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首页> 外文期刊>American Journal of Physiology >Oxidant species trigger late preconditioning against myocardial stunning in conscious rabbits.
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Oxidant species trigger late preconditioning against myocardial stunning in conscious rabbits.

机译：氧化剂会触发清醒兔抗心肌电晕的后期预处理。

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摘要

Conscious rabbits underwent six 4-min occlusion and 4-min reperfusion cycles for 3 consecutive days (day 1, 2, and 3); on day 1, rabbits received intravenous vehicle [preconditioning (PC)] (group I, n = 6), superoxide dismutase (SOD; group II, n = 5), catalase (group III, n = 6), or the hydroxyl radical (. OH) and peroxynitrite (ONOO-)) scavenger N-2-mercaptopropionyl glycine (MPG [group IV], n = 6). In the PC group, the recovery of systolic wall thickening (WTh) after the sixth reperfusion was markedly improved on days 2 and 3 compared with day 1 and the total deficit of WTh was correspondingly reduced, indicating a late PC effect against myocardial stunning. Neither SOD nor catalase had any significant effect on the severity of stunning on day 1 or on the development of late PC on days 2 and 3, despite high plasma levels. In contrast, MPG markedly attenuated the severity of stunning on day 1 and prevented the development of late PC on day 2. Two additional groups of rabbits received an intracoronary infusion of vehicle (group V, n = 4) or the reactive oxygen species (ROS) generating solution [cumene hydroperoxide (CuOOH, group VI, n = 7)] on day 0, and were then subjected to the six occlusion/reperfusion cycles on days 1, 2, and 3. In group VI, infusion of CuOOH elicited a late PC effect 24 h later (on day 1). Taken together, these results demonstrate that oxidant species play an essential role in triggering the development of late PC against stunning in conscious rabbits. The fact that late PC was blocked by MPG and mimicked by CuOOH implicate ONOO- and/or .OH as the oxygen species responsible for the initiation of this phenomenon. In addition, the finding that exogenous ROS (CuOOH) reproduced the phenotype of late PC indicates that ROS are not only necessary but also sufficient to trigger this defensive adaptation of the heart to stress.
机译：清醒的兔子连续三个天（第1、2和3天）经历6次4分钟闭塞和4分钟再灌注周期;在第1天，兔子接受了静脉溶媒[预处理（PC）]（I组，n = 6），超氧化物歧化酶（SOD; II组，n = 5），过氧化氢酶（III组，n = 6）或羟基自由基（。OH）和过氧亚硝酸盐（ONOO-））清除剂N-2-巯基丙酰甘氨酸（MPG [IV组]，n = 6）。在PC组中，与第1天相比，第6天再灌注后第6和第3天的收缩期壁增厚（WTh）的恢复显着改善，并且WTh的总缺乏症相应减少，表明晚期PC效应可防止心肌电晕。尽管血浆水平很高，但SOD和过氧化氢酶对第1天惊厥的严重程度或第2天和第3天晚期PC的发育均无明显影响。相比之下，MPG在第1天显着减轻了惊厥的严重性，并在第2天阻止了晚期PC的发展。另外两组兔子接受了冠状动脉内注入媒介物（V组，n = 4）或活性氧（ROS） ）在第0天产生溶液[氢过氧化枯烯（CuOOH，VI组，n = 7）]，然后在第1、2和3天进行六个闭塞/再灌注循环。在VI组中，注入CuOOH引起晚期PC效应在24小时后（第1天）。综上所述，这些结果表明，氧化剂物种在触发晚期PC的发展中起着至关重要的作用。晚期PC被MPG阻止并被CuOOH模仿的事实暗示ONOO-和/或.OH是导致这种现象发生的氧。此外，外源性ROS（CuOOH）再现了晚期PC的表型的发现表明，ROS不仅是触发心脏防御性适应压力的必要条件，而且还足以触发这种防御方式。

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