Whittle B J, Boughton-Smith N K, Hutcheson I R, Esplugues J V, Wallace J L
Department of Mediator Pharmacology, Wellcome Research Laboratories, Beckenham, Kent.
Br J Pharmacol. 1987 Sep;92(1):3-4. doi: 10.1111/j.1476-5381.1987.tb11287.x.
Platelet-activating factor (Paf) has been proposed as a mediator of the gastrointestinal damage in endotoxic shock. The formation of Paf in rat jejunal tissue, determined following extraction and bioassay on rabbit washed platelets has therefore been correlated with the induction of damage following endotoxin administration. Intravenous injection of E. coli endotoxin led to a time-dependent increase in the jejunal formation of Paf, which after 20 min was twenty fold greater than the control level. There was a significant correlation between elevated Paf release and intestinal hyperaemia and haemorrhage, thus supporting a role for Paf as a mediator of such damage.
血小板活化因子(PAF)被认为是内毒素休克时胃肠道损伤的介质。因此,通过对兔洗涤血小板进行提取和生物测定来确定大鼠空肠组织中PAF的形成,已与内毒素给药后损伤的诱导相关联。静脉注射大肠杆菌内毒素导致空肠PAF形成呈时间依赖性增加,20分钟后比对照水平高20倍。PAF释放升高与肠道充血和出血之间存在显著相关性,从而支持PAF作为这种损伤介质的作用。