左甲状腺素诱导的心脏肥大加重大鼠的缺血性损伤和再灌注心律失常。

Heart hypertrophy induced by levothyroxine aggravates ischemic lesions and reperfusion arrhythmias in rats.

作者信息

Yu F, Dai D Z, An L F, Guo X F

机构信息

Research Division of Pharmacology, China Pharmaceutical University, Nanjing, China.

出版信息

Zhongguo Yao Li Xue Bao. 1997 Jan;18(1):71-4.

PMID:10072899

Abstract

AIM

To develop a cardiac hypertrophic model in rats.

METHODS

Rats were i.p. levothyroxine 0.5 mg.kg-1.d-1 x 10 d. The action potentials of right papillary muscles were recorded by standard glass-microelectrode technique. The left coronary artery was ligated followed by reperfusion and the apparent infarcted zone (AIZ) was determined by tetracycline fluoresence, and the superoxide dismutase (SOD) activity and malondialdehyde (MDA) product in myocardium were also measured.

RESULTS

In the rats treated by levothyroxine, the heart was hypertrophic and the action potential duration (APD) and effective refractory period (ERP) were prolonged, the APD20, APD50, APD90, and ERP were prolonged by 80%, 79%, 74%, and 68%, respectively. No changes in resting potential (RP), action potential amplitude (APA), and Vmax were produced. The incidence of heart arrest (8/8) and the risk of death (67 +/- 0) induced by ischemia-reperfusion in rats with hypertrophic heart was higher than those in normal rats (4/10 and 44 +/- 19, respectively). The AIZ was expanded markedly in hypertrophic heart, and attenuated by lidocaine and propranolol.

CONCLUSION

Levothyroxine-induced heart hypertrophy is a suitable model for severe ischemia and arrhythmias in rats.

摘要

目的

建立大鼠心脏肥厚模型。

方法

大鼠腹腔注射左旋甲状腺素0.5mg·kg-1·d-1，共10天。采用标准玻璃微电极技术记录右乳头肌动作电位。结扎左冠状动脉后再灌注，通过四环素荧光法测定明显梗死区（AIZ），并检测心肌中超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量。

结果

左旋甲状腺素处理的大鼠心脏肥厚，动作电位时程（APD）和有效不应期（ERP）延长，APD20、APD50、APD90和ERP分别延长80%、79%、74%和68%。静息电位（RP）、动作电位幅度（APA）和最大上升速率（Vmax）无变化。肥厚心脏大鼠缺血再灌注诱导的心脏停搏发生率（8/8）和死亡风险（67±0）高于正常大鼠（分别为4/10和44±19）。肥厚心脏的AIZ明显扩大，利多卡因和普萘洛尔可使其减轻。