Carter L S, Mueller R A, Norfleet E A, Payne F B, Saltzman L S
Circ Res. 1987 May;60(5):649-52. doi: 10.1161/01.res.60.5.649.
Isolated perfused paced hearts from rats rendered hypothyroid by chronic administration of propylthiouracil have a delayed onset of ischemia-induced myocardial contracture in contrast to hearts from control rats. In addition, the time to reach maximum contracture is delayed, and the magnitude of the contracture pressure is reduced. Preischemia myocardial adenosine triphosphate (ATP) values in the hypothyroid rat hearts are similar to those of control, but the rate of decrease in ATP is slower in the hearts of hypothyroid rats. Thus, it appears that in the hypothyroid state the development of ischemic contracture is associated with a slower fall of ATP.
通过长期给予丙硫氧嘧啶使大鼠甲状腺功能减退，分离灌注并起搏的这些大鼠心脏，与对照大鼠的心脏相比，缺血诱导的心肌挛缩起始延迟。此外，达到最大挛缩的时间延迟，并且挛缩压力的幅度降低。甲状腺功能减退大鼠心脏缺血前的心肌三磷酸腺苷（ATP）值与对照相似，但甲状腺功能减退大鼠心脏中ATP的降低速率较慢。因此，似乎在甲状腺功能减退状态下，缺血性挛缩的发展与ATP的较慢下降有关。
