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出 处:《中国病理生理杂志》1999年第9期829-831,共3页Chinese Journal of Pathophysiology
基 金:国家自然科学基金!39560031;云南省自然科学基金!95C072M
摘 要:目的:探讨血小板活化因子(PAF)与单胺类神经递质缺血性脑损伤中的可能机制,并观察PAF拮抗剂银杏内酯B对抗PAF所致脑缺血中心区及半暗区病理生理改变及其逆转单胺类递质代谢紊乱的作用。方法:采用光化学诱导树血栓性脑缺血模型,舌下静脉一次性注射银杏内酯B5mg·kg-1(光化学反应后6h),观察给药后缺血中心区及半暗区单胺类递质及脑水含量的变化。结果:给药组半暗区NE、DA及5-HT依次为(403.64±50.94)ng/gwt、(474.96±44.12)ng/gwt和(495.79±33.19)ng/gwt,均分别高于缺血组(254.95±42.26)ng/gwt(P<0.01)、(403.28±34.86)ngwt(P<0.01)和(410.58±33.24)ng/wt(P<0.01);而给药组半暗区脑水份含量为(81.75±0.80)%低于缺血组(83.85±0.96)%(P<0.01)。结论:PAF与单胺类神经递质共同参与缺血性脑损伤,并且银杏内酯B能特异性拮抗PAF受体及减少单胺递质的释放而具有抗脑缺血效应。AIM: To investigate the potential mechanism of platelet activating factor (PAF) and monoamine neurotransmitters in ischemic cerebral injury, and to observe the effects of PAF antagonist ginkgolide B on PAF and on the reversing of monoamine neurotransmitters. METHODS: Thrombotic cerebral ischemic model induced by photochemical reaction in tree shrews was used. Ginkgolide B was given intravenously at 6h following photochemical reaction and the alterations of monoamine neurotransmitters and water contents after the treatment were monitored in ischemic core, and penumbra regions.RESULTS:The contents of NE, DA and 5-HT in ischemic penumbra were(403. 64±50. 94)ng/g wt, (474. 96±44. 12)ng/g wt and (495. 79± 33. 19)ng/g wt in the treatmnt group, and they were higher than those in the ischemic group, respectively (P < 0. 01 ). While water content was (81. 75% ± 0. 80% ) in the treatment group, was lower than that in the ischemic group (P < 0. 01 ). CONCLUSION: PAF and monoamine neurotransmitters may participate in the ischemic injury and ginkgolide B may possess cerebral protection against ischemic cerebral damage by inhibiting PAF receptor and decreasing the release of monoamine neurotransmitters.
分 类 号:R743.310.2[医药卫生—神经病学与精神病学]
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