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.