Zwemer C F, Whitesall S E, Nachreiner R F, Mayor G H, D'Alecy L G
Department of Physiology, University of Michigan Medical School, Ann Arbor 48109-0622, USA.
Resuscitation. 1997 Jan;33(3):271-80. doi: 10.1016/s0300-9572(96)01040-4.
This study determined the acute effects of intravenous levothyroxine sodium (LT4) on systemic oxygen delivery and consumption for 6 h following resuscitation from 9 min of normothermic cardiac arrest in dogs. Male mongrel dogs (15-25 kg) were randomly assigned to two groups of seven. The treated group received a pre-cardiac arrest infusion of 15 micrograms/kg per h of LT4 for 1.5 h prior to arrest and for 6 h after, while controls received a comparable volume of 0.9 N saline infusion. Neurologic outcome was recorded at 1, 2 and 6 h following resuscitation. Systemic oxygen consumption (VO2), carbon dioxide production (VCO2) and respiratory quotient (RQ) were calculated from directly measured cardiac output, arterial and mixed venous blood gases and contents. Serum levels of circulating canine thyroid-stimulating hormone (cTSH), total thyroxine (T4), free thyroxine (FT4), total 3,5,3'-triiodothyronine (T3), free 3,5,3'-triiodothyronine (FT3), reverse 3,3',5'-triiodothyronine (rT3), and plasma markers of oxidant injury (malonaldehyde (MDA), 4-hydroxynonenal (4-OH) and erythrocyte GSH) were measured before administration and after resuscitation. Following resuscitation, treated dogs maintained significantly higher cardiac output when compared with their control counterparts at 4 h (5.5 ml/g per h vs. 2.9 ml/g per h, respectively, P < 0.05) and at 6 h (5.5 ml/g per h vs. 3.0 mg/g per h, respectively, P < 0.05). The level of VO2 was significantly higher in treated dogs than control dogs at 1, 4 and 6 h (P < 0.05). Treated dogs had significantly elevated levels of T4, FT4, T3, FT3 and rT3 (P < 0.01), compared with control dogs. No changes in cTSH were detected between groups or over time. Acute administration of LT4 enhances systemic oxygen delivery and apparently, therefore, oxygen consumption following resuscitation.
本研究确定了静脉注射左甲状腺素钠（LT4）对犬常温心脏骤停9分钟复苏后6小时内全身氧输送及氧消耗的急性影响。雄性杂种犬（15 - 25千克）被随机分为两组，每组7只。治疗组在心脏骤停前1.5小时及骤停后6小时接受每小时15微克/千克的LT4预心脏骤停输注，而对照组接受等量的0.9N盐水输注。在复苏后1小时、2小时和6小时记录神经学结果。根据直接测量的心输出量、动脉血和混合静脉血的气体及成分计算全身氧消耗（VO2）、二氧化碳产生量（VCO2）和呼吸商（RQ）。在给药前和复苏后测量血清中循环犬促甲状腺激素（cTSH）、总甲状腺素（T4）、游离甲状腺素（FT4）、总3,5,3'-三碘甲状腺原氨酸（T3）、游离3,5,3'-三碘甲状腺原氨酸（FT3）、反式3,3',5'-三碘甲状腺原氨酸（rT3）以及氧化损伤的血浆标志物（丙二醛（MDA）、4-羟基壬烯醛（4-OH）和红细胞谷胱甘肽（GSH））。复苏后，治疗组犬在4小时（分别为5.5毫升/克每小时和2.9毫升/克每小时，P < 0.05）和6小时（分别为5.5毫升/克每小时和3.0毫克/克每小时，P < 0.05）时的心输出量显著高于对照组。治疗组犬在1小时、4小时和6小时的VO2水平显著高于对照组犬（P < 0.05）。与对照组犬相比，治疗组犬的T4、FT4、T3、FT3和rT3水平显著升高（P < 0.01）。两组之间或随时间未检测到cTSH的变化。急性给予LT4可增强全身氧输送，因此显然也能增强复苏后的氧消耗。
