McDonough K H, Chen V, Spitzer J J
Am J Physiol. 1987 Apr;252(4 Pt 2):H788-95. doi: 10.1152/ajpheart.1987.252.4.H788.
Effect of a chronic excess or deficit of thyroid hormone on intrinsic myocardial performance in rats was assessed. Animals were thyroidectomized or treated with thyroid hormone or vehicle 6-7 wk before the study. Body weight and heart weight were decreased in the hypothyroid group, and heart weight was elevated in the hyperthyroid group. Hearts were removed from thyroidectomized, euthyroid or thyroid-treated animals and studied as isolated, perfused working heart preparations. Ventricular function curves were generated by increasing left atrial filling pressure, whereas outflow resistance was not varied. Coronary flow, aortic outflow (and thus cardiac output), heart rate, and peak aortic systolic pressure were measured as a function of preload. These studies showed that performance of hearts from hyperthyroid animals was similar to that of euthyroid controls. Hearts from hypothyroid rats had decreased rate, pressure, and cardiac output but normal stroke volume. Since heart weight was 55% lower than control, normalization of volume work to dry heart weight reversed the difference in cardiac output. Comparison of hearts from hypothyroid animals to control rats of similar weight showed minimal differences in pump function. Thus hyperthyroidism did not result in altered in vitro cardiac output or peak systolic pressure as a function of changing preload when compared with age-matched euthyroid controls, hypothyroidism resulted in a decreased in vitro heart rate but greater cardiac output normalized to heart weight when compared with age-matched controls and hyperthyroid animals; external pacing of hypothyroid hearts yielded myocardial work parameters that were comparable to euthyroid control rats of similar body weight; and cardiac efficiency was significantly greater in hypothyroid hearts than in hyperthyroid hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
评估了甲状腺激素长期过量或不足对大鼠心肌内在性能的影响。在研究前6 - 7周，对动物进行甲状腺切除、甲状腺激素治疗或给予赋形剂。甲状腺功能减退组的体重和心脏重量降低，甲状腺功能亢进组的心脏重量升高。从甲状腺切除、甲状腺功能正常或接受甲状腺治疗的动物身上取出心脏，作为离体灌注工作心脏标本进行研究。通过增加左心房充盈压生成心室功能曲线，而流出阻力不变。测量冠状动脉血流量、主动脉流出量（从而计算心输出量）、心率和主动脉收缩压峰值作为前负荷的函数。这些研究表明，甲状腺功能亢进动物的心脏性能与甲状腺功能正常的对照组相似。甲状腺功能减退大鼠的心脏心率、压力和心输出量降低，但每搏量正常。由于心脏重量比对照组低55%，将容积功归一化至干心脏重量可逆转心输出量的差异。将甲状腺功能减退动物的心脏与体重相似的对照大鼠的心脏进行比较，发现泵功能差异极小。因此，与年龄匹配的甲状腺功能正常的对照组相比，甲状腺功能亢进在改变前负荷时不会导致体外心输出量或收缩压峰值改变；与年龄匹配的对照组和甲状腺功能亢进动物相比，甲状腺功能减退导致体外心率降低，但以心脏重量归一化后的心脏输出量更大；甲状腺功能减退心脏的外部起搏产生的心肌工作参数与体重相似的甲状腺功能正常的对照大鼠相当；甲状腺功能减退心脏的心脏效率明显高于甲状腺功能亢进心脏。（摘要截选至25０字）
