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目的 观察实验性感染性脑水肿时β -内啡肽 (β -EP)的变化以探讨感染性脑水肿的发病机理。方法 采用兔百日咳菌液感染性脑水肿模型 ,观察生理盐水组 (NS ,n =7)、百日咳菌液组 (PB ,n =7)两组兔脑组织含水量、大脑皮层、海马、血浆及脑脊液中 β -EP含量变化。 结果 PB组脑组织含水量显著高于NS组 (P<0 0 1) ,大脑皮层、海马、血浆及脑脊液中 β -EP含量分别为 (5 6 2 8± 11 6 6 )pg/mg ,(85 97± 33 76 )pg/mg ,(10 6 33± 2 4 96 )ng/ml,(2 4 9± 0 6 6 )ng/ml,均显著高于NS组 (18 5 0± 2 0 1)pg/mg ,(2 2 5 2± 6 0 7)pg/mg ,(43 80± 19 6 3)ng/ml,(1 14± 0 39)ng/ml,P均小于 0 0 1)。结论 感染性脑水肿时 ,大脑皮层、海马、血浆及脑脊液中β -EP含量明显增加 ,引起脑水肿的发生和发展。
Objective To observe the changes of β-endorphin (β-EP) in experimental infectious brain edema to explore the pathogenesis of infectious brain edema. Methods The cerebral edema model of infective cerebral edema in rabbits was used to observe the changes of brain water content, cerebral cortex, hippocampus, plasma and brain tissue in NS group (n = 7) and pertussis bacilli group (PB, n = 7) Changes of β-EP in cerebrospinal fluid. Results The brain water content in PB group was significantly higher than that in NS group (P <0.01). The β-EP contents in cerebral cortex, hippocampus, plasma and cerebrospinal fluid were (562 ± 11 6 6) pg / mg, 85 97 ± 33 76) pg / mg, (10 6 33 ± 2 496) ng / ml and (249 ± 0 6 6) ng / ml, respectively, were significantly higher than those in NS group (18 50 ± 2 0 1 pg / mg, (2252 ± 607) pg / mg, (4380 ± 1963) ng / ml and (114 ± 039) ng / ml, respectively, P <0.01). Conclusions Infectious brain edema, β-EP content in cerebral cortex, hippocampus, plasma and cerebrospinal fluid was significantly increased, causing the occurrence and development of cerebral edema.