1. The influence of hyperthyroidism on electrophysiological characteristics and on reperfusion arrhythmias was examined in rat hearts. 2. Electrophysiological studies were performed with glass microelectrodes, and the experiments on reperfusion arrhythmias were done in isolated perfused hearts. 3. Ventricular muscle from hyperthyroid rats was more prone than that from euthyroid rats to develop triggered activity under conditions believed to cause myoplasmic Ca2+ overload. 4. The severity of reperfusion arrhythmias was significantly enhanced in hyperthyroid preparations as compared with euthyroid ones. 5. The enhanced reperfusion arrhythmias in hyperthyroid rats were significantly reduced by propranolol (3 x 10(-7) M), lignocaine (1 x 10(-5) M) and verapamil (3 x 10(-8) M), but not by nadolol (3 x 10(-7) M) or prazosin (3 x 10(-7) M). 6. These results suggest that increased heart rate due to hyperthyroidism and responses mediated via either alpha- or beta-adrenoceptors were not dominant causes of enhanced reperfusion arrhythmias in hyperthyroid hearts. 7. The increased tendency to develop triggered activity which was observed in the electrophysiological study, may be one possible explanation of enhanced reperfusion arrhythmias in hyperthyroid hearts.
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机译：1.在大鼠心脏中检查了甲亢对电生理特征和对再灌注心律失常的影响。 2.用玻璃微电极进行电生理学研究，并在离体的灌注心脏中进行再灌注心律不齐的实验。 3.在认为会导致肌质Ca2 +超负荷的条件下，甲状腺功能亢进大鼠的心室肌比正常甲状腺大鼠的肌更容易触发活动。 4.与正常甲状腺的制剂相比，甲状腺功能亢进的制剂的再灌注心律不齐的严重程度明显增加。 5.普萘洛尔（3 x 10（-7）M），利多卡因（1 x 10（-5）M）和维拉帕米（3 x 10（-8）M）显着降低了甲状腺功能亢进大鼠的增强的再灌注性心律失常。而不是纳多洛尔（3 x 10（-7）M）或哌唑嗪（3 x 10（-7）M）。 6.这些结果表明，甲状腺功能亢进引起的心律加快以及通过α-或β-肾上腺素受体介导的反应并不是甲亢心脏中再灌注性心律失常增强的主要原因。 7.在电生理研究中观察到，发展触发活动的趋势增加，可能是甲状腺机能亢进心脏再灌注心律失常增强的一种可能解释。
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