Nishio M L, Ornatsky O I, Hood D A
School of Physical Education, York University, Canada.
Med Sci Sports Exerc. 1995 Nov;27(11):1500-8.
We evaluated mitochondrial adaptations in the hearts of euthyroid and hypothyroid rats subject to aortic constriction for 2, 4, 7, 14, 21, and 28 d to induce a pressure-overload (PO), compared to sham-operated (SH) controls. PO animals attained higher arterial pressures than SH animals, by 55% in the euthyroid group, but only 14% in hypothyroid rats after 28 d. The left ventricle/body weight ratio was increased 44% by PO in the euthyroid group, and 26% in the hypothyroid group. PO attenuated the decline in cardiac growth in the hypothyroid group. Thus, hypothyroidism reduces the magnitude of the PO, but not the potential for hypertrophy in response to PO. Cytochrome c oxidase activity (CYTOX) was unchanged by PO in the euthyroid animals, indicating that the synthesis of mitochondria paralleled adaptive growth. However, CYTOX activity decreased up to 20% in the hypothyroid groups (P < 0.05) and was unaltered by PO. Thus, PO prevented the decline in growth, but not the decline in mitochondrial enzymes due to hypothyroidism. The lack of effect of PO on mitochondria was partly due to pretranslational changes since CYTOX subunit VIc mRNA was reduced by PO in the hypothyroid animals, but not in the euthyroid group. Levels of the chaperones HSP60 and GRP75, as well as HSP60 mRNA were unaffected by hypothyroidism, but paralleled adaptive growth induced by PO. Hypothyroidism changes the pattern of gene expression within the heart leading to altered mitochondrial composition. This cannot be compensated for by conditions of increased physiological demand.
我们评估了甲状腺功能正常和甲状腺功能减退大鼠在主动脉缩窄2、4、7、14、21和28天以诱导压力超负荷（PO）后心脏中的线粒体适应性变化，并与假手术（SH）对照组进行比较。PO动物的动脉压高于SH动物，甲状腺功能正常组升高了55%，但甲状腺功能减退大鼠在28天后仅升高了14%。甲状腺功能正常组中PO使左心室/体重比增加了44%，甲状腺功能减退组增加了26%。PO减轻了甲状腺功能减退组心脏生长的下降。因此，甲状腺功能减退会降低PO的幅度，但不会降低对PO反应的肥大潜力。甲状腺功能正常的动物中PO未改变细胞色素c氧化酶活性（CYTOX），表明线粒体的合成与适应性生长平行。然而，甲状腺功能减退组中CYTOX活性下降高达20%（P<0.05），且不受PO影响。因此，PO阻止了生长下降，但没有阻止由于甲状腺功能减退导致的线粒体酶下降。PO对线粒体缺乏影响部分归因于翻译前的变化，因为甲状腺功能减退动物中PO使CYTOX亚基VIc mRNA减少，但甲状腺功能正常组未减少。伴侣蛋白HSP60和GRP75以及HSP60 mRNA的水平不受甲状腺功能减退影响，但与PO诱导的适应性生长平行。甲状腺功能减退会改变心脏内的基因表达模式，导致线粒体组成改变。这种情况无法通过生理需求增加的条件得到补偿。
