室旁核及其加压素能系统对大鼠胃缺血再灌注损伤的调控

The effects of paraventricular nucleus (PVN) stimulation and vasopressin on gastric ischemia-reperfusion injury (GI-RI) were investigated in male SD rats of which the celiac artery was clamped for 30 min and reperfused for 1h by removal of the clamp. we used electrical stimulation,eletrolytic lesion of the PVN and intranuclear microinjection, eletron microscopic , Fos immun-histochemical method.The gastric juice volume, acidity, total acid output, gastric barrier mucus, pepsin activity, MDA contents and SOD activity were measured to analyse the role of PVN in GI-RI, meanwhile by using vagotomy, sympathectomy, injection of antagonist and a high dose of capsaicin to ablate the capsaicin-sensitive afferent neurons , we studied the role of peripheral nerves in PVN regulating GI-RI.The results were as follows:.(1) Electric stimulation of the PVN and L-glutamic acid microinjection into PVN decreased the GI-RI, These results indicate that the PVN is an important brain site regulating the development of GI-RI..(2) Gastric mucosal MDA contents, gastric pepsin acitivity, acidity are involved in the protection of PVN stimulation on GI-RI. The gastric juice volume, total acid output, gastric barrier mucus have no effect in the protection of PVN stimulation on I-RI..(3) Parasympathetic, sympathetic nervous systems, capsaicin-sensitive afferent neurons and NO take part in the protection of PVN stimulation on GI-RI ..(4) Bilateral electrolytic lesion of the NTS or microinjection of AVP-V1 receptor antagonist into the NTS could eliminate the protective effect of electrical stimulation of the PVN on GI-RI. .(5) Microinjection of arginine-vasopressin (AVP) into the PVN also attenuated the effect on GI-RI.Hypophysectomy did not influence the effect of electrical stimulation of the PVN. This effect might be mediated by the activation of VP-ergic neurons in PVN and influenced the activities of neurons in the NTS while PVN-neural hypophysis pathway might not involved in the protection of PVN stimulation on GI-RI..(6) Using Fos immunohistochemical method （ABC method）examined the c-fos expression within PVN and NTS. The Fos-like immunoreactive neurons were present bilaterally PVN and NTS..Both electrical and chemical stimulation of the PVN could obviously attenuate the GI-RI. Bilateral electrolytic lesion of the NTS or microinjection of AVP-V1 receptor antagonist into the NTS could eliminate the protective effect of electrical stimulation of the PVN on GI-RI. Hypophysectomy did not influence the effect of electrical stimulation of the PVN. Both vagotomy or sympathectomy could increase the effect of stimulating PVN on GI-RI. Microinjection of arginine-vasopressin (AVP) into the PVN also attenuated the effect on GI-RI. These results suggest that the PVN and AVP participate in the regulation of GI-RI and play an important role in the protection on the GI-RI. This protective effect of PVN on GI-RI might be mediated by the activation of AVP-ergic neurons in the PVN, which release AVP from the descending projection fibers and activate the AVP-V1 receptors on the NTS neurons. The vagus and sympathetic nerves are involved in the efferent pathway and then effecting the GI-RI. Hypophysis does not seem to play an important role in the protective effect of PVN stimulation. .Key words： paraventricular nucleus (PVN); gastric ischemia-reperfusion injury (GI-RI) ;

运用在体核团刺激、损毁、微量注射和免疫组织化学、放免测定、生化、电镜技术等手段，探讨下丘脑室旁核及其加压素能神经元系统对大鼠胃缺血--再灌注损伤的外周及中枢调控机理，为研究其损伤的机理及临床防治提供新的理论、实验依据和研究途径，从而进一步拓宽对多脏器缺血再灌注损伤的认识。