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机构地区:[1]浙江大学医学院附属第二医院临床药学室,杭州310009 [2]浙江大学生物医学工程教育部重点实验室,杭州310027
出 处:《中国药学杂志》2007年第23期1786-1789,共4页Chinese Pharmaceutical Journal
摘 要:目的在海马脑片水平观察左旋四氢巴马汀(L-tetrahydropalmatine,L-THP)对脑组织缺氧后及恢复给氧早期突触功能的影响。方法大鼠离体海马脑片以人工脑脊液孵育,观察缺氧后海马CA1区诱发群峰电位(population spike,PS)开始减小的时间和消失时间,缺氧损伤电位(hypoxic injury potential,HIP)出现时间、出现率和保持时间,复氧后PS的恢复率和恢复程度等指标并观察L-THP对这些指标的影响。结果L-THP(0.028,0.14,0.28 mmol.L-1)组脑片PS减小时间、消失时间与缺氧组相比后延,并有显著差异(P<0.05),但其作用强度随剂量递减。缺氧组脑片平均在658.8 s出现HIP,L-THP 0.028 mmol.L-1组,0.14 mmol.L-1组和0.28 mmol.L-1组脑片出现时间分别推迟为1 152.4和851.1,723.5 s,与缺氧组相比均有显著差异(P<0.05)。各组的HIP出现率分别为100%,33.3%,67.0%,83.3%。复氧30 min后,氧-葡萄糖剥夺(oxygen-glucose dep-rivation,OGD)组的恢复率为8.33%,恢复程度为19.8%。在L-THP组(0.028,0.14,0.28 mmol.L-1),PS的恢复率分别为92%、75%和33.3%,恢复程度分别为82.5%,70.4%和58.6%,与对照组比有非常显著的差异(P<0.01)。结论L-THP能减缓缺氧时PS幅度的降低速度,减轻和防止脑片突触功能的不可逆损伤,提高脑片的耐缺氧能力,但随着剂量增加而作用减弱。OBJECTIVE To investigate the effect of L-tetrahydropalmatine on synaptic function after ischemia and reperfusion in hippocampal slices. METHODS Rat hippoeampal slices placed in two compartment of a dual chamber were immersed in the superfusing artificial cerebral fluid(ACSF) with 95% O2 + 5% CO2. The population spike(PS) were recorded in CA1 pyramidal cells by stimulating Schffer collateral pathways. The appearance time of attenuation and disappearance time of PS, the appearance of hypoxic injury potential and the recovery rate of PS after reoxygenation were recorded. RESULTS After the treatment with L-tetrahydropalmatine at the doses of 0. 028,0. 14,0. 28 mmol·L^-1 , the appearance of attenuation and disappearance of population spike (PS) were significantly postponed comparing with the ischemia group. The appearance of hypoxie injury potential (HIP) was delayed significantly and the appearance probability of HIP was lower in L-tetrahydropalmatine group and the recovery amplitude of PS after reoxygenation was significantly higher than that of oxygen-glucose deprivation (OGD) group. CONCLUSION L-THP increased the ability against brain hypoxic injury and relieved the reversible and irreversible hypoxic injury in bippocampal slices.
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