Klemperer J D, Ojamaa K, Klein I
Department of Medicine, North Shore University Hospital, Cornell University Medical College, Manhasset, NY 11030, USA.
Prog Cardiovasc Dis. 1996 Jan-Feb;38(4):329-36. doi: 10.1016/s0033-0620(96)80017-x.
The relationship between thyroid disease states and cardiovascular hemodynamics is well recognized. Although the long-term effects of thyroid hormone are thought to result from changes in myocardial gene expression, attention has recently focused on acute, non-nuclear-mediated actions of L-triidothyronine (T3), the biologically active form of the hormone. Various lines of evidence have documented that T3 can act as a vasodilator and inotrope. With this recognition have come novel treatment strategies targeted at specific clinical conditions including heart failure and cardiac surgery that are associated with impaired cardiovascular performance and low serum T3 levels. An understanding of the mechanisms of action of thyroid hormone on the heart and peripheral vasculature is essential for the rational implementation of thyroid hormone as a therapeutic agent. As outlined in this review, initial clinical experience suggests that the ability of thyroid hormone to increase cardiac output and to lower systemic vascular resistance may provide a novel treatment option for physicians caring for patients with cardiovascular illness.
甲状腺疾病状态与心血管血流动力学之间的关系已得到充分认识。尽管甲状腺激素的长期作用被认为是由心肌基因表达的变化引起的，但最近注意力集中在L-三碘甲状腺原氨酸（T3）的急性、非核介导作用上，T3是该激素的生物活性形式。各种证据表明，T3可作为血管扩张剂和正性肌力药。随着这种认识的出现，针对特定临床情况（包括与心血管功能受损和血清T3水平低相关的心力衰竭和心脏手术）的新型治疗策略应运而生。了解甲状腺激素对心脏和外周血管系统的作用机制对于合理使用甲状腺激素作为治疗药物至关重要。如本综述所述，初步临床经验表明，甲状腺激素增加心输出量和降低全身血管阻力的能力可能为治疗心血管疾病患者的医生提供一种新的治疗选择。
