Moulakakis Konstantinos G, Sokolis Dimitrios P, Perrea Despina N, Dosios Theodosios, Dontas Ismene, Poulakou Maria V, Dimitriou Constantinos A, Sandris George, Karayannacos Panayotis E
Center for Experimental Surgery, Foundation of Biomedical Research, Academy of Athens, Greece.
Angiology. 2007 Jun-Jul;58(3):343-52. doi: 10.1177/0003319707301759.
Thyroid hormones decrease systemic vascular resistance by directly affecting vascular smooth muscle relaxation. There is limited literature about their effect on the mechanical performance of the aortic wall. Therefore, the authors determined the influence of hyperthyroidism on the mechanical properties and histomorphological structure of the descending thoracic aorta in rats. Severe hyperthyroidism was induced in 20 male Wistar rats by administering L-thyroxine (T(4)) in their drinking water for 8 weeks; age-matched normal euthyroid rats acted as controls. Animals were sacrificed, and the mechanical and histomorphometrical characteristics of the descending thoracic aorta were studied. The aortic wall of hyperthyroid rats was stiffer than that of euthyroid animals at the upper physiologic levels of stress or strain (p < 0.05) but less stiff at the lower physiologic and lower levels (p < 0.05). The aorta of hyperthyroid animals compared with that of euthyroid ones showed an increase of the internal and external diameters (p < 0.05), the media area (p < 0.05), the number of smooth muscle cell nuclei (p < 0.05), and the collagen density (p < 0.05) and a decrease in the elastin laminae thickness (p < 0.001) and elastin density (p < 0.001). In hyperthyroid rats, the aortic wall was stiffer at the upper physiologic and higher levels of stress and strain. These changes correlated with microstructural changes of the aortic wall. The coexistence of hyperthyroidism with disease states or clinical conditions that predispose to increased arterial pressure may be associated with increased arterial stiffness and have undesirable consequences on the mechanical performance of the thoracic aorta and hemodynamic homeostasis. These changes could lead to an increased risk for developing vascular complications.
甲状腺激素通过直接影响血管平滑肌舒张来降低全身血管阻力。关于它们对主动脉壁力学性能影响的文献有限。因此,作者确定了甲状腺功能亢进对大鼠胸降主动脉力学性能和组织形态结构的影响。通过在20只雄性Wistar大鼠的饮用水中给予L-甲状腺素(T4)8周来诱导严重甲状腺功能亢进;年龄匹配的正常甲状腺功能正常的大鼠作为对照。处死动物,研究胸降主动脉的力学和组织形态学特征。在较高生理应力或应变水平下,甲状腺功能亢进大鼠的主动脉壁比甲状腺功能正常动物的更硬(p<0.05),但在较低生理和更低水平下则较软(p<0.05)。与甲状腺功能正常动物相比,甲状腺功能亢进动物的主动脉内径和外径增加(p<0.05),中膜面积增加(p<0.05),平滑肌细胞核数量增加(p<0.05),胶原密度增加(p<0.05),而弹性膜厚度(p<0.001)和弹性蛋白密度降低(p<0.001)。在甲状腺功能亢进大鼠中,主动脉壁在较高生理和更高应力及应变水平下更硬。这些变化与主动脉壁的微观结构变化相关。甲状腺功能亢进与易导致动脉压升高的疾病状态或临床情况并存,可能与动脉僵硬度增加有关,并对胸主动脉的力学性能和血流动力学稳态产生不良影响。这些变化可能导致发生血管并发症的风险增加。