EFFECTS OF BRAIN-DEATH ON MYOCARDIAL-FUNCTION AND ISCHEMIC TOLERANCE OF POTENTIAL DONOR HEARTS

Citation
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
ISSN journal
10532498
Volume
17
Issue
9
Year of publication
1998
Pages
921 - 930
Database
ISI
SICI code
1053-2498(1998)17:9<921:EOBOMA>2.0.ZU;2-L
Abstract
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.