Institute for Pathophysiology West German Heart and Vascular Center, University of Essen Medical School, Essen, Germany.
Environmentally-induced cardiovascular degeneration, Institute of Clinical Chemistry and Diagnostics, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany.
Int J Cardiol. 2022 Sep 15;363:159-162. doi: 10.1016/j.ijcard.2022.06.050. Epub 2022 Jun 18.
In patients undergoing interventional or surgical coronary revascularization, subclinical hypothyroidism is common and associated with worse outcome, including the need for postoperative inotropic support. In isolated rat hearts with global ischemia/reperfusion, exogenous triiodothyronine (T3) reduces infarct size. Aim of this study was, to investigate whether or not exogenous T3 protects human myocardium from ischemia/reperfusion injury.
Right atrial trabeculae from patients undergoing routine coronary artery bypass grafting were isolated and transferred to Tyrode's buffer. Electrically initiated (1 Hz) contractile stress (mN/mm) was recorded for 10 min at baseline (95% O/ 5% CO, glucose). Sixty min hypoxia were induced by changing buffer gas and increasing stimulation rate (95% N/ 5% CO, choline chloride, 3 Hz) before return to reoxygenation for 30 min. T3 (500 μg/l) vs. NaOH (solvent control) was administered A) throughout (n = 11 vs. n = 9) or B) only 15 min before and during reoxygenation (n = 12 vs. n = 13). Western blot analyses of established cardioprotective signaling proteins were performed.
At baseline, contractile stress was comparable. T3 improved the cumulative recovery of contractile stress during reoxygenation from 41 ± 16 with NaOH to 55 ± 11% of baseline with T3, when given continuously in A or from 52 ± 13 with NaOH to 63 ± 11% of baseline with T3 when given just before and during reoxygenation in B. The ratio of mitochondrial complex I matrix arm to membrane NADH:ubiquinone oxidoreductase subunits (NDUF)V2 to NDUFA9 was reduced, reflecting increased complex I activity.
T3 increases contractile recovery of human right atrial trabeculae from hypoxia/reoxygenation.
在接受介入或手术冠状动脉血运重建的患者中，亚临床甲状腺功能减退症很常见，并且与更差的结果相关，包括需要术后正性肌力支持。在整体缺血/再灌注的孤立大鼠心脏中，外源性三碘甲状腺原氨酸（T3）可减少梗死面积。本研究的目的是，研究外源性 T3 是否可以保护人体心肌免受缺血/再灌注损伤。
从接受常规冠状动脉旁路移植术的患者的右心房小梁中分离出来，并转移到 Tyrode 缓冲液中。以 1 Hz 的电刺激引发收缩力（mN/mm），在基线时记录 10 分钟（95% O/5% CO，葡萄糖）。60 分钟缺氧通过改变缓冲气体并增加刺激率（95% N/5% CO，氯化胆碱，3 Hz）来诱导，然后再进行 30 分钟的复氧。T3（500 μg/l）与 NaOH（溶剂对照）A）持续（n=11 与 n=9）或 B）仅在复氧前 15 分钟和复氧期间给予（n=12 与 n=13）。进行了已建立的心脏保护信号蛋白的 Western blot 分析。
在基线时，收缩力是可比的。T3 改善了复氧期间收缩力的累积恢复，从用 NaOH 的 41±16%恢复到用 T3 的 55±11%的基线，当持续给予 A 或从用 NaOH 的 52±13%恢复到用 T3 的 63±11%的基线，当仅在复氧前和复氧期间给予 B 时。线粒体复合物 I 基质臂与膜 NADH：泛醌氧化还原酶亚基（NDUF）V2 到 NDUFA9 的比值降低，反映出复合物 I 活性增加。
T3 增加了人右心房小梁从缺氧/再氧合中收缩力的恢复。
