Levitt M A, Stahl G, Lefer A M
Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107.
Resuscitation. 1988 Jul;16(3):211-20. doi: 10.1016/0300-9572(88)90047-0.
The effects of a thromboxane receptor antagonist having lipoxygenase inhibitory activity, L-655,240 (3-[1-(4-chlorobenzyl)-5-fluoro-3-methyl-indol-2-yl]2,2-dimethylpropa noic acid) (1 mg/kg per h) were studied in a standardized model of traumatic shock. Pentobarbital (35 mg/kg) anesthetized rats subjected to Noble-Collip drum trauma were characterized by a 82 +/- 12 min survival time, a 20-fold increase in plasma cathepsin D activity, and a 6-fold increase in plasma myocardial depressant factor (MDF) activity. L-655,240 significantly attenuated the accumulation of MDF activity in the plasma (74 +/- 3 vs. 46 +/- 4 units/ml), vehicle vs. drug, respectively, and significantly (P less than 0.01) prolonged survival time to 206 +/- 26 min. However, plasma cathepsin D was not significantly altered with L-655,240 administration during traumatic shock. L-655,240 at 20 micrograms/ml markedly attenuated minced rat lung fragments from producing LTC4 and LTD4.L-655,240 exhibited significant anti-proteolytic activity in pancreatic homogenates. Therefore, L-655,2340 does not stabilize lysosomal membranes directly, but exerts an anti-proteolytic action which appears to curtail the production of a myocardial depressant factor by the ischemic pancreas, thus protecting during traumatic shock. A combination anti-eicosanoid drug such as L-655,240 may therefore prove to be an important therapeutic agent in acute ischemic disorders including traumatic shock.
在创伤性休克的标准化模型中研究了具有脂氧合酶抑制活性的血栓素受体拮抗剂L-655,240(3-[1-(4-氯苄基)-5-氟-3-甲基-吲哚-2-基]-2,2-二甲基丙酸)(每小时1毫克/千克)的作用。戊巴比妥(35毫克/千克)麻醉下遭受Noble-Collip鼓式创伤的大鼠的特征为存活时间82±12分钟、血浆组织蛋白酶D活性增加20倍以及血浆心肌抑制因子(MDF)活性增加6倍。L-655,240显著减弱了血浆中MDF活性的积累(分别为74±3与46±4单位/毫升,溶剂对照与药物组),并显著(P<0.01)延长存活时间至206±26分钟。然而,在创伤性休克期间给予L-655,240后,血浆组织蛋白酶D没有显著改变。20微克/毫升的L-655,240显著减弱了大鼠肺组织碎块产生LTC4和LTD4的能力。L-655,240在胰腺匀浆中表现出显著的抗蛋白水解活性。因此,L-655,2340不是直接稳定溶酶体膜,而是发挥抗蛋白水解作用,这似乎减少了缺血胰腺产生的心肌抑制因子,从而在创伤性休克期间起到保护作用。因此,像L-655,240这样的联合抗类花生酸药物可能被证明是包括创伤性休克在内的急性缺血性疾病的重要治疗药物。