Hsu R B, Huang T S, Chen Y S, Chu S H
Department of Surgery, National Taiwan University Hospital, Taipei.
J Endocrinol Invest. 1995 Oct;18(9):702-9. doi: 10.1007/BF03349792.
Twelve healthy pigs were subjected to a 20-min, period of regional myocardial ischemia by snaring the left anterior descending coronary artery (LAD) between its first and second diagonal branches. The resulting myocardial injury caused significant acute hemodynamic impairments. Cardiac index declined significantly during reperfusion interval and returned to preischemic level by postoperative day 7. Plasma total triiodothyronine (TT3), free triiodothyronine (FT3) and free fatty acid (FFA) decreased gradually and reached the nadir at 6 h after LAD occlusion. In contrast, plasma reverse triiodothyronine (rT3) increased progressively after LAD occlusion and reperfusion. To investigate the effect of T3 on ischemic myocardium, T3 (0.2 microgram/kg/dose; n = 5) or saline (placebo; n = 6) was administered immediately, 30 min, 60 min, 90 min, and 120 min after reperfusion. Plasma TT3 and FT3 increased dramatically after triiodothyronine supplement but declined to presichemic level at six h after LAD occlusion. The pigs treated with T3 demonstrated a rapid improvement in cardiac index over the reperfusion interval, whereas cardiac index in the placebo group remained depressed. Myocardial oxygen consumption estimated by rate pressure product showed no difference between placebo and T3-treated groups. Oxygen extraction as O2 saturation difference between aorta and coronary sinus was less in T3-treated group. Nine pigs (four in the T3-treated group and five in the placebo group) were subjected to euthanasia with hypertonic KCl solution on postoperative day 7. Myocardial infarct size determined by triphenyltetrazolium chloride (TTC) tissue enzyme staining technique was not significantly different between T3-treated and placebo groups. We concluded that this animal model is a useful model of myocardial injury simulating "euthyroid sick syndrome" as seen in patients with cardiopulmonary bypass, and T3 supplementation after reperfusion significantly enhanced postischemic left ventricular functional recovery but did not affect myocardial oxygen consumption and myocardial infarct size.
12只健康猪通过在左前降支冠状动脉（LAD）的第一和第二对角支之间套扎，使其经历20分钟的局部心肌缺血。由此产生的心肌损伤导致了显著的急性血流动力学损害。心脏指数在再灌注期间显著下降，并在术后第7天恢复到缺血前水平。血浆总三碘甲状腺原氨酸（TT3）、游离三碘甲状腺原氨酸（FT3）和游离脂肪酸（FFA）逐渐降低，并在LAD闭塞后6小时达到最低点。相反，血浆反三碘甲状腺原氨酸（rT3）在LAD闭塞和再灌注后逐渐升高。为了研究T3对缺血心肌的影响，在再灌注后立即、30分钟、60分钟、90分钟和120分钟给予T3（0.2微克/千克/剂量；n = 5）或生理盐水（安慰剂；n = 6）。补充三碘甲状腺原氨酸后血浆TT3和FT3显著升高，但在LAD闭塞后6小时降至缺血前水平。接受T3治疗的猪在再灌注期间心脏指数迅速改善,而安慰剂组的心脏指数仍处于较低水平。通过心率血压乘积估算的心肌耗氧量在安慰剂组和T3治疗组之间没有差异。T3治疗组中作为主动脉和冠状窦之间O2饱和度差异的氧摄取较少。9只猪（T3治疗组4只，安慰剂组5只）在术后第7天用高渗KCl溶液实施安乐死。通过氯化三苯基四氮唑（TTC）组织酶染色技术测定的心肌梗死面积在T3治疗组和安慰剂组之间没有显著差异。我们得出结论，该动物模型是一种模拟体外循环患者所见“正常甲状腺病态综合征”的心肌损伤有用模型，再灌注后补充T3显著增强了缺血后左心室功能恢复，但不影响心肌耗氧量和心肌梗死面积。
