Abstract: Objective To investigate the effects of sympathetic excitation and dendritic cell activation on myocardial injury in LPS-induced rats. Methods：The rats were randomly divided into control group, LPS group (intraperitoneal injection of LPS :10 mg/kg), the intervention group was given beta receptor blocker Ate (5 mg/kg) and DC inhibitor VAG539 (30 mg/kg gavage 2 times a day for 2 days) respectively after LPS administration. The powerlab system was used to record the hemodynamic and sympathetic data. The concentration of norepinephrine (NE) in plasma was measured by high performance liquid chromatography (HPLC), and the expression and positive cells of TNF-αand DCs in myocardium were detected by immunohistochemistry. Results Compared with the control group, the plasma NE level significantly increased(P<0.05);The expression of TNF-αand DCs in heart tissue significantly increased (P<0.05);the renal sympathetic nerve activity（SNA） significantly increased between the three groups after LPS administration for 24h. Compared with the LPS group, the plasma NE level significantly decreased(P<0.05);The expression of TNF-αand DCs in heart tissue significantly decreased (P<0.05);the renal SNA significantly decreased after Ate and VAG539 administration(P<0.05).Conclusions Excessive activation of sympathetic nervous system and activation of DC aggravate myocardial injury induced by LPS in LPS-induced rats.

Key words: sympathetic excitation, dendritic cell, sepsis, myocardial injury