Bio-energetic response of the heart to dopamine following brain death-related reduced myocardial workload: A phosphorus-31 magnetic resonance spectroscopy study in the cat

Objective: Long-term exposure of the donor heart to high dosages of dopamin e in the treatment of brain death-related hemodynamic deterioration has bee n shown to reduce myocardial phosphocreatine (PCr) and adenosine triphospha te (ATP) in myocardial biopsy specimens and may preclude heart donation for transplantation. Short-term exposure to the acute catecholamine release du ring the onset of brain death has shown an unchanged PCr/ATP ratio using in vivo phosphorus-31 magnetic resonance spectroscopy (P-31 MRS). In this stu dy P-31 MRS was used to evaluate in vivo myocardial energy metabolism durin g long-term dopamine treatment. Methods: Twelve cats were studied in a 4.7 Tesla magnet:for 360 minutes. At t = 0 minutes, brain death was induced (n = 6). At 210 minutes, when myoca rdial workload in the brain-death group was reduced significantly, dopamine was infused (n = 12) at 5 mu g/kg/min and its dose was consecutively doubl ed every 30 minutes and was withheld during the last 30 minutes of the expe riment. Phosphorus-31 magnetic resonance spectra were obtained from the lef t ventricular wall during 5-minute time frames, and PCr/ATP ratios were cal culated. The hearts were histologically examined. Results: Although significant changes in myocardial workload were observed after the induction of brain death and during support and withdrawal of dop amine in both groups, the initial PCr/ATP ratio of 2.00 +/- 0.12 and the co ntents of PCr and ATP did not vary significantly. Histologically identified sub-endocardial hemorrhage was observed in 3 of 6 of the brain-dead animal s and in 1 of 6 of the control animals. Conclusions: High dosages of dopamine in the treatment of brain death-relat ed reduced myocardial workload do not alter PCr/ATP ratios and the contents of PCr and ATP of the potential donor heart despite histologic damage.