Levitt M A, Lefer A M
Crit Care Med. 1987 Aug;15(8):769-73. doi: 10.1097/00003246-198708000-00012.
The effects of prostaglandin E1 (PGE1) were studied in a standardized model of traumatic shock in rats. Pentobarbital anesthetized rats were subjected to standardized drum trauma of 525 revolutions in a Noble-Collip drum. These traumatized rats were characterized by a survival time of 108 +/- 19 min, a 12-fold increase in plasma cathepsin D activity, and a three-fold increase in plasma myocardial depressant factor (MDF) activity. PGE1 (1.2 micrograms/kg X min) significantly improved survival time during traumatic shock (191 +/- 29 vs. 108 +/- 19 min), drug vs. vehicle, respectively (p less than .03). In addition, PGE1 significantly attenuated plasma MDF activity during traumatic shock (58 +/- 10 vs. 27 +/- 7 U/ml), vehicle vs. drug, respectively (p less than .02). Plasma cathepsin D activity was also significantly retarded (12.1 +/- 1.8 vs. 1.70 +/- 1.50 U/ml), vehicle vs. drug, respectively (p less than .01). PGE1 appears to exert a membrane stabilizing effect, decreasing plasma cathepsin D and attenuating MDF production. PGE1 thus appears to have significant antishock activity.
在大鼠创伤性休克的标准化模型中研究了前列腺素E1(PGE1)的作用。用戊巴比妥麻醉大鼠,使其在Noble - Collip鼓中接受525次旋转的标准化鼓式创伤。这些受创伤的大鼠的特征为存活时间为108±19分钟,血浆组织蛋白酶D活性增加12倍,血浆心肌抑制因子(MDF)活性增加3倍。PGE1(1.2微克/千克×分钟)显著改善了创伤性休克期间的存活时间(分别为191±29分钟与108±19分钟,药物组与溶媒组,p<0.03)。此外,PGE1显著减弱了创伤性休克期间的血浆MDF活性(分别为58±10与27±7 U/ml,溶媒组与药物组,p<0.02)。血浆组织蛋白酶D活性也显著受到抑制(分别为12.1±1.8与1.70±1.50 U/ml,溶媒组与药物组,p<0.01)。PGE1似乎发挥了膜稳定作用,降低了血浆组织蛋白酶D并减弱了MDF的产生。因此,PGE1似乎具有显著的抗休克活性。