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兴奋性氨基酸拮抗剂对大鼠急性硬膜下血肿相关半球肿胀的减轻作用

Attenuation of hemispheric swelling associated with acute subdural hematomas by excitatory amino acid antagonist in rats.

作者信息

Kinoshita K, Katayama Y, Kano T, Hirayama T, Tsubokawa T

机构信息

Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan.

出版信息

Acta Neurochir Suppl (Wien). 1994;60:505-7. doi: 10.1007/978-3-7091-9334-1_138.

DOI:10.1007/978-3-7091-9334-1_138
PMID:7976631
Abstract

Acute subdural hematoma (ASDH) gives rise to a mass effect not only by itself but also through unilateral hemispheric swelling. The present study tested the hypothesis that hemispheric swelling is mediated by mechanisms which involve excitatory amino acids (EAAs). After removal of the subdural clot, introduced by homologous blood (0.1-0.2 ml), the % brain water was determined from the formula: ((wet weight--dry weight)/wet weight) x 100. The % brain water of the left hemisphere was significantly greater than that of the right hemisphere during the initial 6 hours after induction of ASDH in animals injected with 0.2 ml blood. A less marked but significant increase was observed in the animals injected with 0.1 ml blood. Systemic pretreatment with kynurenic acid (KYN; 800 mg/kg, i.p.), a broad-spectrum EAA antagonist, attenuated the increase in % brain water in the animals injected with 0.2 ml blood. In order to determine the changes in cerebral metabolism induced by the model of ASDH employed in the present study, we measured the cortical cytochrome oxidase (CYO) activity, a marker of mitochondrial respiration, in a separate group of animals. The CYO activity estimated densitometrically from the histochemical staining was not significantly altered in the animals injected with either 0.1 or 0.2 ml blood, suggesting absence of ischemia. These results indicated that the hemispheric swelling associated with thin ASDHs may be partially mediated by mechanisms other than ischemia, in which EAAs appear to be involved.

摘要

急性硬膜下血肿(ASDH)不仅自身会产生占位效应,还会通过单侧半球肿胀产生占位效应。本研究检验了以下假设:半球肿胀是由涉及兴奋性氨基酸(EAA)的机制介导的。在注入同源血液(0.1 - 0.2 ml)形成硬膜下血凝块后,通过以下公式确定脑含水量百分比:((湿重 - 干重)/湿重)×100。在注入0.2 ml血液诱导ASDH后的最初6小时内,注射0.2 ml血液的动物左半球脑含水量百分比显著高于右半球。在注射0.1 ml血液的动物中观察到不太明显但显著的增加。用广谱EAA拮抗剂犬尿喹啉酸(KYN;800 mg/kg,腹腔注射)进行全身预处理,可减轻注射0.2 ml血液的动物脑含水量百分比的增加。为了确定本研究中使用的ASDH模型诱导的脑代谢变化,我们在另一组动物中测量了皮质细胞色素氧化酶(CYO)活性,这是线粒体呼吸的一个标志物。通过组织化学染色密度测定法估计的CYO活性在注射0.1或0.2 ml血液的动物中没有显著改变,表明不存在缺血。这些结果表明,与薄层ASDH相关的半球肿胀可能部分由缺血以外的机制介导,其中EAA似乎参与其中。

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