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Ultrastructure and Behaviour of Platelet Thrombi in Injured Arteries

机译:受伤动脉血小板血栓的超微结构和行为

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摘要

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.
机译:电子显微镜检查是在足以产生血小板血栓的损伤后对家兔的脑动脉进行的,轻微的机械损伤(即短暂产生血栓而没有渗血的损伤)均显示动脉壁破裂,止血内部和外部投影的插头;内皮和邻近裂口的介质的损害是不变的。通过施加单极电极0·0457 mm造成电击伤。皮层动脉的直径。带有阴极刺激,直流电压范围3-10 V. 1-50μA的动脉收缩并形成白色小体;他们持续了几分钟达180分钟。由于持续时间的变化,抑制剂难以评估。当血栓停止形成时,通常以极低的浓度形成二磷酸腺苷(ADP),将促使血栓形成的返回。 5-羟色胺的作用较差。电子显微镜检查显示在损伤部位内皮损失并且介质的肌肉细胞广泛受损。培养基通常含有血小板,有时含有红细胞。血小板血栓存在于内皮剥蚀的壁上并与其相邻。在损伤后几分钟获得的标本中,由于电子半透明成分,血小板显示出明显的膨胀。在已经自发停止形成血栓的病变中,但是处于预期可以被ADP激活的状态,血小板边缘覆盖了受伤部位。通常,阳极刺激必须更强才能产生可​​比的血栓形成。从未见过血管收缩。内皮显示出巨大的扩张,腔膜丧失,内含物明显向内爆炸。在非常早期的病变中,在内部弹性薄层上发现了无定形物质的边缘,并以簇状的形式附着在最接近的血小板上,尽管距离较远的血小板则较少。总是发现内侧受伤。最早的伤口未观察到血小板膨胀。在其他方面,变化与发现阴极损伤的变化相似。

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