From the Department of Anesthesiology, University Hospital Duesseldorf, Duesseldorf, Germany.
Institute of Cardiovascular Physiology, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany.
Anesth Analg. 2018 Feb;126(2):439-442. doi: 10.1213/ANE.0000000000002230.
Prior studies have suggested that the antifibrinolytic drug aprotinin increases the infarct size after ischemia and reperfusion (I/R) and attenuates the effect of ischemic preconditioning (IPC). Aprotinin was replaced by tranexamic acid (TXA) in clinical practice. Here, we investigated whether TXA influences I/R injury and/or cardioprotection initiated by IPC and/or remote ischemic preconditioning (RIPC). Anesthetized male Wistar rats were randomized to 6 groups. Control animals were not further treated. Administration of TXA was combined with and without IPC and RIPC. Estimated treatment effect was 20%. Compared to control group (56% ± 11%), IPC reduced infarct size by 46% (30% ± 6%; mean difference, 26%; 95% confidence interval, 19-33; P < .0001), and RIPC reduced infarct size by 29% (40% ± 8%; mean difference, 16%; 95% confidence interval, 9-24; P < .011). Additional application of TXA had no effect on I/R injury and cardioprotection by IPC or RIPC. TXA does not abolish infarct size reduction by IPC or RIPC.
先前的研究表明，抗纤维蛋白溶解药物抑肽酶会增加缺血再灌注（I/R）后的梗死面积，并减弱缺血预处理（IPC）的作用。在临床实践中，抑肽酶已被氨甲环酸（TXA）取代。在这里，我们研究了 TXA 是否会影响由 IPC 和/或远程缺血预处理（RIPC）引发的 I/R 损伤和/或心脏保护作用。麻醉雄性 Wistar 大鼠被随机分为 6 组。对照组未进行进一步治疗。给予 TXA 联合或不联合 IPC 和 RIPC。估计治疗效果为 20%。与对照组（56%±11%）相比，IPC 使梗死面积减少了 46%（30%±6%；平均差异，26%；95%置信区间，19-33；P<.0001），RIPC 使梗死面积减少了 29%（40%±8%；平均差异，16%；95%置信区间，9-24；P<.011）。另外应用 TXA 对 IPC 或 RIPC 的 I/R 损伤和心脏保护作用没有影响。TXA 不会消除 IPC 或 RIPC 引起的梗死面积减少。
