Fountain S W, Martin B A, Musclow C E, Cooper J D
Circ Res. 1980 Feb;46(2):175-80. doi: 10.1161/01.res.46.2.175.
Pulmonary leukostasis, as a result of complement activation, has been invoked as a cause of pulmonary dysfunction. To investigate this phenomenon, we studied the pulmonary response to infusion of autologous complement-activated plasma in sheep and rabbits. Complement activation was produced by plasma incubation with zymosan. Leukopenia, with selective loss of polymorphonuclear leukocytes into the lungs, occurred in all animals immediately after the onset of plasma infusion. Complement-activated plasma infusion in sheep produced a significant fall in the arterial PO2 and a marked rise in pulmonary vascular resistance, whereas no such effects were observed in rabbits. Pretreatment of the sheep with sulfinpyrazone eliminated the pulmonary response to complement-activated plasma without altering the leukopenic response. Pulmonary histology in rabbits and sheep confirmed the presence of intracapillary leukostasis after the plasma infusions, whether or not sulfinpyrazone had been administered previously. The pulmonary response to complement activation is associated with pulmonary capillary leukostasis, but leukostasis alone is not an adequate explanation of the phenomenon.
补体激活导致的肺白细胞淤滞已被认为是肺功能障碍的一个原因。为了研究这一现象，我们在绵羊和兔子身上研究了输注自体补体激活血浆后的肺部反应。补体激活是通过血浆与酵母聚糖孵育产生的。在血浆输注开始后，所有动物立即出现白细胞减少，多形核白细胞选择性地进入肺部。在绵羊中输注补体激活血浆导致动脉血氧分压显著下降和肺血管阻力显著升高，而在兔子中未观察到此类效应。用磺吡酮预处理绵羊可消除对补体激活血浆的肺部反应，而不改变白细胞减少反应。无论之前是否给予磺吡酮，兔子和绵羊的肺部组织学检查均证实血浆输注后存在毛细血管内白细胞淤滞。对补体激活的肺部反应与肺毛细血管白细胞淤滞有关，但仅白细胞淤滞不足以解释这一现象。
