G. Szabo et al., EFFECTS OF BRAIN-DEATH ON MYOCARDIAL-FUNCTION AND ISCHEMIC TOLERANCE OF POTENTIAL DONOR HEARTS, The Journal of heart and lung transplantation, 17(9), 1998, pp. 921-930
Citations number
28
Categorie Soggetti
Cardiac & Cardiovascular System",Transplantation,"Respiratory System
Background: An increasing number of experimental and clinical studies
reports hemodynamic instability in the donor organism after brain deat
h. However, the relative importance of brain death-related cardiac dys
function on posttransplantation cardiac function and the reversibility
of the observed changes remain controversial. In this study a load-in
dependent analysis of cardiac function after brain death was performed
. Special interest was focused on a possible interactive influence of
brain death and cardiac preservation on postischemic cardiac function.
Methods: In 12 anesthetized dogs, brain death was induced by inflatio
n of a subdural balloon; 12 sham-operated animals served as control su
bjects. After a 2-hour observation in situ, the hearts were explanted
and perfused parabiotically either immediately or after hypothermic is
chemic preservation (4 hours, 4 degrees C). Heart rate, cardiac output
, left ventricular pressure, the maximum of left ventricular pressure
development and aortic pressure were measured in situ. In addition, th
e slope of the end-systolic pressure-volume relationship, coronary blo
od flow, and myocardial oxygen consumption were estimated in the cross
-circulated hearts. Results: In spite of a brain death-associated hemo
dynamic deterioration in situ (expressed as low mean aortic pressure a
nd significant decrease of maximal dP/dt), myocardial function was sim
ilar to control after explantation, if assessed ex vivo. Furthermore,
after hypothermic ischemic preservation and reperfusion, complete func
tional recovery of control and brain-dead hearts could be observed. Co
nclusions: These data indicate that hemodynamic instability after brai
n death may rather reflect altered loading conditions than irreversibl
e myocardial damage or primary cardiac dysfunction. Furthermore, there
is no evidence for a brain death-related impairment of ischemic toler
ance.