Hock C E, Lefer A M
Circ Shock. 1985;17(4):263-72.
We studied the effects of a selective antagonist of LTD4 (LY-171883, 2 and 4 mg/kg) in traumatic shock. Anesthetized rats subjected to Noble-Collip drum trauma developed a shock state characterized by a survival time of 1.7 +/- 0.3 h, a sixfold increase in plasma cathepsin D activity, and a fourfold increase in plasma myocardial depressant factor (MDF) activity. Administration of LY-171883 did not significantly inhibit the release of the lysosomal hydrolase cathepsin D during traumatic shock. However, LY-171883 (2 mg/kg) significantly attenuated the accumulation of MDF activity in the plasma (51 +/- 2 vs 37 +/- 3 U/ml), vehicle vs drug, respectively, and significantly (p less than 0.02) prolonged survival time to 2.7 +/- 0.2 h. Administration of the antagonist at a dose of 4 mg/kg further improved survival time (3.4 +/- 0.6 h, p less than 0.01) and additionally blunted circulating MDF activities compared to traumatized rats given only the vehicle. LY-171883 was found to antagonize the bronchoconstrictor effect of LTD4 given intravenously to anesthetized rats as well as the coronary vasoconstrictor actions of LTD4 in vitro. The beneficial effect of LTD4 antagonism in the present study is consistent with the concept that peptide leukotrienes are important mediators of the pathogenesis of traumatic shock.
我们研究了白三烯D4(LTD4)的选择性拮抗剂(LY - 171883,2毫克/千克和4毫克/千克)对创伤性休克的影响。接受诺布尔 - 科利普鼓式创伤的麻醉大鼠出现休克状态,其特征为存活时间为1.7±0.3小时,血浆组织蛋白酶D活性增加6倍,血浆心肌抑制因子(MDF)活性增加4倍。给予LY - 171883并不能显著抑制创伤性休克期间溶酶体水解酶组织蛋白酶D的释放。然而,LY - 171883(2毫克/千克)显著减弱了血浆中MDF活性的积累(分别为51±2与37±3单位/毫升,即对照组与药物组),并显著(p<0.02)延长存活时间至2.7±0.2小时。以4毫克/千克的剂量给予拮抗剂进一步改善了存活时间(3.4±0.6小时,p<0.01),并且与仅给予对照剂的创伤大鼠相比,还减弱了循环中的MDF活性。发现LY - 171883可拮抗静脉注射给麻醉大鼠的LTD4的支气管收缩作用以及LTD4在体外的冠状血管收缩作用。本研究中LTD4拮抗作用的有益效果与肽白三烯是创伤性休克发病机制的重要介质这一概念一致。