Modulation of coronary perfusion pressure can reverse cardiac dysfunction after brain death

被引:33
作者
Szabó, G [1 ]
Hackert, T [1 ]
Sebening, C [1 ]
Vahl, CF [1 ]
Hagl, S [1 ]
机构
[1] Heidelberg Univ, Dept Cardiac Surg, D-69120 Heidelberg, Germany
关键词
D O I
10.1016/S0003-4975(98)01307-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background. Brain death results in a rapid decline in left ventricular function, which has clinical relevance for organ transplantation. The aim of the present study was to investigate coronary perfusion changes during brain death and their role in cardiac dysfunction. Methods. In an in situ isolated canine heart model, brain death was induced by inflation of a subdural balloon catheter. The heart was perfused separately with the animal's own blood by a pressure-controlled roller pump that was coupled to the measured aortic pressure. Myocardial contractility was estimated by the slope of the end-systolic pressure-volume relation. Results. Induction of brain death resulted in a transient hyperdynamic response, followed by a significant decrease in systemic vascular resistance, coronary blood now, and the end-systolic pressure-volume relation (p < 0.05). However, if coronary perfusion pressure was decoupled from aortic pressure and elevated to pre-brain death levels, coronary blood now and the end-systolic pressure-volume relation were also restored to baseline levels. Conclusion. Severe impairment of coronary blood now may contribute to decreased contractility after brain death that can be reversed by modulation of coronary perfusion pressure. (C) 1999 by The Society of Thoracic Surgeons.
引用
收藏
页码:18 / 25
页数:8
相关论文
共 25 条
[1]  
ABEL R M, 1970, Circulation Research, V27, P961
[2]   IMPORTANCE OF PERFUSION PRESSURE IN CORONARY ARTERIES FOR CONTRACTILITY AND OXYGEN CONSUMPTION OF HEART [J].
ARNOLD, G ;
KOSCHE, F ;
MIESSNER, E ;
NEITZERT, A ;
LOCHNER, W .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1968, 299 (04) :339-+
[3]   AUTOREGULATION OF HEART WORK BY CORONARY PERFUSION PRESSURE [J].
ARNOLD, G ;
MORGENSTERN, C ;
LOCHNER, W .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1970, 321 (01) :34-+
[4]   NEURAL MODULATION OF VENTRICULOARTERIAL COUPLING IN CONSCIOUS DOGS [J].
ASANOI, H ;
ISHIZAKA, S ;
KAMEYAMA, T ;
SASAYAMA, S .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 266 (02) :H741-H748
[5]  
Baroldi G, 1997, J HEART LUNG TRANSPL, V16, P994
[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]  
DOWNEY JM, 1976, AM J PHYSIOL, V230, P1
[9]   BRAIN-DEATH-INDUCED CARDIAC CONTRACTILE DYSFUNCTION - STUDIES OF POSSIBLE NEUROHORMONAL AND BLOOD-BORNE MEDIATORS [J].
GALINANES, M ;
HEARSE, DJ .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1994, 26 (04) :481-498
[10]   Changes in organ perfusion after brain death in the rat and its relation to circulating catecholamines [J].
Herijgers, P ;
Leunens, V ;
TjandraMaga, TB ;
Mubagwa, K ;
Flameng, W .
TRANSPLANTATION, 1996, 62 (03) :330-335