Long-term physiological T3 supplementation in hypertensive heart disease in rats.

Long-term physiological T3 supplementation in hypertensive heart disease in rats.
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DOI:
10.1152/ajpheart.00431.2015
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发表时间:
2015-09
期刊:
American journal of physiology. Heart and circulatory physiology
影响因子:
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通讯作者:
N. Weltman;C. Pol;Youhua Zhang;Yibo Wang;Adrienne Koder;Sarah Raza;R. Zucchi;A. Saba;Daria Colli
N. Weltman;C. Pol;Youhua Zhang;Yibo Wang;Adrienne Koder;Sarah Raza;R. Zucchi;A. Saba;Daria Colli
中科院分区:
其他
文献类型:
--
作者:
N. Weltman;C. Pol;Youhua Zhang;Yibo Wang;Adrienne Koder;Sarah Raza;R. Zucchi;A. Saba;Daria Colli

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动物研究表明,高血压会导致心脏组织甲状腺功能减退,这种情况本身就会导致心力衰竭。我们之前已经表明,短期甲状腺激素治疗对心力衰竭附近的自发性高血压心力衰竭(SHHF)大鼠是有益的。本研究验证了SHHF大鼠治疗性长期T3治疗可以预防或减轻心功能障碍的假设。雌性SHHF大鼠于12 ~ 24月龄口服生理剂量T3 (0.04 μg/ml)。年龄匹配的雌性SHHF大鼠和Wistar-Kyoto大鼠分别作为高血压和正常血压的对照组。与血压正常的对照组相比,SHHF大鼠血清游离甲状腺激素水平和心脏组织T3水平降低,左室功能障碍,左室胶原含量升高。t3治疗大鼠血清和心脏组织甲状腺激素水平的恢复与心率无变化相关,但左室收缩功能和胶原蛋白水平有明显改善趋势。例如,与对照组相比,收缩期终末直径、分数缩短、收缩壁应力和左室胶原蛋白水平不再有显著差异。综上所述,长期高血压导致大鼠血清和心脏组织甲状腺激素水平慢性降低。低剂量T3长期治疗是安全的。虽然在没有抗高血压治疗的情况下不能完全预防心功能障碍,但T3作为一种辅助治疗可能会改善舒张功能,从而提供额外的益处。
Animal studies suggest that hypertension leads to cardiac tissue hypothyroidism, a condition that can by itself lead to heart failure. We have previously shown that short-term thyroid hormone treatment in Spontaneously Hypertensive Heart Failure (SHHF) rats near heart failure is beneficial. This study tested the hypothesis that therapeutic, long-term T3 treatment in SHHF rats can prevent or attenuate cardiac dysfunction. Female SHHF rats were treated orally with a physiological T3 dose (0.04 μg/ml) from 12 to 24 mo of age. Age-matched female SHHF and Wistar-Kyoto rats served as hypertensive and normotensive controls, respectively. SHHF rats had reduced serum free thyroid hormone levels and cardiac tissue T3 levels, LV dysfunction, and elevated LV collagen content compared with normotensive controls. Restoration of serum and cardiac tissue thyroid hormone levels in T3-treated rats was associated with no change in heart rate, but strong trends for improvement in LV systolic function and collagen levels. For instance, end-systolic diameter, fractional shortening, systolic wall stress, and LV collagen levels were no longer significantly different from controls. In conclusion, longstanding hypertension in rats led to chronic low serum and cardiac tissue thyroid hormone levels. Long-term treatment with low-dose T3 was safe. While cardiac dysfunction could not be completely prevented in the absence of antihypertensive treatment, T3 may offer additional benefits as an adjunct therapy with possible improvement in diastolic function.