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Neuroprotective effects of nimodipine and MK-801 on acute infectious brain edema induced by injection of pertussis bacilli to neocortex of rats

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Chinese Journal of Traumatology 2003年第2期6卷 118-123页

作者：陈立华刘丽旭杨于嘉刘运生曹美鸿 Department of Neurosurgery

Objective: To explore the mechanism and type of acute infectious brain edema induced by injection of pertussis bacilli (PB) in rat neocortex, to study the neuroprotective effect of non-competitive antagonist of N-methl-D-aspartate ( NMDA ) receptor ( MK-801 ) and antagonist of Ca 2+ channels ( nimodipine )on brain edema, and to investigate the relationship between percentage of water content and cytosolic free calcium concentration ( i) in synaptosomes or content of Evans Blue (EB). Methods: 95 SD rats were randomly divided into five groups, ie, normal control group, sham-operated control group, PB group, nimodipine treatment group and MK-801 pretreatment group. The acute infectious brain edema was induced by injection of PB into the rats. Quantitative measurements of water content and the concentration of EB were performed. i was determined in calcium fluorescent indication Fura-2/AM loaded neuronal synaptosome with a spectrofluorophotometer. To observe the effect of MK-801 and nimodipine, we administered MK-801 48 hours and 24 hours before the injection of PB in MK-801 pretreatment group, and nimodipine after the injection of PB in nimodipine treatment group. The specific binding of NMDA receptor was measured with -MK-801 in the neuronal membrane of cerebral cortex. Results: The levels of water content and EB content of brain tissues, and i in the neuronal synaptosomes increased more significantly in the PB-injected cerebral hemisphere in the PB group than those of normal control group and sham-operated control group (P< 0.05). The water content and i increased with the duration of infectious brain edema. Nimodipine administered after the injection of PB could significantly decrease the water content, EB and i (P< 0.05). MK-801 could significantly decrease the water content, EB and i in 4 h and 24 h groups (P< 0.05). The Kd values were 30.5 nmol/L ±3.0 nmol/L and 42.1 nmol/L ±4.2 nmol/L in PB group and NS group respectively (P< 0.05), and Bmax were 0.606 pmol/mg.p

关键词： pertussis toxins Brain edema Nimodipine MK-801 Rat

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Changes of neuronal calcium channel following brain damage induced by injection of pertussis bacilli in rats

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Chinese Journal of Traumatology 2002年第4期5卷 224-227页

作者：陈立华杨于嘉刘丽旭曹美鸿 Department of Neurosurgery Xiangya HospitalCentral South University

Objective: To explore changes of neuronal calcium channel following brain damage induced by injection of pertussis bacilli in rats, and to investigate the relationship between cytosolic free calcium concentration ([Ca 2+ ] i) in the synaptosome and Ca 2+ ATPase activities of mitochondria. Methods: The level of [Ca 2+ ] i in the synaptosome and Ca 2+ ATPase activities of mitochondria in the acute brain damage induced by injection of pertussis bacilli (PB) in rat was determined and nimodipine was administrated to show its effects on [Ca 2+ ] i in the synaptosome and on alteration of Ca 2+ ATPase activity in the mitochondria. Seventy three rats were randomly divided into four groups, ie, normal control group (Group A), sham operation control group (Group B), PB group (Group C) and nimodipine treatment group (Group D). Results: The level of [Ca 2+ ] i was significantly increased in the PB injected cerebral hemisphere in the Group C as compared with that in the Group A and the Group B at 30 minutes after injection of PB. The level of [Ca 2+ ] i was kept higher in the 4 hours and 24 hours subgroups after the injection in the Group C (P< 0.05 ). In contrast, the Ca 2+ ATPase activities were decreased remarkably among all of the subgroups in the Group C. Nimodipine, which was administered after injection of PB, could significantly decrease the [Ca 2+ ] i and increase the activity of Ca 2+ ATPase (P< 0.05 ). Conclusions: The neuronal calcium channel is opened after injection of PB. There is a negative correlation between activities of Ca 2+ ATPase and [Ca 2+ ] i. Nimodipine can reduce brain damage through stimulating the activities of Ca 2+ ATPase in the mitochondria, and decrease the level of [Ca 2+ ] i in the synaptosome. Treatment with nimodipine dramatically reduces the effects of brain damage induced by injection of PB.

关键词： pertussis toxins Brain damage Nimodipine Ca 2+ transporting ATPase Cytosolic free calcium concentration

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