低甲状腺功能对自发性高血压心力衰竭大鼠心脏结构和功能的影响。
Effect of low thyroid function on cardiac structure and function in spontaneously hypertensive heart failure rats.
作者信息
Kisso Bassel, Patel Ankit, Redetzke Rebecca, Gerdes A Martin
机构信息
Cardiovascular Research Institute, Sanford Research/University of South Dakota, 1100 East 21st Street, Sioux Falls, SD 57105, USA.
出版信息
J Card Fail. 2008 Mar;14(2):167-71. doi: 10.1016/j.cardfail.2007.10.018.
BACKGROUND
Although low thyroid function is known to have detrimental effects on the cardiovascular system, including microvascular impairment, little is known about the pathophysiologic consequences of hypothyroidism in the background of hypertension.
METHODS AND RESULTS
Hypothyroidism was induced in female spontaneously hypertensive heart failure (SHHF) rats by treatment with propylthiouracil (PTU) for 6 months. Untreated SHHF and normotensive Wistar Furth (WF) rats served as controls. In terminal experiments, heart weight, echocardiographic measurements, hemodynamics, and arteriolar morphometry were performed. Left ventricular internal diameter in systole and diastole were increased and wall thickness, ejection fraction, heart rate, systolic blood pressure, and +/-dP/dt were significantly decreased in the treatment group. Surprisingly, there were no observed differences in arteriolar density among the 3 groups.
CONCLUSIONS
As expected, PTU treatment of SHHF rats led to systolic dysfunction and chamber dilation. However, PTU treatment did not lead to arteriolar loss as previously observed in normotensive rats treated with PTU. These finding suggest that induced hypothyroidism leads to detrimental changes in SHHF rats, but the overall effects were no worse than those previously observed in normotensive rats treated with PTU.
背景
尽管已知甲状腺功能低下对心血管系统有不利影响，包括微血管损伤，但对于高血压背景下甲状腺功能减退的病理生理后果知之甚少。
方法与结果
通过用丙硫氧嘧啶（PTU）治疗6个月，诱导雌性自发性高血压心力衰竭（SHHF）大鼠发生甲状腺功能减退。未治疗的SHHF大鼠和血压正常的Wistar Furth（WF）大鼠作为对照。在终末实验中，进行了心脏重量、超声心动图测量、血流动力学和小动脉形态测定。治疗组的左心室收缩末期内径和舒张末期内径增加，而壁厚、射血分数、心率、收缩压和+/-dP/dt显著降低。令人惊讶的是，3组之间的小动脉密度没有观察到差异。
结论
正如预期的那样，PTU治疗SHHF大鼠导致收缩功能障碍和心室扩张。然而，PTU治疗并未导致如先前在用PTU治疗的血压正常大鼠中所观察到的小动脉损失。这些发现表明，诱导的甲状腺功能减退会导致SHHF大鼠出现有害变化，但总体影响并不比先前在用PTU治疗的血压正常大鼠中所观察到的更严重。
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