Department of Cardiovascular Surgery, Nippon Medical School Chiba Hokusoh Hospital, Inzai, Chiba, Japan.
Department of Cardiovascular Surgery, Nippon Medical School, Tokyo, Japan.
Ann Thorac Cardiovasc Surg. 2024;30(1). doi: 10.5761/atcs.oa.24-00034.
Esaxerenone, a mineralocorticoid receptor blocker, attenuates global ischemia-induced myocardial damage and coronary endothelial dysfunction. This study aimed to determine whether esaxerenone exerted cardioprotective effects against cardioplegic arrest in Wistar rat hearts.
Isolated male Wistar rat hearts aerobically perfused via the Langendorff method for 20 min were randomly allocated to the Control (n = 6; perfused for an additional 10 min and subjected to no treatment) or Esax (n = 6; perfused with 0.1 μmol/L esaxerenone in perfusate for 10 min before ischemia) groups. Hearts in both groups were perfused with St. Thomas' Hospital No. 2 solution (STH2) for 2 min and subjected to 28 min of global ischemia. The recovery of left ventricular developed pressure (LVDP) and total troponin T leakage were measured after reperfusion.
The final recovery of LVDP (expressed as a percentage of pre-ischemic value) in the Control and Esax groups was 50.8 ± 3.5% and 62.1 ± 5.6%, respectively (p <0.05, Esax vs. Control). The total troponin T leakage in the Control and Esax groups was 138.8 ± 18.5 ng/g heart wt and 74.3 ± 18.6 ng/g heart wt, respectively (p <0.05, Esax vs. Control).
The administration of esaxerenone before cardioplegic arrest enhanced the cardioprotective effect exerted by STH2.
依普利酮作为一种盐皮质激素受体阻滞剂,可减轻全脑缺血引起的心肌损伤和冠状动脉内皮功能障碍。本研究旨在确定依普利酮是否对 Wistar 大鼠心脏停搏心肌具有保护作用。
采用 Langendorff 法体外循环灌流雄性 Wistar 大鼠心脏 20 min,随机分为对照组(n = 6;再灌流 10 min,不做任何处理)和依普利酮组(n = 6;缺血前用 0.1 μmol/L 依普利酮灌流液灌流 10 min)。两组心脏均用 St.Thomas' Hospital No.2 溶液(STH2)灌流 2 min,然后进行 28 min 全脑缺血。再灌注后测量左心室发展压(LVDP)和总肌钙蛋白 T 漏出的恢复情况。
对照组和依普利酮组的 LVDP 最终恢复率(以缺血前值的百分比表示)分别为 50.8 ± 3.5%和 62.1 ± 5.6%(p <0.05,依普利酮组 vs. 对照组)。对照组和依普利酮组的总肌钙蛋白 T 漏出量分别为 138.8 ± 18.5 ng/g 心脏重和 74.3 ± 18.6 ng/g 心脏重(p <0.05,依普利酮组 vs. 对照组)。
停搏前给予依普利酮可增强 STH2 的心脏保护作用。