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作 者:杨永录[1] 汪云利[1] 赖雁[1] 惠锦[2] 李欣[1] 陈小华[1]
机构地区:[1]成都医学院基础医学院,四川成都610081 [2]解放军第一医院,甘肃兰州730030
出 处:《中国应用生理学杂志》2008年第1期19-23,共5页Chinese Journal of Applied Physiology
基 金:四川省教育厅重点项目(2005A192)
摘 要:目的:观察梭曼对大鼠应激性体温过高的抑制作用以及中枢和外周胆碱能受体阻断剂对其效应的影响。方法:用无线遥测技术测量大鼠的体温,观察皮下注射梭曼、东莨菪碱、甲基东莨菪碱和吡啶斯的明对开放环境中大鼠应激性体温过高的影响。用分光光度技术测定血浆中胆碱酯酶活性。结果:①对照组大鼠在开放实验箱中体温升高达0.96℃,而注射梭曼动物体温只升高了0.55℃。中枢性胆碱能受体阻断剂东莨菪碱几乎完全阻断梭曼对应激体温过高的抑制作用,而外周胆碱能受体阻断剂甲基东莨菪碱则能明显增强梭曼对应激性体温过高的抑制作用。②外周抗胆碱酯酶剂吡啶斯的明能使血浆胆碱酯酶的活性降低至52%,同时明显提高开放环境中大鼠应激性体温过高的反应。甲基东莨菪碱几乎可以阻断吡啶斯的明对应激体温过高反应的影响。结论:神经毒剂梭曼可改变大鼠在开放环境中应激性体温过高的反应能力,其作用主要是通过中枢毒蕈碱型胆碱能通路所致。此外,外周胆碱能神经参与大鼠开放应激性体温过高的形成过程。Aim: To determine the effect of soman on stress induced hyperthermia and the influence of central and peripheral cholinergic antagonists.Methods: Effects of subcutaneous injection of soman, scopolamine, methylscopolamine and pyridostigmine on stress-induced hyperthermia were observed in rats by radio telemetry in an open-field environment. Plasma cholinesterase (ChE) activity was measured by a spectrophotometry.Results: (1)Core temperature of the control group increased by 0.96℃ when exposed to open-field, whereas core temperature only increased by 0.55℃ in soman treated animals. Scopolamine, a central cholinergic antagonist, nearly abolished inhibitory effects of soman on core temperature when exposed to open-fidd. Methylscopolamine,a peripheral cholinergic antagonist, coadministered with soman reduced significantly the hyperthermic response to open-fidd exposure compared with rats dosed with soman. (2)Pyridostigmine, a peripheral anti-ChE agent that caused a 52 % decrease in plasma ChE activity led to a significant enhancement of the hyperthermic response to open-field exposure. Methyl scopolamine nearly abolished the effects of pyridostigmine on stress-induced hyperthermia response. Conclusion: Inhibitory effect of soman on the open fidd hyperthermia suggesed that soman treatment hampered the ability of the rat to develop a normal hyperthermic response when placed in the open-field environment. Its inhibitory effects were mediated primarily through a central muscarinic pathway. In addition, peripheral cholinergic nerve was involved in the control of stress hyperthermic response.
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