Chick T W, Goldblum S E, Smith N D, Butler C, Skipper B J, Winkelstein J A, Cork L C, Reed W P
J Lab Clin Med. 1984 Feb;103(2):180-92.
In the present study we investigated the cardiopulmonary dysfunction caused by systemic pneumococcal (PNC) disease. We studied the hemodynamic and hematologic effects of intravascular challenge with nonviable PNC in normal, granulocyte-depleted, and genetically C3-deficient dogs. In normal dogs PNC administration caused a decrease in cardiac output (CO) of 58% (p less than 0.001), an increase in pulmonary vascular resistance (PVR) of 151% (p less than 0.02), and an increase in systemic vascular resistance (SVR) of 72% (p less than 0.02). The PNC challenge also caused significant decreases in both circulating granulocytes (-73%; p less than 0.02) and platelets (-58%; p less than 0.02). Histologic examination revealed granulocyte plugging within small pulmonary vessels. PNC challenge in granulocyte-depleted and C3-deficient dogs resulted in hemodynamic and hematologic changes that were not significantly different from those seen in normal PNC-challenged animals. Infusion of PNC-activated plasma resulted in hematologic changes that were not significantly different from those seen in PNC-challenged animals. Infusion of plasma treated with ethylenediamenetetraacetic acid (EDTA) prior to PNC incubation induced the same hematologic alterations but the hemodynamic response was less pronounced. To control for PNC constituents not removed by centrifugation and filtration, saline was incubated with PNC. After the PNC was removed, infusion of the saline induced no significant hemodynamic changes, although profound granulocytopenia occurred. We conclude that an intact complement system, but not normal numbers of circulating granulocytes, is essential to PNC-induced hemodynamic changes. PNC generates a plasma factor in vitro that does not require an intact complement system or cellular machinery to induce granulocytopenia without hemodynamic effect.
在本研究中，我们调查了全身性肺炎球菌（PNC）疾病引起的心肺功能障碍。我们研究了在正常、粒细胞缺乏和遗传性C3缺陷犬中，用无活力的PNC进行血管内刺激对血流动力学和血液学的影响。在正常犬中，给予PNC导致心输出量（CO）降低58%（p<0.001），肺血管阻力（PVR）增加151%（p<0.02），全身血管阻力（SVR）增加72%（p<0.02）。PNC刺激还导致循环粒细胞（-73%；p<0.02）和血小板（-58%；p<0.02）显著减少。组织学检查显示小肺血管内有粒细胞阻塞。在粒细胞缺乏和C3缺陷犬中进行PNC刺激导致的血流动力学和血液学变化与正常PNC刺激动物中所见的变化无显著差异。输注PNC激活的血浆导致的血液学变化与PNC刺激动物中所见的变化无显著差异。在PNC孵育前用乙二胺四乙酸（EDTA）处理的血浆输注诱导了相同的血液学改变，但血流动力学反应不那么明显。为了控制未通过离心和过滤去除的PNC成分，将盐水与PNC一起孵育。去除PNC后，输注盐水未引起显著的血流动力学变化，尽管出现了严重的粒细胞减少。我们得出结论，完整的补体系统对PNC诱导的血流动力学变化至关重要，而循环粒细胞数量正常并非必需。PNC在体外产生一种血浆因子，该因子在不影响血流动力学的情况下诱导粒细胞减少不需要完整的补体系统或细胞机制。
