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目的观察实验性感染性脑水肿时β－内啡肽（β－ＥＰ）活性的变化及阿片肽受体拮抗剂金尔伦（ＪＥＬ）对其影响。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）及金尔伦治疗组（ＪＥＬ，ｎ＝７）３组兔脑组织含水量、伊文思蓝含量及大脑皮层、海马、血浆和脑脊液中β－ＥＰ变化。结果ＰＢ组兔脑含水量、伊文思蓝含量显著高于ＮＳ组（Ｐ＜０．０１），血浆、脑脊液及大脑皮层、海马β－ＥＰ分别为１０６．３３±２４．９６ｎｇ／ｍｌ，２．４９±０．６６ｎｇ／ｍｌ，５６．２８±１１．６６ｎｇ／ｍｇ，８５．９７±３３．７６ｎｇ／ｍｇ，均显著高于ＮＳ组（４３．８０±１９．６３ｎｇ／ｍｌ，１．１４±０．３９ｎｇ／ｍｌ，１８．５０±２．０１ｎｇ／ｍｇ，２２．５２±６．０９ｎｇ／ｍｇ，Ｐ值均＜０．０１）；而ＪＥＬ组血浆、脑脊液及大脑皮层、海马β－ＥＰ分别为６９．３８±４．６７ｍｇ／ｍｌ，１．４４±０．２６ｎｇ／ｍｌ，３１．１６±７．０１ｎｇ／ｍｇ，４５．０３±９．９８ｎｇ／ｍｇ，均较ＰＢ组明显减低（Ｐ值均＜０．０１）。结论β－内啡肽在感染性脑水肿发生中起重要作用，金尔伦可有效地减轻脑水肿并降低β－ＥＰ?
Objective To observe the changes of β-endorphin (β-EP) activity and the effect of opioid receptor antagonist JEL on experimental infectious brain edema. Methods Infectious cerebral edema model of rabbits pertussis was used to observe the effects of NS, n = 7, pertussis bacilli (PB, n = 7) and JEL (n = 7) Rabbit brain tissue water content, Evans blue content and changes of β-EP in cerebral cortex, hippocampus, plasma and cerebrospinal fluid. Results The brain water content and Evans blue content in PB group were significantly higher than those in NS group (P <0.01). The levels of β-EP in plasma, cerebrospinal fluid and cerebral cortex and hippocampus were 106.33 ± 24.96ng / ml, 2 respectively. 49 ± 0.66ng / ml, 56.28 ± 11.66ng / mg and 85.97 ± 33.76ng / mg respectively, which were significantly higher than those in NS group (43.80 ± 19.63ng / ml, 1.14 ± 0 P <0.01). However, β-EP in plasma, cerebrospinal fluid, cerebral cortex and hippocampus in JEL group were 69.38 ± 4.67mg / ml, 1.44 ± 0.26ng / ml, 31.16 ± 7.01ng / mg, 45.03 ± 9.98ng / mg respectively, which were significantly lower than those in PB group <0.01). Conclusion β-endorphin plays an important role in the pathogenesis of infectious brain edema. Treating the brain edema effectively and decreasing β-EP?