甲状腺激素T_3增补于心脏停搏液中对心肌的保护作用

Effects of triiodothyronine supplement in cardioplegia on postischemic myocardium

目的 探讨Ｔ３ 增补于停搏液中的心肌保护作用。方法 离体鼠心（ ｎ ＝ １６） 在改良的ＬａｎｇｅｎｄｏｒｆｆＮｅｅｌｙ 灌注模型上、３７ ℃下经历２０ 分钟预灌注、２０ 分钟停搏、３０ 分钟再灌注。结果 再灌注３０ 分钟时，左室功能指标（ＬＶＤＰｄｐ／ｄｔ）百分恢复率治疗组显著高于对照组（ Ｐ ＜０ ．０１），心肌超氧化物歧化酶（ＳＯＤ） 治疗组显著高于对照组（ Ｐ＜ ０．０１），过氧化脂质（ＬＰＯ） 治疗组显著低于对照组（ Ｐ ＜０．０５）；心肌酶（ＨＢＤＨ．ＬＤＨ）释放量再灌注期对应时点组间比较，治疗组显著低于对照组（ Ｐ＜ ０ ．０１） ；电镜观察心肌超微结构，治疗组显著优于对照组。结论 Ｔ３ 增补于心脏停搏液中可以显著地促进缺血后左室功能的恢复，显著减轻心肌缺血再灌注损伤，具有良好的心肌保护作用。

Objective To study the protective effects of triiodothyronine supplement in cardioplegia on postischemic myocardium. Methods Isolated rat hearts (n=16) were subjected to preperfusion for 20 min, ischemia for 20min and reperfusion for 30 min using a modified Langendorff Neely model with modified Krebs Henseleit buffer at 37℃. Results Percent recovery of left ventricular developing pressure (LVDP) and its first derivate (dp/dt) in the treated group 30 min after reperfusion were significantly increased as compared with control group (P<0.01). Comparison of postischemic myocardial superoxidas dismutase (SOD) between two groups demonstrated a significant increase in the treated group (P<0.01), while the comparison of postischemic myocardial lipid peroxide (LPO) between two groups demonstrated a significant decrease in the treated group (P<0.05). The release of postischemic myocardial enzyme (HBDH, LDH) in the treated group was significantly lower than in the control group (P<0.01). Myocardial ultrastructure was well preserved in the treated group. Conclusion T 3 supplement in cardioplegia significantly improve the recovery of postischemic left ventricular function, alleviated reperfusion mediated myocardial injury after global ischemia, suggesting good myocardioprotective actions.