Effects of brain death on myocardial function and ischemic tolerance of potential donor hearts.
BACKGROUND
An increasing number of experimental and clinical studies reports hemodynamic instability in the donor organism after brain death. However, the relative importance of brain death-related cardiac dysfunction on posttransplantation cardiac function and the reversibility of the observed changes remain controversial. In this study a load-independent 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 inflation of a subdural balloon; 12 sham-operated animals served as control subjects. After a 2-hour observation in situ, the hearts were explanted and perfused parabiotically either immediately or after hypothermic ischemic 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, the slope of the end-systolic pressure-volume relationship, coronary blood flow, and myocardial oxygen consumption were estimated in the cross-circulated hearts.


RESULTS
In spite of a brain death-associated hemodynamic deterioration in situ (expressed as low mean aortic pressure and significant decrease of maximal dP/dt), myocardial function was similar to control after explantation, if assessed ex vivo. Furthermore, after hypothermic ischemic preservation and reperfusion, complete functional recovery of control and brain-dead hearts could be observed.


CONCLUSIONS
These data indicate that hemodynamic instability after brain death may rather reflect altered loading conditions than irreversible myocardial damage or primary cardiac dysfunction. Furthermore, there is no evidence for a brain death-related impairment of ischemic tolerance.
Szabó
G
G
Department of Cardiac Surgery, University of Heidelberg, Germany.
Sebening
C
C
Hackert
T
T
Hagl
C
C
Tochtermann
U
U
Vahl
C F
CF
Hagl
S
S
D000818:Animals; D001794:Blood Pressure; D001926:Brain Death / Q000503:physiopathology*; D002302:Cardiac Output; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate; D017202:Myocardial Ischemia / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury; D010101:Oxygen Consumption; D014019:Tissue Donors; D014021:Tissue Preservation; D016277:Ventricular Function, Left