In vivo and in vitro acute cardiovascular effects of bimoclomol

Andrea Jednákovits , Péter Ferdinándy , László Jaszlits , Tamás Bányász , János Magyar , Péter Szigligeti , Agnes Körtvély , József A Szentmiklósi , Péter P Nánási
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引用次数: 11

Abstract

Effects of bimoclomol, the novel heat shock protein (HSP) coinducer, was studied in various mammalian cardiac and rabbit aortic preparations. Bimoclomol decreased the ST-segment elevation induced by coronary occlusion in anesthetized dogs (56% and 80% reduction with 1 and 5 mg/kg, respectively). In isolated working rat hearts, bimoclomol increased coronary flow (CF), decreased the reduction of cardiac output (CO) and left ventricular developed pressure (LVDP) developing after coronary occlusion, and prevented ventricular fibrillation (VF) during reperfusion. In rabbit aortic preparations, precontracted with phenylephrine, bimoclomol induced relaxation (EC50=214 μM). Bimoclomol produced partial relaxation against 20 mM KCl, however, bimoclomol failed to relax preparations precontracted with serotonin, PGF2 or angiotensin II. All these effects were evident within a few minutes after application of bimoclomol. A rapid bimoclomol-induced compartmental translocation of the already preformed HSPs may explain the protective action of the compound.

双氯酚对体内和体外急性心血管的影响
本文研究了新型热休克蛋白(HSP)共诱导剂双氯酚在各种哺乳动物心脏和兔主动脉制剂中的作用。双氯酚降低麻醉犬冠状动脉闭塞引起的st段抬高(1和5 mg/kg分别降低56%和80%)。在离体工作大鼠心脏中,双氯酚增加冠状动脉血流(CF),降低冠状动脉闭塞后心输出量(CO)和左室发展压(LVDP)的减少,防止再灌注时心室颤动(VF)。在兔主动脉预备物中,苯肾上腺素预收缩,双氯酚诱导舒张(EC50=214 μM)。bimoclool对20mm KCl产生部分松弛作用,然而,bimoclool不能使血清素、PGF2或血管紧张素II预收缩的制剂松弛。所有这些效果在应用双氯苯后的几分钟内都很明显。双氯苯酚诱导的已经形成的热休克蛋白的快速区室易位可以解释该化合物的保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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