【摘要】 目的　探讨百日咳菌液诱导的急性感染性脑水肿的发生机制和类型 ,并观察尼莫地平和MK - 80 1的作用。方法　测定脑组织水分含量和EB含量 ,Fura 2 /AM测定突触体 [Ca2 + ]i,放射性配基结合法测定NMDA受体的结合量。结果　 [Ca2 + ]i随脑水肿时间的延长而持续进行性升高 ,伴随脑组织水分含量和EB含量增加。MK 80 1预处理和尼莫地平治疗后 ,脑组织含水量和EB含量及[Ca2 + ]i明显下降 (P <0 0 5 )。PB组与NS组相比Kd值有显著性差异 ,而Bmax差异无显著性。结论　感染性脑水肿是混合性脑水肿 ,它的发生与Ca2 + 通道开放和NMDA受体介导的迟发性钙离子内流及BBB通透性增加密切相关。MK 80 1和尼莫地平通过缓解细胞内钙离子超载和改善BBB的通透性 ,从而减轻脑水肿。更多还原

【Abstract】 Objective To study the mechanism and type of infective brain edema induced by injection of Pertussis Bacilli(PB),and the neuroprotection effect of antagonist of Non competition NMDA receptor(MK 801)and antagonist of Ca 2+ channels on the neuron.Methods The infective brain edema in SD rats was induced by injection of PB. A quantitative measurement of water content and the contentration of Evan blue(EB) were done. Cytosolic free calcium ([Ca 2+ ]i) was determined in calcium fluorscent indication Fura 2/AM loaded neuronal synaptosomes by using spectroflurophtometer. MK 801 was pretreated at 48 hours and 24 hours before brain edema by injection of PB. Nimodipine was administered after infective brain injury induced by PB for observing their influence on brain edema. The specific binding of NMDA receptor were measured with 3[KG2/5]H MK 801 in the neuronal membrane of cerebral cortex. Results The level of water content and EB of brain tissues, and [Ca 2+ ]i within neuronal synoptosomes significantly increased in the injective PB cerebral hemisphere in the PB group as compared with that of Nor and NS group (P<0 05). The water content and [Ca 2+ ]i increased with the increasing time of infective brain edema. Nimodipine could decreased remarkably water content EB and [Ca 2+ ]i (P<0 05). MK 801 is selective non competitive inhibitor of NMDA receptor, which could significantly decreased water content and [Ca 2+ ]i at 4 and 24 hours after injection of PB (P<0 05). The Kd values were 30 5±3 0 and 42 1±4 2 nmol/L in BP group and NS group respectively(P<0 05).Conclusion It is suggested that the changes of the permeability of BBB, and Ca 2+ overloaded may participate in the pathogenesis of infective brain edema. Nimodipine through inhibiting the excess of Ca 2+ influx, and decreased the permeability of BBB, and possess the protective effect on brain edema. MK 801 pretreatment could inhibit the inflow of Ca 2+ into the neurons. It was not only occurred cytotoxic brain edema(intracellular edema) but also occurred vasogenic brain edema(extracellular edema)followed by BBB breakdown eariler,so infective brain edema is mixed brain edema.更多还原