Effects of transection of cervical sympathetic trunk on left ventricular remodeling after acute myocardial infarction in rats

Objective To investigate the effects of right or left transaction of cervical sympathetic trunk (TCST) on left ventricalar remodeling (LVRM) after acute myocardial infarction in rats and the mechanism. Methods Sixty-four adult mule pathogen-free SD rats (230-250 g) were randomly divided into 4 groups (n=16 each): group Ⅰsham operation (group S) ; group Ⅱ LVRM; group Ⅲ left TCST and group Ⅳ right TCST. Myocardial infarct was induced by ligation of left anterior descending branch (LAD) of coronary artery in group Ⅱ, Ⅲ and Ⅳ. Left and right TCST were performed immediately after myocardial infarct was successfully induced in group Ⅲ and Ⅳ respectively. In group S LAD and cervical sympathetic trunk were exposed but not ligated and transected. The animals were killed at 4 weeks after ligation of LAD and TCST. The weight of left ventricle was measured and left ventricle weight index calculated, Left veatricular myocardial tissue volume (V_t), the volume density of myocardial cells (V_v) and myocardial cell volmne (V_c) were quantitatively analyzed by stereological method. The c-fos mRNA expression in myocardium was determined by RT-PCR. Results The left ventricle weight index, V_t, V_c and c-fos mRNA expression were significantly increased in group LVRM (Ⅱ), left and right TCST (Ⅲ, Ⅳ) as compared with group S. Left ventricle weight index, V_v, V_t, V_c and c-fos mRNA expression were all significantly decreased in fight TCST group (Ⅳ), while left ventricle weight index, V_t, V_c and c-fos mRNA expression were significantly increased in left TCST group (Ⅲ) as compared with LVRM group (Ⅱ). Conclusion Right TCST down-regulates the increase in c-fos mRNA expression after acute myocardial infarction and inhibits the left ventricular remodeling while left TCST up-regulates the c-fos mRNA expression and promotes the development of left ventricular remodeling. Key words: Ganglia;  sympathetic;  Sympathectomy;  Myocardial infarction;  Ventricular remodeling