Surgical trauma stress has been reported to induce immunosuppression. The mechanisms involved are still unclear. The present study was designed to assess the role of the sympathetic nervous system in regulating splenocyte apoptosis induced by surgical trauma stress. Our results showed that the rats that underwent surgical trauma stress exhibited a significant reduction in splenic cellularity, the loss of splenocytes was likely mediated by apoptosis, for a substantial increase in apoptosis was observed by using DNA gel electrophoresis and TUNEL assay. At the same time, an increase in Fas(CD95/Apo-1) protein expression in splenocytes was also observed. These effects were significantly abolished by either chemical sympathectomy or beta-adrenergic receptor antagonist propranolol. The data clearly revealed that the sympathetic nervous system especially beta-adrenergic receptors was involved in surgical trauma-induced immune alterations via a mechanism of apoptotic cell death.