Yu P, Xiao G, Fu W
Burn Research Institute, Southwest Hospital, Third Military Medical College, Chongquing.
Zhonghua Wai Ke Za Zhi. 1995 Jul;33(7):393-5.
In order to investigate the roles of platelet activating factor (PAF) in postburn intestinal barrier injury, the changes in intestinal mucosal potential difference (PD), intestinal PAF, Phospholipase A2 (PLA2), myeloperoxidase (MPO) and malondialdehyde (MDA) were measured in a model of rats with 30% TBSA III degrees burns. The results showed that the intestinal PAF level was significantly elevated after severe burn and was negatively correlated with the decrease of intestinal mucosal PD (r = -0.94, P < 0.01). PAF antagonist WEB 2170 treatment could significantly inhibite the increase of PAF in intestinal tissue, enhance intestinal mucosal PD, attenuate the levels of PLA2, MPO and MDA in intestinal tissue, and alleviate the pathological changes in ileal mucosa, compared with the burn group. The results suggest that PAF is an important factor causing postburn intestinal mucosal barrier injury, and activation of leukocyte and PLA2 as well as the release of superoxide are important intermediate mechanisms for PAF leading to intestinal mucosal injury.
为探讨血小板活化因子(PAF)在烧伤后肠屏障损伤中的作用,在30%总体表面积Ⅲ度烧伤大鼠模型中,测定肠黏膜电位差(PD)、肠PAF、磷脂酶A2(PLA2)、髓过氧化物酶(MPO)和丙二醛(MDA)的变化。结果显示,严重烧伤后肠PAF水平显著升高,且与肠黏膜PD降低呈负相关(r = -0.94,P < 0.01)。与烧伤组相比,PAF拮抗剂WEB 2170治疗可显著抑制肠组织中PAF的增加,增强肠黏膜PD,降低肠组织中PLA2、MPO和MDA水平,并减轻回肠黏膜的病理变化。结果提示,PAF是导致烧伤后肠黏膜屏障损伤的重要因素,白细胞和PLA2的激活以及超氧化物的释放是PAF导致肠黏膜损伤的重要中间机制。