| Abstrakt: |
Brain-dead donors frequently show circulatory deterioration and often require so much inotropic support that the donor heart is of questionable value. This experimental study quantifies the cardiac metabolic consequences of brain death and the role of warm blood cardioplegic solution for induction of cardioplegia to improve the quality of potential donor hearts with impaired hemodynamics. Twelve dogs were subjected to brain death by interrupting cerebral blood flow (ligation of innominate artery, carotid arteries, and superior vena cava) and were followed up for as long as 6 hours. Each showed progressive hemodynamic deterioration, necessitating inotropic support (dopamine, calcium, and epinephrine) and large amounts of volume replacement (hetastarch; Hespan) to support the circulation (maintain mean arterial blood pressure greater than 60 mm Hg). Biopsy specimens were taken after 6 hours, or when irreversible ventricular fibrillation occurred, and were analyzed for adenosine triphosphate, creatine phosphate, glycogen, glutamate, and lactate. In six dogs the aorta was then clamped, and a 10-minute infusion of warm (37° C) substrate-enriched aspartate/glutamate blood cardioplegic solution (with the dog’s own blood) was given by roller pump to simulate warm induction during the harvesting process. Biopsies were then repeated. Myocardial metabolism, expressed as percent of control values, during brain death was characterized by the following: (1) moderate energy depletion (adenosine triphosphate fell 25% ± 8%, creatine phosphate fell 55% ± 15%; p < 0.05 versus control: mean ± standard error of the mean); (2) substrate depletion (tissue glutamate fell 48% ± 9.5%, glycogen fell 66% ± 7.5%; p < 0.05 versus control: mean ± standard error of the mean); and (3) evidence of anaerobic metabolism (lactate increased 374% ±95%; p < 0.05 versus control: mean ± standard error of the mean). Warm induction of blood cardioplegia in these energy- and substrate-depleted ischemic hearts showed (1) return of creatine phosphate levels to normal (113% ± 16.8%), (2) replenishment of glutamate (201% ± 24% of control; p < 0.05 versus control: mean ± standard error of the mean), and (3) 43% ± 14% reduction in myocardial lactate content; (p < 0.05 versus brain-dead animals). These data suggest that brain-dead donors requiring inotropic support sustain energy and substrate depletion and ischemic damage that can be reversed by a brief period of induction of cardioplegia with a warm substrate-enriched blood cardioplegic solution before harvesting. Warm substrate-enriched blood cardioplegic solution may increase the tolerance to subsequent ischemia during organ storage, provide potential expansion of the donor pool, or improve the potential function of hearts harvested from hemodynamically impaired donors. |
