Blood-arterial wall barrier disruption to various sized tracers following subarachnoid haemorrhage-猫眼课题宝

蛛网膜下腔出血后各种大小示踪剂对血动脉壁屏障的破坏

DOI：

10.1007/bf01407780

发表时间：

2005

期刊：

Acta Neurochirurgica

影响因子：

2.4

通讯作者：

中科院分区：

医学3区

文献类型：

作者：

T. Nakagomi;N. Kassell;H. Johshita;R. Lehman;S. Fujiwara;Tsutomu Sasaki

蛛网膜下腔出血（SAH）后主要脑动脉的血-动脉壁屏障破坏，可能与脑血管痉挛的发病机制有关。使用不同大小的FITC葡聚糖，进行本研究以确定SAH后不久屏障破坏是否与各种大小的示踪剂相同。将42只SD大鼠分为5组。四组注射不同分子量（MW）的FITC-葡聚糖：FD 4（MW= 4，080）、FD 40（MW= 40，500）、FD 70（MW= 71，400）和FD 150（MW= 156，900）。一组注射辣根过氧化物酶（HRP：MW= 40，000）。每组又分为两个亚组：伴或不伴SAH。蛛网膜下腔出血（SAH）是通过向枕大池注入动脉血来诱导的。为了通过透射电子显微镜评估血动脉壁屏障的完整性，在处死动物之前静脉注射示踪剂。没有SAH的组显示示踪剂没有渗透到基底动脉的内皮下空间。相比之下，除FD 150外，在内皮下间隙中观察到FITC-葡聚糖（FD 4、FD 40、FD 70）。FITC-葡聚糖在弹性膜中的分布与HRP相似。这些结果表明，尽管较大分子的渗透似乎存在一些限制，但各种分子大小的FITC-dextrans都会发生屏障破坏。目前的研究表明，在SAH后的急性期主要脑动脉屏障破坏的机制可能是囊泡，而不是通过分离的紧密连接。

SummaryDisruption of the blood-arterial wall barrier in the major cerebral arteries occurs following subarachnoid haemorrhage (SAH) and may be related to the pathogenesis of cerebral vasospasm. Using FITC dextrans of various sizes, the present study was undertaken to determine if the barrier disruption shortly after SAH occurs equally to various sized tracers. Forty-two Sprague-Dawley rats were divided into 5 groups. Four groups were injected with FITC-dextrans of differing molecular weights (MW): FD4 (MW=4,080), FD40 (MW=40,500), FD 70 (MW=71,400), and FD 150 (MW=156,900). One group was injected with horseradish peroxidase (HRP: MW=40,000). Each group was further divided into two subgroups: with or without SAH. SAH was induced by injecting arterial blood into the cisterna magna. To assess the integrity of the blood-arterial wall barrier by transmission electron microscope, the tracers were intravenously injected prior to sacrificing the animals. The groups without SAH showed no permeability of tracers into the subendothelial spaces of the basilar arteries. In contrast, with the exception of FD 150, FITC-dextrans (FD 4, FD 40, FD 70) were noticed in the subendothelial spaces. The distribution of FITC-dextrans in the elastic lamina was similar to that of HRP. These results suggest that barrier disruption occurs with a wide range of molecular sizes of FITC-dextrans, although there seems to be some limitation to the permeation of the larger molecules. The present study suggests that the mechanism of barrier disruption of the major cerebral arteries in the acute stage following SAH may be vesicular rather than by separation of tight junctions.

Platelet-derived growth factor binds specifically to receptors on vascular smooth muscle cells and the binding becomes nondissociable.