McAllister R M, Luther K L, Pfeifer P C
Departments of Kinesiology and Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506, USA.
Am J Physiol Endocrinol Metab. 2000 Aug;279(2):E252-8. doi: 10.1152/ajpendo.2000.279.2.E252.
We have previously reported that changes in thyroid status are associated with significant alterations in skeletal muscle blood flow during exercise and that changes in endothelium-dependent vasodilation may contribute to these blood flow abnormalities. The purpose of this study was to test the hypothesis that altered endothelium-dependent vasoconstriction is also associated with changes in thyroid status. To test this hypothesis, rats were rendered hypothyroid with propylthiouracil (Hypo, n = 14) or hyperthyroid with triiodothyronine (Hyper, n = 14) over approximately 3 mo. Treatment efficacy was confirmed by altered (P < 0.05) citrate synthase activity in several hindlimb skeletal muscles from Hypo and Hyper, compared with that in muscles from euthyroid rats (Eut, n = 12). Vascular rings were prepared from abdominal aortae, and responses to several vasoactive agents were determined in vitro. As found previously, maximal acetylcholine-induced vasorelaxation was modulated by thyroid status (Eut, 47 +/- 9; Hypo, 28 +/- 6; Hyper, 68 +/- 5%; P < 0.05). Contractile responses of vascular rings with intact endothelium to the endothelium-derived constrictor endothelin-1 (ET-1), however, were similar among groups across a range of ET-1 concentrations. In addition, maximal responses [Eut, 3.75 +/- 0.47; Hypo, 2.72 +/- 0.25; Hyper, 3.22 +/- 0.42 g; not significant (NS)] and sensitivities (Eut, 8.12 +/- 0.09; Hypo, 8.10 +/- 0.06; Hyper, 8.28 +/- 0.09 -log M; NS) to ET-1 were similar among groups. If these findings from the conduit-type abdominal aorta extend into resistance vasculature, it appears that changes in endothelium-dependent vasoconstriction do not contribute to skeletal muscle blood flow abnormalities associated with thyroid disease states.
我们之前曾报道，甲状腺状态的变化与运动期间骨骼肌血流的显著改变相关，并且内皮依赖性血管舒张的变化可能导致这些血流异常。本研究的目的是检验以下假设：内皮依赖性血管收缩的改变也与甲状腺状态的变化相关。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 = 14），或用三碘甲状腺原氨酸使大鼠甲状腺功能亢进（甲亢组，n = 14），持续约3个月。与正常甲状腺大鼠（正常组，n = 12）的肌肉相比，甲减组和甲亢组几只后肢骨骼肌中柠檬酸合酶活性的改变（P < 0.05）证实了治疗效果。从腹主动脉制备血管环，并在体外测定对几种血管活性药物的反应。如之前所发现的，最大乙酰胆碱诱导的血管舒张受甲状腺状态调节（正常组，47±9；甲减组，28±6；甲亢组，68±5%；P < 0.05）。然而，在内皮完整的血管环对内皮源性收缩剂内皮素-1（ET-1）的收缩反应在不同浓度的ET-1范围内各组相似。此外，各组对ET-1的最大反应[正常组，3.75±0.47；甲减组，2.72±0.25；甲亢组，3.22±0.42 g；无显著差异（NS）]和敏感性（正常组，8.12±0.09；甲减组，8.10±0.06；甲亢组，8.28±0.09 -log M；NS）相似。如果来自导管型腹主动脉的这些发现扩展到阻力血管系统，似乎内皮依赖性血管收缩的变化不会导致与甲状腺疾病状态相关的骨骼肌血流异常。
