Portman M A, Fearneyhough C, Ning X H, Duncan B W, Rosenthal G L, Lupinetti F M
Division of Cardiology, Department of Pediatrics, University of Washington and Children's Hospital and Regional Medical Center, Seattle, WA 98105, USA.
J Thorac Cardiovasc Surg. 2000 Sep;120(3):604-8. doi: 10.1067/mtc.2000.108900.
Cardiopulmonary bypass suppresses circulating thyroid hormone levels. Although acute triiodothyronine repletion has been evaluated in adult patients after cardiopulmonary bypass, triiodothyronine pharmacokinetics and effects have not previously been studied in infants undergoing operations for congenital heart disease. We hypothesized that triiodothyronine deficiency in the developing heart after bypass may adversely affect cardiac function reserve postoperatively.
Infants less than 1 year old undergoing ventricular septal defect or tetralogy of Fallot repair were randomized into 2 groups. Group T (n = 7) received triiodothyronine (0.4 microg/kg) immediately before the start of cardiopulmonary bypass and again with myocardial reperfusion. Control (NT, n = 7) patients received saline solution placebo or no treatment.
These groups underwent similar ischemic and bypass times and received similar quantities of inotropic agents after the operation. The NT group demonstrated significant depression in circulating levels, compared with prebypass levels, for free triiodothyronine and total triiodothyronine at 1, 24, and 72 hours after bypass. Group T demonstrated similar low thyroxine values, but free and total triiodothyronine levels were maintained at prebypass levels for 24 hours and remained elevated over those of group NT (P <.05) at 72 hours. Heart rate was transiently elevated in group T compared with group NT (P <.05), and peak systolic pressure-rate product increased after 6 hours.
These data imply that (1) triiodothyronine in the prescribed dose prevents circulating triiodothyronine deficiencies and (2) triiodothyronine repletion promotes elevation in heart rate without concomitant decrease in systemic blood pressure. Elevation of peak systolic pressure-rate product implies that triiodothyronine repletion improves myocardial oxygen consumption and may enhance cardiac function reserve after cardiopulmonary bypass in infants.
体外循环会抑制循环甲状腺激素水平。尽管已对成年患者体外循环后急性补充三碘甲状腺原氨酸进行了评估，但此前尚未对患有先天性心脏病接受手术的婴儿的三碘甲状腺原氨酸药代动力学及作用进行研究。我们推测，体外循环后发育中的心脏出现三碘甲状腺原氨酸缺乏可能会对术后心脏功能储备产生不利影响。
将年龄小于1岁接受室间隔缺损或法洛四联症修复手术的婴儿随机分为2组。T组（n = 7）在体外循环开始前即刻及心肌再灌注时各接受一次三碘甲状腺原氨酸（0.4μg/kg）。对照组（NT组，n = 7）患者接受盐溶液安慰剂或不接受治疗。
这些组的缺血和体外循环时间相似，术后接受的强心剂用量也相似。与体外循环前水平相比，NT组在体外循环后1、24和72小时的游离三碘甲状腺原氨酸和总三碘甲状腺原氨酸循环水平显著降低。T组甲状腺素值同样较低，但游离和总三碘甲状腺原氨酸水平在24小时内维持在体外循环前水平，且在72小时时高于NT组（P <.05）。与NT组相比，T组心率短暂升高（P <.05），6小时后收缩压-心率峰值乘积增加。
这些数据表明，（1）规定剂量的三碘甲状腺原氨酸可预防循环三碘甲状腺原氨酸缺乏，（2）补充三碘甲状腺原氨酸可促进心率升高，而不会伴随全身血压下降。收缩压-心率峰值乘积升高表明，补充三碘甲状腺原氨酸可改善心肌氧消耗，并可能增强婴儿体外循环后的心脏功能储备。
