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Acupuncture analgesia (AA) caused by low frequency stimulation of the acupuncture point (AP) was abolished by hypophysectomy and adrenalectomy. Termination of the AA producing pathway from the AP to the pituitary gland was in the medial hypothalamic arcuate nucleus (M-HARN). The origin of the descending pain inhibitory system associated with AA was in the posterior HARN (P-HARN). AA in the hypophysectomized rats, and enhanced neuronal activity in the P-HARN that were abolished during acupuncture stimulation, were both restored by intraperitoneal microinjection of 0.5 mg/kg morphine or 0.1 micrograms beta-endorphin into the P-HARN during acupuncture stimulation. Of the analgesia produced by dopamine or beta-endorphin injected into the P-HARN, that caused by beta-endorphin disappeared after denervation of the M-HARN. The P-HARN neurons that responded to acupuncture stimulation also responded to iontophoretic dopamine, but not to iontophoretic morphine nor ultramicroinjected beta-endorphin. The transmission between the M-HARN and P-HARN may be dopaminergic, and beta-endorphin might presynaptically modulate this transmission. Reduction of sodium ions may have been the reason for abolition of AA after adrenalectomy.  相似文献   
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(张明敏)(刘沛霖)(叶望云)EffectofTripterygiumVilfordiionAdrenalCortexinRatwithAdjuvantArthritis¥ZHANGMing-min;LIUPei-lin;YEWang-yun(Tongji...  相似文献   
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The peptide melittin, the main constituent of bee venom is a potent stimulus for the generation of an eosinophil chemotactic factor (ECF) from human polymorphonuclear neutrophils, rat mast cells and rat peritoneal cells depleted in mast cells. Optimal EFC induction required a sublytic activation of the cells. With each cell type the kinetics of ECF generation were similar in that after an early rise in activity a steep fall off occurred at later times of incubation suggesting a mechanism of inactivation. The induction of ECF by melittin is increased in the presence of calcium. The polar portion of the melittin molecule (aminoacids 20–26) is responsible for the generation of the chemotactic activity. Other peptides of honey bee venom such as the mast cell degranulating peptide (MCD) or apamine do not initiate ECF release. It appears that melittin leads to ECF induction via the phospholipase A2-arachidonic acid dependent pathway of cell activation. Our data suggests that the lipid mediator ECF can be obtained from phagocytes and mast cells thus indicating the interdependence of inflammatory reactions.  相似文献   
5.
White male rabbits, weighing about 3 kg, were injected intravenously with 5 ml of 0.1% saponin solution dissolved in physiological saline once a week for six months. The sequential histological changes in the kidneys were observed by repeated biopsies and, in addition, the animals were subjected to necropsy for light and electron microscopic examinations. Amyloid protein was purified from the animal tissues, estimated at approximately 6,300 daltons in molecular weight by SDS-PAGE and considered as an AA type protein based on its amino acid sequence study. The antibody against the purified amyloid protein was produced in guinea pigs and was used for immunohistochemical studies. The deposition of amyloid started initially in mesangial matrices and subendothelial regions of the glomeruli, but at the end the spleen, kidney and bowels were found to be frequent sites of deposition. The amyloid deposited in the tissues was specifically positive by the indirect immunohistochemistry using the prepared antibody. This antibody also reacted positively to human materials with secondary amyloidosis. These results indicate that amyloidosis induced by saponin is a good model of secondary amyloidosis.  相似文献   
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Kidney biopsies from one patient with primary (AL) and three with secondary (AA) amyloidosis were used for an ultrastructural study of the collocalization of basement membrane proteins and the extracellular matrix protein fibronectin within amyloid deposits. Antibodies against amyloid P component, laminin, and heparan sulphate proteoglycan core protein all reacted with the basement membranes and the amyloid depositions in AA and AL amyloidosis. Monoclonal and polyclonal antibodies against collagen type IV reacted only with the basement membranes. Anti-fibronectin reaction was found in association with the basement membranes in all four cases, while labelling of amyloid depositions was found only in one of the AA amyloid cases and in the AL amyloid depositions. It is concluded that basement membrane components may be of importance for the formation of amyloid fibrils.  相似文献   
8.
The outcome of antidepressant drug treatment was measured in 200 patients, 145 seen in psychiatric out-patient clinics and 55 in general practice, after 4 weeks of therapy. The results of the 200 patients taken together suggested that prognosis was largely determined by factors dependent on the natural history of the disorder and that clinical symptoms were unimportant, but when the results for patients in each drug group were analysed separately symptoms were more important than natural history factors. We conclude that clinical symptoms are only important predictors of response to antidepressant drugs when the patients studied are homogeneous with regard to natural history factors, particularly duration of illness.  相似文献   
9.
目的 研究右酮洛芬氨丁三醇 (D KPT)对佐剂性关节炎大鼠的治疗作用及胃肠道损伤作用。方法 采用大鼠佐剂性关节炎模型 ,观察D KPT对佐剂性关节炎大鼠原发和继发性症状的作用以及对前列腺素E2 和胃、十二指肠的影响。结果 D KPT(2 5、5、10mg·kg-1)不仅能抑制佐剂性关节炎大鼠的原发性炎症 ,而且对继发性炎症和多发性关节炎有抑制作用。D KPT(10 -8、10 -7、10 -6 、10 -5、10 -4 mol·L-1)体外对佐剂性关节炎大鼠腹腔巨噬细胞产生过高的PGE2 有抑制作用。D KPT(10mg·kg-1)对胃、十二指肠黏膜有损伤作用 ,但损伤程度小于酮洛芬 (KP) (10mg·kg-1)。结论 D KPT对佐剂性关节炎大鼠有治疗作用 ,同时对胃、十二指肠损伤小于KP。  相似文献   
10.
目的对脑血通颗粒剂进行定性定量分析。方法采用茚三酮、蒽醌定性反应和大黄素、补骨脂素、异补骨脂素薄层色谱鉴别进行定性控制;对补骨脂素、异补骨脂素应用高效液相色谱法定量测定;运用等离子发射光谱仪、氨基酸自动分析仪进行无机元素和氨基酸的测定。结果定性鉴别简便易行;含量测定方法中同分异构体补骨脂素、异补骨脂素分离较好,分离度大于2,补骨脂素、异补骨脂素柱效比较理想,理论塔板数均大于4000。结论此法分离效果好、重现性好、精密度高;元素分析和氨基酸分析结果可信度高,可用于脑血通颗粒剂的质量控制。  相似文献   
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