Brüngger M, Hulter H N, Krapf R
Klinik B für Innere Medizin, Kantonsspital, St. Gallen, Switzerland.
Am J Physiol. 1997 May;272(5 Pt 2):F648-53. doi: 10.1152/ajprenal.1997.272.5.F648.
The effects of metabolic acidosis on thyroid function are unknown. We investigated the effects of chronic extrarenal acidosis on the hypothalamic-pituitary-thyroid axis. Chronic metabolic acidosis was induced by administering NH4Cl (4.2 mmol.kg body wt-1.day-1) to six normal male volunteers during metabolic balance conditions. Plasma bicarbonate concentration decreased from 25.0 +/- 0.4 to 15.5 +/- 0.9 mmol/l (P < 0.001). Metabolic acidosis significantly decreased serum-free 3,5,3'-triiodothyronine (T3) concentrations from 373 +/- 18 (control) to 251 +/- 13 pg/dl (P < 0.001) and decreased serum-free L-thyroxine (T4) from 1.55 +/- 0.42 to 1.25 +/- 0.37 ng/dl (P < 0.002), whereas serum total reverse T3 did not change significantly. Consequently, the reverse T3-to-free T4 ratio increased. Serum thyroid-stimulating hormone (TSH) levels increased significantly from 0.70 +/- 0.07 during control to 1.30 +/- 0.12 mU/l during acidosis (P < 0.003). The TSH response to thyrotropin (TRH, 2 mg intranasally) was exaggerated in acidosis: the partial area under the concentration curve for the TSH response (210 min post-TRH) was 902 +/- 167 during control compared with 1.394 +/- 209 mU.min.l-1 during acidosis (P = 0.0139). Chronic metabolic acidosis, as produced by the model employed here, induces a decrease in thyroid hormone secretion and might exert additional effects on thyroid hormone metabolism in humans. The acidosis-induced decrease in thyroid function might modulate some of the reported effects of metabolic acidosis, such as on nitrogen balance, protein synthesis, lean body mass, insulin-like growth factor I levels, renal acidification, and cardiac contractile function.
代谢性酸中毒对甲状腺功能的影响尚不清楚。我们研究了慢性肾外酸中毒对下丘脑 - 垂体 - 甲状腺轴的影响。在代谢平衡条件下，给6名正常男性志愿者服用氯化铵（4.2 mmol·kg体重-1·天-1）诱导慢性代谢性酸中毒。血浆碳酸氢盐浓度从25.0±0.4降至15.5±0.9 mmol/l（P<0.001）。代谢性酸中毒使血清游离3,5,3'-三碘甲状腺原氨酸（T3）浓度从373±18（对照）显著降至251±13 pg/dl（P<0.001），血清游离L-甲状腺素（T4）从1.55±0.42降至1.25±0.37 ng/dl（P<0.002），而血清总反三碘甲状腺原氨酸没有显著变化。因此，反T3与游离T4的比值增加。血清促甲状腺激素（TSH）水平从对照时的0.70±0.07显著升高至酸中毒时的1.30±0.12 mU/l（P<0.003）。酸中毒时TSH对促甲状腺激素释放激素（TRH，鼻内注射2 mg）的反应增强：TSH反应浓度曲线下的部分面积（TRH后210分钟）在对照时为902±167，而在酸中毒时为1394±209 mU·min·l-1（P = 0.0139）。此处采用的模型所产生的慢性代谢性酸中毒会导致甲状腺激素分泌减少，并可能对人体甲状腺激素代谢产生额外影响。酸中毒引起的甲状腺功能减退可能会调节一些已报道的代谢性酸中毒的影响，如对氮平衡、蛋白质合成、瘦体重、胰岛素样生长因子I水平、肾酸化和心脏收缩功能的影响。
