Gaskins R A, Dalldorf F G
Arch Pathol Lab Med. 1976 Jun;100(6):318-24.
The pathogenesis of experimental meningococcal septicemia and the efficacy of heparin sodium therapy were evaluated by inoculating rabbits intraperitoneally with type B meningococci in mucin. Half the rabbits died, and the respiratory distress and circulatory failure that occurred during the terminal phase of the disease were associated with diffuse pulmonary capillary and venular thrombosis and with renal glomerular fibrin deposition. Platelet and leukocyte counts and plasma fibrinogen levels decreased in all rabbits, and prothrombin and partial thromboplastin times were prolonged. Pretreatment with heparin sodium diminished intravascular fibrin deposition but failed to prevent the pulmonary microthrombi and did not either reduce the mortality or improve the survival time. We conclude that death in meningococcal septicemia is due to widespread thrombosis of the pulmonary microcirculation. The disease is complicated by diffuse intravascular coagulation, which can be controlled with heparin sodium but which is not immediately life-threatening.
通过给家兔腹腔注射含有B型脑膜炎球菌的粘蛋白来评估实验性脑膜炎球菌败血症的发病机制及肝素钠治疗的疗效。半数家兔死亡，疾病终末期出现的呼吸窘迫和循环衰竭与弥漫性肺毛细血管和小静脉血栓形成以及肾小球纤维蛋白沉积有关。所有家兔的血小板和白细胞计数及血浆纤维蛋白原水平均降低，凝血酶原时间和部分凝血活酶时间延长。肝素钠预处理可减少血管内纤维蛋白沉积，但未能预防肺微血栓形成，也未降低死亡率或延长生存时间。我们得出结论，脑膜炎球菌败血症的死亡是由于肺微循环广泛血栓形成所致。该疾病并发弥漫性血管内凝血，可用肝素钠控制，但并非立即危及生命。
