Gong S, Yin W P, Yin Q Z
Laboratory of Neurobiology, Suzhou Medical College.
Sheng Li Xue Bao. 1992 Oct;44(5):434-41.
It has been demonstrated in animal model of somatic pain that hypothalamic paraventricular nucleus (PVN) participates in acupuncture analgesia, probably by mediation of vasopressin release. The role of PVN in acupuncture analgesia for experimental visceral pain in rats was further investigated in the present study. Experimental results demonstrated that electroacupuncture could inhibit the writhing response, produced by intraperitoneal injection of antimonium potassium tartrate and this inhibitory effect could be enhanced by electrical stimulation of PVN, but decreased by electrolytical lesion of PVN, intracerebroventricular injection of vasopressin antiserum (14 microliters) or the vasopressin antagonist, d(CH2)5Tyr(Me)-AVP (500 ng/5 microliters). Intraperitoneal administration of the latter drug (10 micrograms/kg), however, was ineffective. The above experimental results suggest that vasopressinergic neurons in PVN also participate in the inhibition of visceral pain by electroacupuncture.
在躯体痛动物模型中已证实，下丘脑室旁核（PVN）参与针刺镇痛，可能是通过介导血管加压素释放来实现的。本研究进一步探讨了PVN在大鼠实验性内脏痛针刺镇痛中的作用。实验结果表明，电针可抑制腹腔注射酒石酸锑钾引起的扭体反应，电刺激PVN可增强这种抑制作用，而PVN电解损伤、脑室内注射血管加压素抗血清（14微升）或血管加压素拮抗剂d(CH2)5Tyr(Me)-AVP（500纳克/5微升）则可使其减弱。然而，腹腔注射后一种药物（10微克/千克）无效。上述实验结果提示，PVN中的血管加压素能神经元也参与电针对内脏痛的抑制作用。
