Brain death-related energetic failure of the donor heart becomes apparent only during storage and reperfusion: an ex vivo phosphorus-31 magnetic resonance spectroscopy study on the feline heart.
OBJECTIVE
Recently, we have shown, by using localized in vivo phosphorus-31 magnetic resonance spectroscopy (31P MRS) of the anterior left ventricular wall, that brain death (BD) is not associated with reduced myocardial energy status. In this study, we applied ex vivo 31P MRS of the entire heart to study the effects of BD on the energy status of the feline donor heart following explantation.


METHODS
We used cats (6 BD and 6 controls [C]) in a 26-hour protocol. After 2 hours of preparation, we induced BD by filling an intracranial balloon at t = 0 hour. At t = 6 hours, the hearts were arrested with St. Thomas' Hospital cardioplegic solution, explanted, and stored in the same solution at 4 degrees C in a 4.7 Tesla magnet for 17 hours. Subsequently, the hearts were reperfused in the Langendorff mode at 38 degrees C for 1 hour. The first 5-minute 31P MRS spectrum was obtained 1 hour after crossclamping the aorta; we obtained subsequent spectra every hour during storage and every 5 minutes during reperfusion. At the end, the hearts were dried and weighed. Phosphocreatine (PCr), gamma-adenosine triphosphate (gamma-ATP), inorganic phosphate (Pi), and phosphomonoesters (PME), were expressed per g dry heart weight. The intracellular pH (pH(i)) and the PCr/ATP ratio were calculated.


RESULTS
During storage, we identified a significant but similar decrease of pH(i), PCr/ATP ratio, and PCr in both groups. During reperfusion, pH(i) and PCr/ATP ratio recovered similarly in both groups, whereas the recovery of PCr in the BD group was significantly lower (p < 0.05). The Pi and PME increased in both groups during storage but to a lesser extent in the BD group (p < 0.05). This difference disappeared during reperfusion. The gamma-ATP was already significantly lower in the BD group at the onset of storage, and this remained so throughout storage and reperfusion (p < 0.05 vs C). Contractile capacity was lost in all hearts, except for 1 heart in the BD group.


CONCLUSIONS
Brain death-related failure of the energetic integrity of the feline donor heart becomes apparent only when using 31P MRS during ischemic preservation and subsequent reperfusion.
Bruinsma
G J
GJ
Heart Lung Institute, University Medical Center, Utrecht, The Netherlands. g.j.bbb@planet.nl
Van de Kolk
C W
CW
Nederhoff
M G
MG
Bredée
J J
JJ
Ruigrok
T J
TJ
Van Echteld
C J
CJ
D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001826:Body Fluids / Q000378:metabolism; D001831:Body Temperature / Q000502:physiology; D001926:Brain Death / Q000000981:diagnostic imaging* / Q000378:metabolism*; D002415:Cats; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology*; D006321:Heart / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D016027:Heart Transplantation / Q000000981:diagnostic imaging*; D006439:Hemodynamics / Q000502:physiology; D006863:Hydrogen-Ion Concentration; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism; D011877:Radionuclide Imaging; D014019:Tissue Donors
D010758:Phosphorus