FORMATION OF TRANSENDOTHELIAL CHANNELS IN TRAUMATIC HUMAN-BRAIN EDEMA
FORMATION OF TRANSENDOTHELIAL CHANNELS IN TRAUMATIC HUMAN-BRAIN EDEMA
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DOI：
10.1016/s0344-0338(84)80054-0
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发表时间：
1984-01-01
影响因子：
2.8
通讯作者：
CASTEJON, OJ
中科院分区：
文献类型：
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作者：
CASTEJON, OJ
本文报告4例创伤性脑损伤合并硬膜下或硬膜外血肿或积液的不完全跨内皮细胞通道的形成。观察到这些结构与增加的跨内皮细胞空泡和囊泡转运共存。主要表现为：腔内皮细胞膜深陷形成电子透明通道，膜融合和裂解共同作用形成链状球形或细长空泡连接腔内皮细胞膜，含大蛋白的空泡或微吞饮小泡占据整个外周内皮细胞质的宽度，扩张的基底膜扩张的腔面轮廓延伸至内皮管腔质膜附近。大多数病例内皮细胞连接完好。跨内皮细胞通道显然代表了对创伤性脑损伤的跨细胞反应。它们可以为水肿的形成提供特定的细胞质通道，便于运输，包括管腔内的毛细血管内容物，穿过内皮细胞质的外围区域，并在管腔表面将其排空，进入周围的基底膜，从那里充斥邻近神经桩的细胞间隙。由扩张的基底膜分叉形成的蛋白跨内皮细胞通道可能是内源性物质从实质裂隙向血液移动的反向穿梭，作为消肿的毛细血管机制。
The formation of incomplete transendothelial channels is reported in 4 cases of traumatic human brain injury complicated with subdural or epidural hematoma or hygroma. Such structures were observed coexisting with increased transendothelial vacuolar and vesicular transport. They appeared in the following manners: as electron lucent corridors formed by deep invaginations of luminal endothelial plasma membranes, as chained spheroidal or elongated vacuoles connected with the luminal and abluminal endothelial membranes, as a result of a combined process of membrane fusion and fission, as a large protein containing vacuole or a micropinocytotic vesicle occupying the entire width of peripheral endothelial cytoplasm, as abluminal profiles of dilated basement membrane expansions, extending their course to the vicinity of endothelial luminal plasma membrane. The endothelial junctions appeared intact in most cases. The transendothelial channels apparently represent a transcytosis response to the traumatic brain injury. They may provide specific cytoplasmic corridors of facilitated transport for edema formation, which incorporate the intraluminal capillary content, ferry it across the peripheral zone of endothelial cytoplasm and empty it at the abluminal surface, into the surrounding basement membrane, from where it floods the intercellular spaces of neighboring neuropile. The albuminal transendothelial channels, formed by the dilated basement membrane bifurcations, might be a reverse shuttle for endogenous substances moving from parenchymal clefts to blood as a capillary mechanism of edema resolution.