THYROID FUNCTION AND CARDIOPULMONARY BYPASS--A EUTHYROID SICK SYNDROME

这项前瞻性研究的目的是确定 体外循环对甲状腺功能的影响。血液样本是 从14名患者入院当天，麻醉后诱导， 肝素治疗后，随着CPBP的建立，体温下降的最低点， CPBP终止前、术后2、8、24小时。TSH、TBG、 总T-4、总T-3和逆转录T-3(RT-3)，T-4的非活性代谢产物， 迄今未见CPBP报道，均采用放射免疫法测定。免费 平衡透析法测定T-3(FT-3)。数据通过以下方式进行比较 将所有时间间隔的配对T检验与术前值进行比较。总计 最活跃的甲状腺激素T-3(T-3)和FT-3值 CPBP治疗24小时后显著抑郁(分别为75%和50%) (P&lt；0.05)。反向T-3在8小时和24小时显示出四倍的上升 术后(P&lt；0.05)，术后2小时无明显变化。TBG是 在所有采样时间(p&lt；0)均降低。TSH、T-4和FT-4维持在 所有采样时间的正常范围。这些结果表明CPBP 模拟严重烧伤和严重烧伤后的“正常甲状腺病态综合症” 危重病人。术后T-3明显降低。 和FT-3，RT-3升高，而TSH、T-4和FT-4保持在 正常范围。这些数据表明FT-3及其配套设备的使用情况 T-4到RT-3的异常脱碘或RR-3到T2的异常脱碘 (RT-3的分解产物)。结论是CPBP产生了一种 促甲状腺激素对低T-3和T-4反应迟钝。有害的血液动力学 甲状腺功能减退症的影响是公认的。这些数据提供了依据 静脉注射T-3治疗低心动过速 体外循环后的输出综合征。

The purpose of this prospective study was to define the effect of cardiopulmonary bypass (CPBP) on thyroid function. Blood samples were obtained from 14 patients the day of admission, postanesthetic induction, post-heparination, following institution of CPBP, the nadir of hypothermia, before termination of CPBP, and 2, 8, and 24 hrs postoperatively. TSH, TBG, Total T-4, Total T-3 and reverse T-3 (rT-3), an inactive metabolite of T-4, heretofore never reported with CPBP, were assayed by radioimmunoassay. Free T-3 (ft-3) was assayed by equilibrium dialysis. Data were compared by paired T-tests for all time intervals against preoperative values. Total T-3 (T-3), the most active thyroid hormone, and fT-3 values were significantly depressed (75 and 50% respectively) following CPBP for 24 hrs (p<0.05). Reverse T-3 demonstrated a four-fold rise at 8 and 24 hrs postoperatively (p<0.05), but no change at 2 hrs postoperatively. TBG was decreased at all sampling time (p<0.)5). TSH, T-4 and fT-4 remained within normal ranges at all sampling times. These results indicate that CPBP simulates the "Euthyroid Sick Syndrome" as seen in severe burn and critically ill patients. There was marked postoperative depression of T-3 and fT-3 with increased rT-3, while TSH, T-4 and fT-4 remained within normal ranges. These data indicate utilization of fT-3 with concomitant abnormal deiodination of T-4 to rT-3 or abnormal deiodination of rR-3 to T2 (the breakdown product of rT-3). It is concluded that CPBP produces a blunted response of TSH to low T-3 and T-4. The deleterious hemodynamic effects of hypothyroidism are well established. These data provide a basis for intravenous administration of T-3 in the treatment of low cardiac output syndrome following cardiopulmonary bypass.