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本文应用胶体碳作为示踪物,对小鼠在大肠杆菌内毒素引起休克时的肺,小肠和膈肌进行了血管通透性的形态学研究。 结果表明,注射内毒素30min后,属於体循环系统的支气管微静脉。小肠粘膜下层的微静脉以及膈肌血管树的微静脉及毛细血管后徼静脉段开始有碳黑颗粒沉着,这些徼静脉在电镜下发现为内皮细胞间连结开放,碳黑颗粒通过开放的连结进入内皮下,形成静脉漏,或称碳漏。它是血管通透性增高的标志之一。随着内毒素作用时间的延长,微静脉漏的数目增加,表明内毒素对血管通透性的影响,随着休克进展而不断加重。但属於肺循环系统中的微血管,只见毛细血管管腔内嗜中性白细胞、血小板逐渐增多,在内毒素注射后60min,嗜中性白细胞的特殊颗粒减少,吞噬泡出现,并发现这些血液有形成分粘附在内皮细胞表面,说明肺微血管的变化和血管通透性变化是相应的。最后对微静脉漏产生的可能机制进行了讨论。
In this paper, colloidal carbon was used as a tracer to study the morphological changes of vascular permeability of lung, small intestine and diaphragm in E. coli endotoxin-induced shock. The results showed that 30 min after injection of endotoxin, belong to the systemic circulation of bronchial vein. Microvessels of the small intestinal submucosa, as well as the venules of the vascular tree of the diaphragm and the posterior commissure of the capillaries, begin to have carbon black granules that are found under electron microscopy to be open to endothelial cell junctions and into which the carbon black particles enter through open connections Subcutaneous, the formation of venous leakage, or carbon leakage. It is one of the hallmarks of increased vascular permeability. With the prolongation of the action time of endotoxin, the number of venules of venules increased, indicating that the effect of endotoxin on vascular permeability was aggravating with the progression of shock. However, the microvessels belonging to the pulmonary circulation system showed capillary neutrophils in the lumen of the capillaries and gradually increased platelets. After 60 min of injection of endotoxin, the special particles of neutrophils decreased, and the phagocytic vesicles appeared and found to have formed Adhesion on the surface of endothelial cells, indicating changes in pulmonary microvascular and vascular permeability changes are corresponding. Finally, the possible mechanism of venous leakage is discussed.