EFFECTS OF LEUKOCYTES ON BRAIN METABOLISM IN GRANULOCYTIC BRAIN EDEMA
EFFECTS OF LEUKOCYTES ON BRAIN METABOLISM IN GRANULOCYTIC BRAIN EDEMA
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DOI：
10.1002/ana.410020202
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发表时间：
1977-01-01
影响因子：
11.2
通讯作者：
HAKE, RB
中科院分区：
文献类型：
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作者：
FISHMAN, RA;SLIGAR, K;HAKE, RB
利用体外模型研究粒细胞白细胞（WBC）对脑代谢的影响，阐明化脓性脑膜炎、脑脓肿等脑病、脑水肿的发生机制。将单个第一大鼠皮质脑切片在正常培养基或含有由腹膜内糖原诱导的大鼠腹膜渗出细胞制备的WBC膜部分的培养基中孵育。膜部分引起“细胞毒性”脑水肿，导致脑水分增加、细胞肿胀（菊粉空间减少）、细胞内钠增加和细胞内钾丢失。大脑还显示出与能量消耗相关的葡萄糖氧化和乳酸生成增加，这通过磷酸肌酸、三磷酸腺苷和能量电荷电位的降低来证明。脓性脑脊液的低葡萄糖和高乳酸反映了脑代谢的这些变化。粒细胞脑水肿模型不受地塞米松影响。白细胞中导致这些变化的因素是膜结合的，不存在于细胞质中，并且对热不稳定。使用的浓度与病理渗出液中的浓度相容。脓液中的有毒因子会改变脑细胞膜的完整性，从而导致与化脓性脑膜炎和脑脓肿相关的脑病和脑水肿。
An in vitro model has been used to study the effects of granulocytic leukocytes (WBC) on brain metabolism to elucidate the mechanism of the encephalopathy and cerebral edema of purulent meningitis and brain abscess. Single first rat cortical brain slices were incubated in normal medium or medium containing a membrane fraction of WBC prepared from rat peritoneal exudate cells induced by intraperitoneal glycogen. Membrane fraction caused “cytotoxic” brain edema with increased brain water, cellular swelling (decreased inulin space), increased intracellular sodium, and loss of intracellular potassium. The brain also showed increased glucose oxidation and lactate production associated with energy depletion demonstrated by decreases in phosphocreatine, adenosine triphosphate, and energy charge potential. The low glucose and high lactate of purulent cerebrospinal fluid reflect these changes in brain metabolism. The model of granulocytic brain edema was not affected by dexamethasone. The factors in WBC responsible for these changes were membrane bound, absent from the cytosol, and heat labile. The concentrations used are compatible with concentrations in pathological exudates. Toxic factors in pus alter the integrity of brain cell membranes and thus contribute to the encephalopathy and brain edema associated with purulent meningitis and brain abscess.