Cellular mechanism of heart injury in the early stage of crush injury in rats.
- Author:
Shui-Ping LIU
1
;
Xiao-Shan LIU
;
Hua-Lan JING
;
Zhao-Hui LI
;
Yu-Chuan CHEN
Author Information
1. Department of Forensic Pathology, Preclinical School of Sun Yat-sen University, Guangzhou 510080, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Calcium/metabolism*;
Cell Size/drug effects*;
Cells, Cultured;
Disease Models, Animal;
Extremities/injuries*;
Heart Injuries/pathology*;
Heart Rate/drug effects*;
Immune Sera/pharmacology*;
Myocytes, Cardiac/pathology*;
Proto-Oncogene Proteins c-fos/metabolism*;
Rats;
Rats, Sprague-Dawley
- From:
Journal of Forensic Medicine
2006;22(2):90-92
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To study cellular mechanism of cardiomyocytes injury in the early stage of crush injury by observing some effects of crush injury rat sera on cultured neonatal rat cardiomyocytes.
METHODS:One to three days old neonatal rat cardiomyocytes were cultured in vitro and some effects of crush injury rat sera on beating rate, cell surface area, total protein content, 3H-Leu incorporation, intracellular calcium concentration ([Ca2+]i) and Fos protein expression were observed in cultured rat cardiomyocytes.
RESULTS:Compared with normal rat serum group, crush injury rat sera decreased beating rate(beats/min) of cardiomyocytes from 88.3 to 26.4, cell surface area, total protein content, 3H-Leu incorporation, [Ca2+]i (nmol/L) and PI of Fos protein expression were increased.
CONCLUSION:Crush injury rat sera suppress cell beating, increase intracellular calcium, induce Fos protein synthesis and cause cell hypertrophy, which may cause cardiac injury in the early stage of rush injury.