McAllister R M, Albarracin I, Jasperse J L, Price E M
Department of Anatomy and Physiology, Kansas State University, 228 Coles Hall, Manhattan, KS 66506, USA.
Am J Physiol Regul Integr Comp Physiol. 2005 Jan;288(1):R284-91. doi: 10.1152/ajpregu.00061.2003. Epub 2004 Sep 16.
Cardiovascular dysfunction is characteristic of both hypo- and hyperthyroidism. Endothelium-dependent dilation of conductance vessels is impaired in hypothyroidism but augmented in hyperthyroidism. We hypothesized that these alterations in dilation extend into the resistance vasculature of skeletal muscle. To test this hypothesis, rats were made hypothyroid with propylthiouracil (Hypo; n = 13) or hyperthyroid with triiodothyronine (Hyper; n = 9) over 3-4 mo. Compared with euthyroid controls (Eut; n = 14), Hypo rats were characterized by reduced skeletal muscle oxidative capacity and blunted growth; Hyper rats exhibited increased muscle oxidative capacity and left ventricular hypertrophy (P < 0.05 for all effects). Vasodilation to the endothelium-dependent agent acetylcholine ( approximately 2 x 10(-4) M) in skeletal muscle was determined in situ. Conductance in certain muscles increased from control [e.g., soleus: 0.98 +/- 0.15 (Eut), 0.79 +/- 0.14 (Hypo), and 1.06 +/- 0.24 ml.min(-1).100 g(-1).mmHg(-1) (Hyper); not significant among groups] to acetylcholine [1.91 +/- 0.21 (Eut), 2.28 +/- 0.26 (Hypo), and 2.15 +/- 0.33 ml.min(-1).100 g(-1).mmHg(-1) (Hyper); P < 0.05 vs. control values for all groups] but did not differ among groups. Expression of mRNA for the endothelial isoform of nitric oxide synthase in resistance vessels isolated from various muscles was similarly unchanged with alterations in thyroid status [e.g., soleus 1A arterioles: 33.15 +/- 0.58 (Eut), 32.73 +/- 0.27 (Hypo), and 32.80 +/- 0.54 (Hyper) cycles at threshold; not significant]. These data suggest that endothelium-dependent dilation of resistance vasculature in skeletal muscle is unchanged in both hypo- and hyperthyroidism. These data also emphasize the importance of examining resistance vasculature to improve understanding of effects of chronic disease on integrated cardiovascular function.
心血管功能障碍是甲状腺功能减退和亢进的共同特征。甲状腺功能减退时，传导血管的内皮依赖性舒张功能受损，而甲状腺功能亢进时则增强。我们推测，这些舒张功能的改变也存在于骨骼肌的阻力血管中。为了验证这一假设，用丙硫氧嘧啶使大鼠甲状腺功能减退（甲减组；n = 13），或用三碘甲状腺原氨酸使大鼠甲状腺功能亢进（甲亢组；n = 9），持续3 - 4个月。与甲状腺功能正常的对照组（正常组；n = 14）相比，甲减大鼠的骨骼肌氧化能力降低且生长迟缓；甲亢大鼠的肌肉氧化能力增强且左心室肥厚（所有效应P < 0.05）。在原位测定骨骼肌对内皮依赖性药物乙酰胆碱（约2×10⁻⁴ M）的血管舒张反应。某些肌肉的传导率从对照时[如比目鱼肌：0.98±0.15（正常组）、0.79±0.14（甲减组）和1.06±0.24 ml·min⁻¹·100 g⁻¹·mmHg⁻¹（甲亢组）；各组间无显著差异]升高至乙酰胆碱作用时[1.91±0.21（正常组）、2.28±0.26（甲减组）和2.15±0.33 ml·min⁻¹·100 g⁻¹·mmHg⁻¹（甲亢组）；所有组与对照值相比P < 0.05]，但各组间无差异。从不同肌肉分离出的阻力血管中，一氧化氮合酶内皮型异构体的mRNA表达同样不受甲状腺状态改变的影响[如比目鱼肌1A小动脉：阈值循环数为33.15±0.58（正常组）、32.73±0.27（甲减组）和32.80±0.54（甲亢组）；无显著差异]。这些数据表明，甲状腺功能减退和亢进时，骨骼肌阻力血管的内皮依赖性舒张功能均未改变。这些数据还强调了检查阻力血管对于增进理解慢性疾病对心血管综合功能影响的重要性。
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