Effects of Brain Death on the Myocardium in Canine Brain Death Models.
10.4070/kcj.1996.26.1.100
- Author:
Myeong Chan CHO
;
Gi Byoung NAM
;
Dong Woon KIM
;
Seong Sook KIM
- Publication Type:Original Article
- Keywords:
Brain death;
Hemodynamics;
Myocardium;
Apoptosis
- MeSH:
Animals;
Apoptosis;
Brain Death*;
Brain*;
Catheters;
Chromatin;
Coronary Vessels;
Dogs;
Electrocardiography;
Heart;
Hemodynamics;
In Situ Nick-End Labeling;
Microscopy;
Microscopy, Electron;
Muscle Cells;
Myocardium*;
Nuclear Envelope
- From:Korean Circulation Journal
1996;26(1):100-111
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Clinical and experimental studies have suggested that brain death may cause hemodynamic, electrocardiographic, functional or histopathologic changes of the heart. METHODS: Brain death was induced by increasing intracranial pressure(ICP) abruptly by intermittent bolus injection of saline(model ) or gradually by continuous infusion of saline(model ) to the epidural catheter in 5 mongrel dogs, respectively. Hemodynamic and biochemical changes during the process of brain death and histopathologic changes of the myocardium were analyzed and compared in two brain death models, and the association of apoptosis was also evaluated. RESULTS: 1) Two predominant subsets of acute contraction band lesion were produced in both brain death models : paradiscal and holocystic contraction band lesions. Both contraction band lesions were more prevalent in brain death model . 2) The frequency of both contraction band lesions was lowest in the epicardial layer and highest in the endocardial layer in both models, but no correlation was observed between the degree of contraction band lesions and ICP, LV maximum +dp/dt or catecholamine levels. There was no statistical difference between any of the LV circumferential blocks and either type of contraction band lesion, and transaxial distribution was not also different in both models. 3) There was no remarkable histopathologic changes in the analysis of major epicardial coronary arteries. Apoptotic cells were suggested in the scattered myocytes in the light microscopy and apoptosis was detected by in situ nick end labeling method. Electron microscopy revealed a condensation of nuclear chromatin and convolution of nuclear membrane in those myocytes. CONCLUSIONS: Myocardial changes due to brain were observed frequently, and few apoptotic cells were found in the brain death heart. Studies on the treatment strategy to minimize damages of myocardial structure and function caused by brain death should be followed in the near future.
