Meyers C H, D'Amico T A, Peterseim D S, Jayawant A M, Steenbergen C, Sabiston D C, Van Trigt P
Department of Surgery, Duke University Medical Center, Durham, N.C. 27710.
J Heart Lung Transplant. 1993 Jan-Feb;12(1 Pt 1):68-79; discussion 79-80.
Previous studies have documented decreases in serum-free triiodothyronine (T3) after brain death and improved hemodynamics with its replacement, suggesting its controversial, but promising, clinical utility for managing potential organ donors. Vasopressin is also commonly used clinically as a pressor agent after brain death. A load-independent analysis of cardiac function and an assessment of myocardial blood flow (MBF) with these agents have not been reported, however. Eighteen pigs were instrumented with left ventricular epicardial dimension transducers and a left ventricular micromanometer. MBF was assessed by standard microsphere techniques. Baseline left ventricular pressure-dimension data were collected, and brain death was induced by ligating the innominate and left subclavian arteries. Left ventricular function data were collected every 30 minutes after brain death to 6 hours or until the animal died. Microsphere injections were performed before brain death and hourly thereafter to 4 hours. At 90 minutes after brain death, animals were assigned to a vasopressin (2 units/hr, intravenously, n = 6), T3 (0.05 microgram/kg/hr, intravenously, n = 6), or control (n = 6) treatment group. Preload recruitable stroke work (PRSW), a load-independent index of left ventricular function, was derived from the pressure-dimension data. MBF was calculated by conventional methods. At 4 hours after brain death, PRSW and MBF decreased significantly in the control, vasopressin, and T3 groups relative to the baseline, pre-brain dead state (PRSW: -36% +/- 12%, -48 +/- 7%, -52% +/- 5%; MBF: -27% +/- 15%, -38% +/- 5%, -78% +/- 2%, respectively). Neither vasopressin nor T3, however, showed any advantage over the control group in terms of preserving left ventricular function or prolonging survival. Furthermore, these data show a marked decrease in MBF in the T3 group (p < 0.01 versus control and vasopressin groups) without a significant change in cardiac function. Analysis of endocardial to epicardial flow ratios disclosed no significant differences between groups at any time. In summary, animals treated with T3 had a greater decline in MBF than the control group at 4 hours, without any benefit to cardiac function. Further studies examining the mechanism responsible for the deterioration of MBF and cardiac dysfunction will be necessary to optimally manage the brain dead patient before organ harvest, especially regarding the precise role of T3.
以往研究记录了脑死亡后血清游离三碘甲状腺原氨酸（T3）水平下降，以及补充T3后血流动力学得到改善，这表明其在管理潜在器官捐献者方面具有存在争议但有前景的临床应用价值。血管加压素在临床上也常用于脑死亡后的升压治疗。然而，尚未有关于使用这些药物进行心脏功能的负荷独立分析以及心肌血流量（MBF）评估的报道。18头猪被植入左心室心外膜尺寸换能器和左心室微测压计。通过标准微球技术评估MBF。收集基线左心室压力-尺寸数据，通过结扎无名动脉和左锁骨下动脉诱导脑死亡。脑死亡后每30分钟收集一次左心室功能数据，持续6小时或直至动物死亡。在脑死亡前及之后每小时至4小时进行微球注射。脑死亡后90分钟，将动物分为血管加压素治疗组（2单位/小时，静脉注射，n = 6）、T3治疗组（0.05微克/千克/小时，静脉注射，n = 6）或对照组（n = 6）。预负荷可募集搏功（PRSW）是一种左心室功能的负荷独立指标，由压力-尺寸数据得出。通过传统方法计算MBF。脑死亡后4小时，对照组、血管加压素治疗组和T3治疗组的PRSW和MBF相对于基线脑死亡前状态均显著下降（PRSW：-36%±12%、-48±7%、-52%±5%；MBF：-27%±15%、-38%±5%、-78%±2%）。然而，在保留左心室功能或延长生存期方面，血管加压素和T3均未显示出优于对照组的优势。此外，这些数据显示T3治疗组的MBF显著下降（与对照组和血管加压素治疗组相比，p < 0.01），而心脏功能无显著变化。心内膜与心外膜血流比值分析显示，各时间点组间无显著差异。总之，T3治疗的动物在4小时时MBF下降幅度大于对照组，且对心脏功能无任何益处。有必要进一步研究导致MBF恶化和心脏功能障碍的机制，以便在器官获取前对脑死亡患者进行最佳管理，尤其是关于T3的确切作用。
