title: 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.
abstract: OBJECTIVE
  Long-term exposure of the donor heart to high dosages of dopamine in the treatment of brain death-related hemodynamic deterioration has been shown to reduce myocardial phosphocreatine (PCr) and adenosine triphosphate (ATP) in myocardial biopsy specimens and may preclude heart donation for transplantation. Short-term exposure to the acute catecholamine release during the onset of brain death has shown an unchanged PCr/ATP ratio using in vivo phosphorus-31 magnetic resonance spectroscopy (31P MRS). In this study 31P MRS was used to evaluate in vivo myocardial energy metabolism during 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 myocardial workload in the brain-death group was reduced significantly, dopamine was infused (n = 12) at 5 microg/kg/min and its dose was consecutively doubled every 30 minutes and was withheld during the last 30 minutes of the experiment. Phosphorus-31 magnetic resonance spectra were obtained from the left ventricular wall during 5-minute time frames, and PCr/ATP ratios were calculated. 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 dopamine in both groups, the initial PCr/ATP ratio of 2.00+/-0.12 and the contents of PCr and ATP did not vary significantly. Histologically identified sub-endocardial hemorrhage was observed in 3 of 6 of the brain-dead animals and in 1 of 6 of the control animals.
  
  
  CONCLUSIONS
  High dosages of dopamine in the treatment of brain death-related reduced myocardial workload do not alter PCr/ATP ratios and the contents of PCr and ATP of the potential donor heart despite histologic damage.
authors.affiliation: Heart Lung Institute, University Hospital, Utrecht, The Netherlands.
authors.forename: G J
authors.initials: GJ
authors.lastname: Bruinsma
authors.forename: M G
authors.initials: MG
authors.lastname: Nederhoff
authors.forename: C W
authors.initials: CW
authors.lastname: van de Kolk
authors.forename: M C
authors.initials: MC
authors.lastname: de Groot
authors.forename: P J
authors.initials: PJ
authors.lastname: Slootweg
authors.forename: J J
authors.initials: JJ
authors.lastname: Bredée
authors.forename: T J
authors.initials: TJ
authors.lastname: Ruigrok
authors.forename: C J
authors.initials: CJ
authors.lastname: Van Echteld
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D001926:Brain Death / Q000378:metabolism*; D002415:Cats; D004298:Dopamine / Q000008:administration & dosage / Q000494:pharmacology*; D004734:Energy Metabolism; D006321:Heart / Q000187:drug effects*; D016027:Heart Transplantation; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism*; D010725:Phosphocreatine / Q000032:analysis; D010761:Phosphorus Radioisotopes
chemical_list: D010761:Phosphorus Radioisotopes; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D004298:Dopamine