摘要
目的探讨感染性脑水肿神经细胞钙通道变化，神经元细胞内游离钙离子浓度（［Ｃａ２＋］ｉ）和Ｃａ２＋ＡＴＰ酶活性变化及其之间的关系。方法采用急性感染性脑水肿模型，测定神经元突触体胞浆内［Ｃａ２＋］ｉ和线粒体Ｃａ２＋ＡＴＰ酶活性变化，并选用Ｃａ２＋通道阻滞剂尼莫地平进行治疗，观察其对突触体［Ｃａ２＋］ｉ和线粒体Ｃａ２＋ＡＴＰ酶活性的影响。结果在注菌后３０分钟４、２４小时感染性脑水肿突触体［Ｃａ２＋］ｉ分别为３０５±２７、３５２±２１、４１３±４８ｎｍｏｌ／Ｌ，线粒体Ｃａ２＋ＡＴＰ酶活性分别为０５２±０１２、０３５±００８、０２４±０１２μｍｏｌ／（ｇ·ｈ）；电镜检查结果亦表明，菌液组突触体和线粒体明显肿胀，内有空泡形成。应用尼莫地平治疗后［Ｃａ２＋］ｉ明显下降，而Ｃａ２＋ＡＴＰ酶活性明显恢复，脑水肿减轻。结论感染性脑水肿神经细胞钙离子通道开放，细胞内Ｃａ２＋超载，突触体［Ｃａ２＋］ｉ与线粒体Ｃａ２＋ＡＴＰ酶活性变化呈负相关关系；尼莫地平通过降低突触体胞浆中［Ｃａ２＋］ｉ和恢复线粒体Ｃａ２＋ＡＴＰ酶活性。
Objective To elucidate the changes of neuronal Ca 2+ channel and to investigate the relationship between changes of cytosolic free calcium ([Ca 2+ ]i) concentration in the synaptosomes and mitochondrial Ca 2+ ATPase activities. Methods The authors determined the level of [Ca 2+ ]i in the synaptosomes and activities of mitochondrial Ca 2+ ATPase in the acute brain edema induced by injection of Pertussis bacilli (Pb). Nimodipine, a calcium channel antagonist, was employed to show its effects on [Ca 2+ ]i in the synaptosomes, and alteration of Ca 2+ ATPase activity in the mitochondria. Results The level of [Ca 2+ ]i significantly incrcased in the Pb injected cerebral hemisphere in the Pb group as compared with that of NS group at 30 min after injection. The level of [Ca 2+ ]i kept higher in the Pb group at 4,24 hours after injection of Pb ( P <0.05). In contrast, the activities of mitochondrial Ca 2+ ATPase were decreased remarkably in the Pb group ( P <0.05). Conclusion The neuronal Ca 2+ channel opened after injection of Pb. There was a negative correlation between activities of Ca 2+ ATPase and [Ca 2+ ]i. Nimodipine reduced brain edema through stimulating the activities of Ca 2+ ATPase in the mitochondria, and decreasing the levels of [Ca 2+ ]i in the synaptosomes.
出处
《中华儿科杂志》
CSCD
北大核心
1999年第1期38-41,共4页
Chinese Journal of Pediatrics
基金
国家自然科学基金
关键词
脑水肿
突触体
钙通道
ATP酶
大鼠
Brain edema
Synaptosomes
Calcium channels
Ca(2+) Transponting ATPase
Nimodipine
