric motility comparing beta receptor.ST36 showed an inhibitory effect in M2&3-/-mice,indicating that there may be other receptors in the efferent pathway of ST36 regulating gastric motility.3.DMV injection of glutamate had an effect excitatory toward gastrnc motility.Injection of GABA showed both types of inhibition and exhilaration.After DMV injection of glutamate and y-aminobutyric acid,the effects of EA at CV12 and ST25 on gastric motility in rats were still inhibited,while the effect of ST36 on intragastric pressure was reduced during 30～120 s and after-EA.After injection of glutamate in DMV,the right side PC6 showed an increase during 0-30s,the difference between the ST36-right and PC-right was statistically significant.Conclusion1.The response time of regulating gastric motility differs according the location of acupoints.The response time of abdominal acupoints is short while the acupoints in the extremities is long.The inhibition of sympathetic nerve may be one of the key factor to the long response time of acupoints in extremities,with the receptor mechanism is relating with 01 and 32 receptors.2.The vagus-CNS circuit of the upper limbs acupoints and the lower limbs acupoints regulating gastric motility is not completely consistent.The DMV vagals-vagal reflex may be an important neural pathway for ST36 to regulate gastric motility. |
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