CYTOTOXIC EFFECTS OF BLOODY CEREBROSPINAL-FLUID ON CEREBRAL ENDOTHELIAL-CELLS IN CULTURE
CYTOTOXIC EFFECTS OF BLOODY CEREBROSPINAL-FLUID ON CEREBRAL ENDOTHELIAL-CELLS IN CULTURE
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DOI：
10.3171/jns.1994.81.1.0087
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发表时间：
1994-07-01
影响因子：
4.1
通讯作者：
LEE, KS
中科院分区：
文献类型：
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作者：
FOLEY, PL;TAKENAKA, K;LEE, KS
裂解血细胞内产物的释放被认为在脑出血后血管病理的病因学中起着关键作用。本文研究了血液和脑脊液(CSF)的混合物对培养的牛脑内皮细胞的影响。用H-3-亮氨酸掺入内皮细胞作为细胞活力的指标。脑脊液本身并不改变细胞内H-3-亮氨酸的掺入。相比之下，在治疗前预先与血液孵育3天或更长时间的脑脊液可引起亮氨酸掺入显著减少。用预先与血液孵育5~7天的脑脊液处理后，培养的细胞迅速恶化，几乎立即出现大量细胞脱落。在预先孵育超过3天的血液和脑脊液混合物中，血红蛋白浓度显著升高。血红蛋白浓度的升高与血性CSF的细胞毒性影响的增加在时间上有关。这些发现表明，在血液破裂过程中释放的因子对颅内内皮细胞产生有害影响。这种作用的时程与人类蛛网膜下腔出血后血管痉挛的发生密切相关。综上所述，这些观察结果与细胞内血液产物，特别是血红蛋白，通过直接损害内皮功能而导致血管痉挛的假设是一致的。
The release of intracellular products from lysed blood cells is believed to play a critical role in the etiology of vascular pathology following intracerebral hemorrhage. The present studies investigated the effects of a mixture of blood and cerebrospinal fluid (CSF) on bovine intracranial endothelial cells maintained in culture. The incorporation of H-3-leucine into endothelial cells was used as an index of cellular viability. Cerebrospinal fluid alone did not alter the incorporation of H-3-leucine into the cells. In contrast, CSF preincubated with blood for 3 days or longer prior to treatment elicited significant reductions in leucine incorporation. Treatment with CSF preincubated with blood for 5 to 7 days resulted in the rapid deterioration of the culture, with large numbers of cells detaching almost immediately. Concentrations of hemoglobin were elevated profoundly in mixtures of blood and CSF preincubated for periods longer than 3 days. The increases in hemoglobin concentration were related temporally to increases in the cytotoxic impact of the bloody CSF.These findings suggest that factors released during the breakdown of blood exert a deleterious effect on intracranial endothelial cells. The time course of this effect is closely related to the development of vasospasm in humans following subarachnoid hemorrhage. Taken together, these observations are consistent with the hypothesis that intracellular blood products, particularly hemoglobin, contribute to vasospasm by directly compromising endothelial function.