Rowe D J, Gedeon G, Broom J, Fleck A
Br J Exp Pathol. 1979 Dec;60(6):589-95.
After acclimatization to metabolic cages, groups of male Wistar rats were pretreated for 48 h with parenteral indomethacin to observe its effect on the biochemical response to femoral fracture stress. This trauma induced an average 2.3-fold rise in fibrinogen levels in all animals, which was maximal 24 h after injury. Indomethacin pretreatment caused a dose-related decrease in the plasma fibrinogen response 24 h after fracture: 1, 2, 10 or 20 mg/kg/day of drug reduced the response by approximately 3, 10, 13 and 23%. Fibrinogen levels in rats treated with high doses (10 and 20 mg/kg) of drug began to rise before fracture owing to intestinal ulceration. Plasma 11-hydroxycorticosteroids and urine total catecholamine levels did not respond to either indomethacin treatment or to fracture but levels of both compounds rose gradually during the experiment. Indomethacin is an inhibitor of prostaglandin synthesis and prostglandins may therefore be involved in the metabolic response to stress.
雄性Wistar大鼠适应代谢笼后,用胃肠外给予吲哚美辛预处理48小时,以观察其对股骨骨折应激生化反应的影响。这种创伤使所有动物的纤维蛋白原水平平均升高2.3倍,在受伤后24小时达到最大值。吲哚美辛预处理导致骨折后24小时血浆纤维蛋白原反应呈剂量相关下降:药物剂量为1、2、10或20mg/kg/天时,反应分别降低约3%、10%、13%和23%。高剂量(10和20mg/kg)药物治疗的大鼠由于肠道溃疡,在骨折前纤维蛋白原水平就开始升高。血浆11-羟基皮质类固醇和尿总儿茶酚胺水平对吲哚美辛治疗或骨折均无反应,但在实验过程中这两种化合物的水平均逐渐升高。吲哚美辛是前列腺素合成的抑制剂,因此前列腺素可能参与应激的代谢反应。