Brain death and its impact on the donor heart - Lessons from animal models

被引:66
作者
Wilhelm, MJ [1 ]
Pratschke, J [1 ]
Laskowski, IA [1 ]
Paz, DM [1 ]
Tilney, NL [1 ]
机构
[1] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Surg,Surg Res Lab, Boston, MA 02115 USA
关键词
D O I
10.1016/S1053-2498(00)00073-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In the light of increasing shortage of 'suitable' donor organs, donor management has become particularly important. Brain death has been recognized as being a determining factor in donor organ quality. Experimental brain death models demonstrate severe impairment of myocardial function and hemodynamic performance. An excessive catecholamine surge, occurring shortly after central catastrophe, seems to be associated with severe myocardial damage and subsequent cardiovascular changes. Acute neurohormonal failure resulting from extensive brain damage and concurrent metabolic dysbalance contributes to progressive functional deterioration. However, it still remains controversial as to which factors determine whether hearts undergo complete recovery or progress to extensive subendocardial necrosis after brain death and subsequent procurement. Future investigations of the underlying molecular mechanisms may provide further insight into the process accompanying this central catastrophe, and may lead to therapeutic strategies to improve donor organ quality.
引用
收藏
页码:414 / 418
页数:5
相关论文
共 35 条
[1]   Brain death further promotes ischemic reperfusion injury of the rabbit myocardium [J].
Biswas, SS ;
Chen, EP ;
Bittner, HB ;
Davis, RD ;
VanTrigt, P .
ANNALS OF THORACIC SURGERY, 1996, 62 (06) :1808-1815
[2]   Brain death alters cardiopulmonary hemodynamics and impairs right ventricular power reserve against an elevation of pulmonary vascular resistance [J].
Bittner, HB ;
Chen, EP ;
Kendall, SWH ;
VanTrigt, P .
CHEST, 1997, 111 (03) :706-711
[3]  
BITTNER HB, 1995, ANN THORAC SURG, V60, P47
[4]  
Bittner HB, 1996, CIRCULATION, V94, P320
[5]   MYOCARDIAL BETA-ADRENERGIC-RECEPTOR FUNCTION AND HIGH-ENERGY PHOSPHATES IN BRAIN DEATH-RELATED CARDIAC DYSFUNCTION [J].
BITTNER, HB ;
CHEN, EP ;
MILANO, CA ;
KENDALL, SWH ;
JENNINGS, RB ;
SABISTON, DC ;
VANTRIGT, P .
CIRCULATION, 1995, 92 (09) :472-478
[6]  
BITTNER HB, 1995, J HEART LUNG TRANSPL, V14, P308
[7]   Acute increase of myocardial workload, hemodynamic instability, and myocardial histological changes induced by brain death in the cat [J].
Bruinsma, GJBB ;
Nederhoff, MGJ ;
Geertman, HJ ;
vanHuffelen, AC ;
Slootweg, PJ ;
Ferrari, R ;
Galinanes, M ;
Hearse, DJ ;
Bredee, JJ ;
Ruigrok, TJC .
JOURNAL OF SURGICAL RESEARCH, 1997, 68 (01) :7-15
[8]   Hormonal and hemodynamic changes in a validated animal model of brain death [J].
Chen, EP ;
Bittner, HB ;
Kendall, SWH ;
VanTrigt, P .
CRITICAL CARE MEDICINE, 1996, 24 (08) :1352-1359
[9]   Some experimental and clinical observations concerning states of increased intracranial tension. The Mutter Lecture for 1901. [J].
Cushing, H .
AMERICAN JOURNAL OF THE MEDICAL SCIENCES, 1902, 124 :375-400
[10]   DESENSITIZATION OF MYOCARDIAL BETA-ADRENERGIC RECEPTORS AND DETERIORATION OF LEFT-VENTRICULAR FUNCTION AFTER BRAIN-DEATH [J].
DAMICO, TA ;
MEYERS, CH ;
KOUTLAS, TC ;
PETERSEIM, DS ;
SABISTON, DC ;
VANTRIGT, P ;
SCHWINN, DA .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1995, 110 (03) :746-751