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受损动脉中血小板血栓的超微结构与行为

Ultrastructure and behaviour of platelet thrombi in injured arteries.

作者信息

Honour A J, Pickering G W, Sheppard B L

出版信息

Br J Exp Pathol. 1971 Oct;52(5):482-94.

Abstract

An electron microscopy study was made of cerebral arteries in the rabbit after injuries adequate to produce platelet thrombi. Minor mechanical injuries, that is to say injuries which produced thrombi briefly without extravasation of blood, all showed a breach in the artery wall through which a haemostatic plug projected internally and externally; damage to endothelium and media adjacent to breach was invariable. Electrical injuries were inflicted by applying a unipolar electrode 0·0457 mm. in diameter to the pial surface of a cortical artery. With cathodal stimuli, ranging from 3-10 V d.c. 1-50 μA the arteries contracted and white bodies formed; they persisted for a few minutes up to 180 min. Because of the variable duration inhibitors were difficult to evaluate. When thrombi had ceased to form adenosine diphosphate (ADP), often in minute concentrations, would provoke the return of thrombus formation. 5-Hydroxytryptamine had a less constant effect. Electron microscopic examination showed a loss of endothelium and extensive damage to muscle cells of media at the site of injury. The media often contained platelets and sometimes red cells. Platelet thrombi were present on the wall denuded of endothelium and adjacent to it. In specimens obtained a few minutes after injury platelets showed remarkable ballooning by electron translucent contents. In lesions which had ceased to form thrombi spontaneously, but which were in a state when reactivation with ADP was expected, a rim of platelets covered the site of injury. Anodal stimuli had usually to be stronger to produce comparable thrombus formation. Vasoconstriction was never seen. Endothelium showed enormous distension with loss of the luminal membrane and apparent explosion of contents inwards. In very early lesions a rim of amorphous material was found on the internal elastic lamina and stuck in tufts to the most closely adjacent platelets, though less so to those more distant. Medial injury was always found. Ballooning of platelets in the earliest injuries was not observed. In other respects the changes were similar to those found with cathodal injury.

摘要

对家兔脑动脉进行了电子显微镜研究,这些脑动脉受到足以形成血小板血栓的损伤。轻微机械损伤,即那些能短暂形成血栓且无血液外渗的损伤,均显示动脉壁有破损,止血栓由此向内外突出;破损处相邻的内皮和中膜受损是必然的。通过将直径为0·0457毫米的单极电极施加于皮质动脉的软膜表面造成电损伤。施加3 - 10伏直流电、1 - 50微安的阴极刺激时,动脉收缩并形成白色团块;它们持续几分钟至180分钟。由于持续时间可变,抑制剂难以评估。当血栓不再形成时,二磷酸腺苷(ADP),通常是微量浓度,会促使血栓形成再次出现。5 - 羟色胺的作用不太稳定。电子显微镜检查显示损伤部位内皮缺失,中膜肌细胞广泛受损。中膜常含有血小板,有时还有红细胞。血小板血栓存在于内皮剥脱的血管壁及其相邻部位。在损伤后几分钟获取的标本中,血小板因电子透明内容物而显著肿胀。在那些已自发停止形成血栓但处于预期可被ADP重新激活状态的病变中,一圈血小板覆盖着损伤部位。阳极刺激通常需要更强才能产生类似的血栓形成。从未观察到血管收缩。内皮显示出巨大扩张,腔面膜缺失,内容物明显向内爆裂。在非常早期的病变中,在内弹性膜上发现一层无定形物质边缘,并成束地附着于最邻近的血小板上,而与较远的血小板附着较少。总是发现有中膜损伤。在最早的损伤中未观察到血小板肿胀。在其他方面,这些变化与阴极损伤时发现的变化相似。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fff/2072424/e102efdcf50b/brjexppathol00425-0058-a.jpg

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