Romero A, Muniain M A, Mata R, Pozuelo F, Pérez J J, Rodríguez M C, Rodríguez M D
Cátedra de Patología y Clínica Médicas I, Hospital Clínico Universitario Virgen Macarena, Sevilla, España.
Rev Esp Fisiol. 1988 Dec;44(4):407-12.
The effects of 6-methylprednisolone sodium succinate, quinacrine and the synthetic anti-PAF compound L-652,731 were studied on the PAF and complement induced aggregation of rabbit polymorphonuclear leukocytes in vivo. High doses (100-250 mg/kg) of corticosteroid were able to abrogate PAF and complement induced aggregation. Quinacrine (1.25 mg/kg), and L-652,731, partially precluded complement-depending aggregation. The L-652,731 dose employed was just enough to prevent PAF induced aggregation. These results suggest that in those pathological conditions in which polymorphonuclear aggregation occurs, factors other than those derived from plasmatic complement system activation, and laboring jointly with it, may be involved.
研究了琥珀酸甲泼尼龙、氯喹和合成抗血小板活化因子化合物L-652,731对血小板活化因子（PAF）和补体诱导的兔体内多形核白细胞聚集的影响。高剂量（100 - 250mg/kg）的皮质类固醇能够消除PAF和补体诱导的聚集。氯喹（1.25mg/kg）和L-652,731可部分阻止依赖补体的聚集。所使用的L-652,731剂量刚好足以防止PAF诱导的聚集。这些结果表明，在那些发生多形核白细胞聚集的病理状态下，可能涉及除血浆补体系统激活衍生的因素之外并与其共同起作用的其他因素。
