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    Objective To explore the neuroendocrinologic mechanism underlying the regulation effect of eletroacupuncture (EA), the mRNA and protein expression of OFQ ( Nociceptin/Orphanin FQ) and ORLl receptor ( opioid receptor-like receptor 1) in medial basal hypothalamus (MBH) was investigated following EA normalizing the abnormal release of pituitary LH (luteinizing hormone) in ovariectomized rats.
    目的 本文在去卵巢(OVX)大鼠模型上,观察下丘脑孤啡肽(Nociceptin/OrphaninFQ,OFQ)及孤儿受体(opiod receptor-like receptor 1,ORLl)是否参与电针对黄体生成素(luteinizing hormone,LH)超常释放的影响,进一步探讨电针作用的神经内分泌机制。
    Results: The releases of CCK 8 from rat striatum were significantly increased during cerebral ischemia and these abnormal releases of CCK 8 were remarkably inhibited by all three EAA antagonists which were administered before cerebral ischemia.
    结果:脑缺血时纹体CCK-8释放明显增高,缺血前分别给予三种拮抗剂,都明显地降低缺血时纹体CCK-8的不正常释放。
    100% in MODS group. Conclusions The abnormal release of the TNF-α? IL-1β?
    结论 细胞因子TNF -α、IL - 1β、IL - 6、IL - 8、IL - 10的异常释放可能参与了危重病MODS的病理过程。
    Hypothalamic Orphanin FQ Participates in Neuroendocrinologic Mechanism of Electroacupuncture Normalizing Abnormal Release of Pituitary LH in Ovariectomized Rats
    下丘脑孤啡肽参与电针调整去卵巢大鼠LH异常释放的神经内分泌机制
    Some investigators regarded that PCOS may be related to abnormal release of GnRH, hyperandrogenism, hyperinsulinemia and insulin resistance.
    一般认为,高雄激素血症、胰岛素抵抗及高胰岛素血症可能是PCOS的发病机制。
    GM1 did not influence the releases of NPY during cerebral ischemia suggesting that releases of NPY from there synaptsomes were not modulated by GM1.CR1505 was able to significantly inhibit the abnormal release of NPY during cerebral ischemia suggesting a coordinated interaction between NPY and CCK in brain ischemia.
    GM1不影响脑缺血时NPY的释放,表明含NPY的突触释放NPY时不受GM1的调节。
    Findings of this serial studies strongly suggested that the uncontrollable "mediator disease" resuIted from ischemic-reperfusion damage, swelling and edema of visceraI tissues, the endothelial cell damage and abnormal release mediators might be of importance in the pathogenesis of early PB organ damage。
    缺血和再灌流损伤、脏器水肿、内皮细胞损伤及多种炎症介质的异常释放,导致难以控制的介质病,是脏器损害的重要因素;
    The results suggested that HIE caused an abnormal release of AVP into plasma and CSF. AVP in CSF played a role in the pathophysiology of HIE.
    结果提示:HIE时,使AVP异常分泌,血浆和脑脊液中AVP升高,脑脊液中AVP可能参与了HIE的病理生理发病机制;
    Conclusion: The abnormal release of all five kinds of amino acids are involved in the pathophysiological process of cerebral ischemia. The significanly increased release of inhibitory amino acids promoted by L-NNA during global ischemia may be one of the protective mechanisms of this agent on brain ischemia. 
    结论:半球缺血时所有五种氨基酸的不正常释放都参与了脑缺血病理过程,L-NNA促进半球缺血时抑制性氨基酸的释放可能是其保护缺血大脑的机制之一。
 

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