Treatment of dopamine-dependent shock with triiodothyronine.

R D Hesch, M Hüsch, R Ködding, B Höffken, T Meyer
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引用次数: 42

Abstract

At the present time dopamine is the most frequently used treatment in patients with septic shock. The effects of dopamine are mediated by alpha-, beta- and dopaminergic receptors. It has been suggested that these receptors are controlled by triiodothyronine (T3). In acute septic shock circulating T3-concentrations are decreased. We have, therefore, treated in a preliminary study 11 such patients with T2-replacement by continuous infusion of T3 (100-200 micrograms/24h). Dopamine dependence was terminated. In all patients there was an increase of arterial blood pressure (BP) within 24 hrs (systolic BP rose by 34 +/- 4.2 mmHg, diastolic BP by 14.0 +/- 8.2 mmHg, resulting in an increase of the mean BP by 25 +/- 6.1 (SEM mmHg). The pulse rate was not influenced suggesting an effect on minute volume. A hypothesis is offered which explains the T3-effects as a result of its decarboxylation to a dopaminergic iodothyronine which is disturbed during the "low T3-syndrome".

三碘甲状腺原氨酸治疗多巴胺依赖性休克。
目前,多巴胺是脓毒性休克患者最常用的治疗方法。多巴胺的作用是由α、β和多巴胺能受体介导的。这些受体受三碘甲状腺原氨酸(T3)的控制。急性感染性休克时循环t3浓度降低。因此,在一项初步研究中,我们通过持续输注T3(100-200微克/24小时)来治疗11例这样的患者。多巴胺依赖终止。所有患者24小时内动脉血压升高(收缩压升高34 +/- 4.2 mmHg,舒张压升高14.0 +/- 8.2 mmHg,导致平均血压升高25 +/- 6.1 (SEM mmHg)。脉搏率没有受到影响,表明对分钟容量有影响。提出了一种假说,解释了t3效应是由于其脱羧为多巴胺能碘甲状腺原氨酸,在“低t3综合征”期间受到干扰。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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