Yokota Y, Inamura N, Asano M, Yamamoto Y, Nakahara K, Notsu Y, Ono T, Watanabe M
Exploratory Research Laboratories, Fujisawa Pharmaceutical Co., Ltd., Ibaraki, Japan.
Eur J Pharmacol. 1994 Jun 13;258(3):239-46. doi: 10.1016/0014-2999(94)90485-5.
This study aimed to evaluate the effect of FR128998, (1s,6s)-1-benzyl-10-(3-pyridyl-methyl)-7-thia-10-azaspiro [5,6]-dodecan-11-one 7,7-dioxide hydrochloride, a novel platelet activating factor (PAF) receptor antagonist, on endotoxin lipopolysaccharide-induced disseminated intravascular coagulation in rats. Experimental disseminated intravascular coagulation was induced by an infusion of lipopolysaccharide at 0.25 mg/kg/h for 4 h. Simultaneous infusion of FR128998 (0.25 and 1.0 mg/kg/h) with lipopolysaccharide dose dependently inhibited thrombocytopenia, but not leukopenia. The changes in coagulation parameters of disseminated intravascular coagulation, i.e., prolongation of activated partial thromboplastin time and elevated levels of fibrinogen/fibrin degradation products, were also prevented by the treatment with FR128998. In addition, FR128998 attenuated the increase in serum tumor necrosis factor (TNF) which appeared during the initial stage of disseminated intravascular coagulation. FR128998 (10 microM) also inhibited the TNF production by peripheral blood leukocytes or alveolar macrophages stimulated by lipopolysaccharide in vitro. Furthermore, TNF production induced by PAF itself in vitro was also inhibited in the presence of FR128998. These data indicate that PAF plays a pivotal role in the development of disseminated intravascular coagulation via TNF production.
本研究旨在评估新型血小板活化因子(PAF)受体拮抗剂FR128998((1s,6s)-1-苄基-10-(3-吡啶基-甲基)-7-硫杂-10-氮杂螺[5,6]-十二烷-11-酮7,7-二氧化物盐酸盐)对大鼠内毒素脂多糖诱导的弥散性血管内凝血的影响。通过以0.25 mg/kg/h的速度输注脂多糖4小时来诱导实验性弥散性血管内凝血。同时输注FR128998(0.25和1.0 mg/kg/h)与脂多糖可剂量依赖性地抑制血小板减少,但不能抑制白细胞减少。用FR128998治疗也可预防弥散性血管内凝血凝血参数的变化,即活化部分凝血活酶时间延长和纤维蛋白原/纤维蛋白降解产物水平升高。此外,FR128998可减轻弥散性血管内凝血初始阶段出现的血清肿瘤坏死因子(TNF)升高。FR128998(10 microM)在体外也可抑制脂多糖刺激的外周血白细胞或肺泡巨噬细胞产生TNF。此外,在存在FR128998的情况下,PAF自身在体外诱导的TNF产生也受到抑制。这些数据表明,PAF通过产生TNF在弥散性血管内凝血的发生发展中起关键作用。