Myrvold H E, Brandberg A
Eur Surg Res. 1977;9(1):34-47. doi: 10.1159/000127923.
Platelets were labelled with 51Cr, fibrinogen with 125I and erythrocytes with 59Fe. Disintegrated Pseudomonas bacteria were injected intravenously and radioactive measurements were made on whole blood; tissue biopsies and clottable fibrinogen. After the infection there was an immediate but transient increase of 51Cr activity in the lung concomitant with a decrease in platelet count and 51Cr activity of blood. In the liver there was a less pronounced increase of 51Cr activity. The fibrinogen concentration decreased slightly, paralleled by the 125I activity of whole blood and of clottable fibrinogen, whereas the 125I activity in the lung and liver remained fairly constant. There was no changes of 51Cr activity or 125I activity in biopsies from muscle, pancreas, small intestine, kidney or spleen. During the experiment (3h) there were no signs of significant disseminated intravascular coagulation other than platelet aggregation. A consumption of fibrinogen related to the formation of fibrin plugs could not be detected. After injection of disintegrated Pseudomonas bacteria reversible platelet aggregates were formed and temporarily trapped in the pulmonary microcirculation. This microembolism might induce tissue damage and could be of importance for the development of septic pulmonary complication.
用51Cr标记血小板,125I标记纤维蛋白原,59Fe标记红细胞。将破碎的假单胞菌静脉注射,然后对全血、组织活检样本和可凝固纤维蛋白原进行放射性测量。感染后,肺部的51Cr活性立即但短暂升高,同时血小板计数和血液中的51Cr活性降低。肝脏中51Cr活性的升高不太明显。纤维蛋白原浓度略有下降,与全血和可凝固纤维蛋白原的125I活性平行,而肺和肝脏中的125I活性保持相当恒定。肌肉、胰腺、小肠、肾脏或脾脏活检样本中的51Cr活性或125I活性没有变化。在实验过程中(3小时),除了血小板聚集外,没有明显的弥散性血管内凝血迹象。未检测到与纤维蛋白凝块形成相关的纤维蛋白原消耗。注射破碎的假单胞菌后,形成了可逆的血小板聚集体,并暂时滞留在肺微循环中。这种微栓塞可能会导致组织损伤,并且可能对脓毒症肺部并发症的发展具有重要意义。