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Metabolical and morphological study for endothelial cell injry and platelet aggregation in childhood disorders.

儿童疾病中内皮细胞损伤和血小板聚集的代谢和形态学研究。

基本信息

批准号：
62570432
负责人：
MIIKE Teruhisa
金额：
$ 1.22万
依托单位：
Kumamoto University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1987
资助国家：
日本
起止时间：
1987 至 1988
项目状态：
已结题

项目摘要

It has been reported that endothelial alterations including blister-like swelling, were observed in experimental serotonin myopathy as well as Duchenne muscular dystrophy (DMD).In the first study, we observed blood vessels in rat muscle tissues after serotonin injection.(1).Serotonin experiment. serotonin (75mg/Kg) was injected to Wister rats intraperitoneally. Althouge no structural damage was observed with the light microscope, ultrastructural changes were prominent in-muscle capillaries. One of the more impressive abnormalities consisted of large blister-like swelling, which appeared to originate from the luminal surface of the endothelial cell and extend into the lumen, at times almost completely occluding it. These phnomena were quite similar to those seen in DMD muscle tissue.(2).Immunohistochemical study using antibodies against DMD gene product (dystrophin). Dystrophin was clearly localized in the surface membrane of smooth muscle layers (tunica media) of blood vessels of any kinds and sizes, especially muscular arteries, in various tissues from rats and mice. Ten hours after serotonin injection, bolld vesse in lung , even muscular arteries, lost dystrophin reaction. These results suggested that, dysfunction of tunica media, due to defective dystrophin and secondary damage by serotonin injection for instance, induce endothelial cell damage and platelet aggregation. On second thought, it wa suggested that, any conditions which induce platelet aggregation resulting abundant serotonin release in blood vessels, also produce endothelial cell injury.

在实验性5-羟色胺肌病（serotonemyopathy）和杜氏肌营养不良症（Duchenne muscular dystrophy，DMD）中，均观察到血管内皮细胞的改变，包括水泡样肿胀。（1）血清素实验。Wister大鼠腹腔注射5-羟色胺（75 mg/Kg）。光镜下虽未见结构损伤，但肌毛细血管超微结构改变明显。其中一个更令人印象深刻的异常包括大的水泡样肿胀，它似乎起源于内皮细胞的管腔表面并延伸到管腔中，有时几乎完全阻塞它。这些现象与DMD肌肉组织中所见的非常相似。（2）DMD基因产物抗肌营养不良蛋白（dystrophin）抗体的免疫组化研究。在大鼠和小鼠的各种组织中，肌营养不良蛋白明显定位于任何种类和大小的血管，特别是肌动脉的平滑肌层（图尼卡中膜）的表面膜。注射5-羟色胺10小时后，肺内血管，甚至肌内动脉的dystrophin反应消失。这些结果表明，由于dystrophin缺陷和5-羟色胺注射引起的继发性损伤，图尼卡中膜功能障碍，诱导内皮细胞损伤和血小板聚集。进一步考虑，这表明，任何诱导血小板聚集导致血管中大量5-羟色胺释放的条件也会导致内皮细胞损伤。