Ultrastructural changes of rat cardiac myocytes in a time-dependent manner after traumatic brain injury

被引:25
作者
Ozisik, K [1 ]
Yildirim, E
Kaplan, S
Solaroglu, I
Sargon, MF
Kilinc, K
机构
[1] Ankara Numune Educ & Res Hosp, Dept Thorac & Cardiovasc Surg, Ankara, Turkey
[2] TYIH, Dept Cardiovasc Surg, Ankara, Turkey
[3] Ankara Numune Educ & Res Hosp, Dept Neurosurg, Ankara, Turkey
[4] Hacettepe Univ, Fac Med, Dept Biochem, TR-06100 Ankara, Turkey
关键词
heart; histology; rat; reactive oxygen species;
D O I
10.1111/j.1600-6143.2004.00448.x
中图分类号
R61 [外科手术学];
学科分类号
摘要
We suggest an ultrastructural scoring system to evaluate the degree of damage in a time-dependent manner in cardiac myocytes after traumatic brain injury (TBI). Forty Wistar-Albino female rats weighing 170-200 g were randomly allocated into five groups. Group 1 was the control and Group 2 was the sham-operated group. Group 3, Group 4 and Group 5 were trauma groups. Weight-drop technique was used for achieving TBI. Lipid peroxidation was estimated by thiobarbituric acid test. An electron microscopic scoring model was used to grade the subcellular changes. Results of heart injury score (HIS) showed that the 24-h trauma group had statistically significant levels in nuclear damage compared with the other groups (p<0.05). Sarcoplasmic reticulum and mitochondria scores of all trauma groups were significantly different from the control and sham groups (p<0.05). The results showed that lipid per oxidation levels were statistically significant different between the control and all trauma groups (p<0.05). The electron microscopic scoring model worked well in depicting the traumatic changes, which were supported by lipid peroxidation levels. Traumatic brain injury produced obvious gradual damage on the ultrastructure of the cardiac myocytes and this damage was more significant in the 24-h trauma group.
引用
收藏
页码:900 / 904
页数:5
相关论文
共 16 条
[1]  
Allen A., 1911, J AM MED ASS, V57, P878, DOI 10.1001/jama.1911.04260090100008
[2]   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
[3]   Nimodipine attenuates lipid peroxidation during the acute phase of head trauma in rats [J].
Ercan, M ;
Inci, S ;
Kilinc, K ;
Palaoglu, S ;
Aypar, Ü .
NEUROSURGICAL REVIEW, 2001, 24 (2-3) :127-130
[4]   BRAIN DEATH-INDUCED IMPAIRMENT OF CARDIAC CONTRACTILE PERFORMANCE CAN BE REVERSED BY EXPLANTATION AND MAY NOT PRECLUDE THE USE OF HEARTS FOR TRANSPLANTATION [J].
GALINANES, M ;
HEARSE, DJ .
CIRCULATION RESEARCH, 1992, 71 (05) :1213-1219
[5]  
GILBERT EM, 1988, J THORAC CARDIOV SUR, V95, P1003
[6]   Antioxidant therapy in acute central nervous system injury: Current state [J].
Gilgun-Sherki, Y ;
Rosenbaum, Z ;
Melamed, E ;
Offen, D .
PHARMACOLOGICAL REVIEWS, 2002, 54 (02) :271-284
[7]   CARDIAC INJURY AND SUBARACHNOID HEMORRHAGE - A CLINICAL PATHOLOGICAL AND PHYSIOLOGICAL CORRELATION [J].
GREENHOO.JH ;
REICHENB.DD .
JOURNAL OF NEUROSURGERY, 1969, 30 (05) :521-&
[8]  
Hall SRR, 2002, ANESTH ANALG, V94, P948
[9]   CATECHOLAMINES PREDICT OUTCOME IN TRAUMATIC BRAIN INJURY [J].
HAMILL, RW ;
WOOLF, PD ;
MCDONALD, JV ;
LEE, LA ;
KELLY, M .
ANNALS OF NEUROLOGY, 1987, 21 (05) :438-443
[10]   MYOCARDIAL DAMAGE FROM ACUTE CEREBRAL-LESIONS [J].
KOLIN, A ;
NORRIS, JW .
STROKE, 1984, 15 (06) :990-993