Correlation of cell apoptosis with brain edema and elevated intracranial pressure in traumatic brain injury.
- Author:
Xiao-feng YANG
1
;
Wei-guo LIU
;
Hong SHEN
;
Jiang-biao GONG
;
Jun YU
;
Wei-wei HU
;
Shi-ting LÜ
;
Xiu-jue ZHENG
;
Wei-ming FU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Brain Edema; etiology; metabolism; pathology; Brain Injuries; complications; pathology; physiopathology; Cell Count; Disease Models, Animal; In Situ Nick-End Labeling; Intracranial Hypertension; etiology; pathology; physiopathology; Male; Necrosis; genetics; pathology; Rabbits; Reference Values; Telencephalon; metabolism; Water; metabolism
- From: Chinese Journal of Traumatology 2005;8(2):96-100
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI).
METHODSIn this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain.
RESULTSApoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP.
CONCLUSIONSIn TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.
