Napoli Raffaele, Biondi Bernadette, Guardasole Vincenzo, D'Anna Carolina, De Sena Antonietta, Pirozzi Concetta, Terracciano Daniela, Mazzarella Claudia, Matarazzo Margherita, Saccà Luigi
Department of Internal Medicine and Cardiovascular Sciences, University Federico II, Via Pansini 5, Naples, Italy.
J Clin Endocrinol Metab. 2008 May;93(5):1959-63. doi: 10.1210/jc.2007-2797. Epub 2008 Mar 11.
The cardiovascular consequences of thyroid diseases are attributed to the altered secretion of thyroid hormones. The possibility that TSH also affects the cardiovascular system has been poorly explored. Endothelial cells and vascular smooth muscle cells possess TSH receptors.
The study was designed to determine whether TSH exerts any effect on vascular homeostasis.
Two different double-blind, controlled studies were performed, one in eight healthy volunteers and the other in six thyroidectomized patients. Recombinant human (rh) TSH (or saline) was infused intrabrachially (1 mU/min) to raise TSH to severe hypothyroidism levels (approximately 100 microU/ml). Endothelium-dependent and -independent vasodilation was tested by intraarterial infusion of acetylcholine and sodium nitroprusside, respectively, and forearm blood flow was measured by plethysmography.
Endothelium-dependent vasodilation was potentiated by rhTSH (P < 0.05 for the treatment effect; general linear model). The dynamics of the response was also profoundly affected by rhTSH because the dose-response curve was much steeper than in controls (P < 0.02 for the interaction between TSH and acetylcholine). rhTSH had no effect on endothelium-independent vasodilation (P = NS for both treatment and interaction). During rhTSH infusion, free T(3) levels increased slowly from 2.3 +/- 0.2 to 3.6 +/- 0.2 pg/ml. In thyroidectomized patients, rhTSH potentiated endothelium-mediated vasodilation to an extent similar to that of healthy subjects (P = 0.05 for the treatment effect and P = 0.01 for the interaction), without affecting the response to nitroprusside. In these patients, thyroid hormones remained unchanged during rhTSH infusion.
rhTSH exerts marked effects on the resistance vessels by enhancing endothelial-mediated vasodilation, independent of changes in thyroid hormone concentration.
甲状腺疾病的心血管后果归因于甲状腺激素分泌的改变。促甲状腺激素（TSH）是否也影响心血管系统的可能性尚未得到充分研究。内皮细胞和血管平滑肌细胞具有TSH受体。
本研究旨在确定TSH是否对血管稳态有任何影响。
进行了两项不同的双盲对照研究，一项针对8名健康志愿者，另一项针对6名甲状腺切除患者。通过肱动脉内输注重组人（rh）TSH（或生理盐水）（1 mU/分钟），使TSH升高至严重甲状腺功能减退水平（约100 μU/ml）。分别通过动脉内输注乙酰胆碱和硝普钠测试内皮依赖性和非内皮依赖性血管舒张，并通过体积描记法测量前臂血流量。
rhTSH增强了内皮依赖性血管舒张（治疗效果P<0.05；一般线性模型）。rhTSH也对反应动力学产生了深远影响，因为剂量反应曲线比对照组陡得多（TSH与乙酰胆碱之间的相互作用P<0.02）。rhTSH对非内皮依赖性血管舒张无影响（治疗和相互作用的P均为无统计学意义）。在rhTSH输注期间，游离T3水平从2.3±0.2缓慢增加至3.6±0.2 pg/ml。在甲状腺切除患者中，rhTSH增强内皮介导的血管舒张的程度与健康受试者相似（治疗效果P = 0.05，相互作用P = 0.01），而不影响对硝普钠的反应。在这些患者中，rhTSH输注期间甲状腺激素保持不变。
rhTSH通过增强内皮介导的血管舒张对阻力血管产生显著影响，与甲状腺激素浓度的变化无关。
