Background: Cerebral ischemia and reperfusion affects not only cellular necrosis at acute stage, but also delayed neuronal apoptosis in central neural system. Objective: To observe apoptosis rate, necrosis rate and expression of Bcl-2 and Bax apoptosis-regulating proteins in hippocampal neurons at various reperfusion stages of complete cerebral ischemia in rats so as to probe into the regulation of injury induced by complete cerebral ischemia and reperfusion. Design: Randomized control experiment. Setting: Department of Neurosurgery and Department of Anesthesiology in Beijing Tiantan Hospital Affiliated to Capital University of Medical Sciences. Materials: The experiment was performed in Beijing Institute of Neurosurgery Affiliated to Capital University of Medical Sciences from January 2003 to January 2004. Totally 33 healthy adult male Wistar rats of clean grade were employed, randomized in 5 groups, named ischemia + reperfusion 24 hours group (24 hours group) (7 rats), ischemia + reperfusion 48 hours group (48 hours group) (7 rats), ischemia + reperfusion 72 hours group (72 hours group) (7 rats), ischemia + reperfusion 7 days group (7 days group) (7 rats) and sham-operation control (control) (5 rats). Interventions: Model of complete cerebral ischemia and reperfusion was prepared in rat. Cerebral hippocampal tissues were collected in 24, 48, 72 hours and 7 days after reperfusion successively. The flow cytometer was used to determine cellular apoptosis rate and necrosis rate and expression of Bcl-2 and Bax proteins in cerebral hippocampal neurons in rats. Main outcome measures: 1 Apoptosis rate and necrosis rate of cells-in rats of every group determined with flow cytometer. 2 Expression percentages of Bcl-2 and Bax proteins. Results: All of the 33 rats entered result analysis. 1 Apoptosis rate of hippocampal neurons in 7 days group was the highest [(24.59±0.97) %]. The peak value of necrosis rate presented in 24 hours group [(16.67 ±1.04)%], which was remarkably higher than the control [(1.28±0.50)%, (0.90±0.38)%] (P < 0.01). 2 In the control, Bcl-2 expression was extremely low [(1.07±0.27)%], but high expression of Bax presented [(46.09±5.37)%]. 3 The peak value of Bcl-2 protein presented in 48 hours after ischemia and reperfusion [(14.41±0.67)%] and the peak value of Bax protein presented in 72 hours after ischemia and reperfusion [(77.38±1.52)%]. Conclusion: Hippocampal neuronal apoptosis rate is increased gradually and expression of Bcl-2 and Bax apoptosis-regulating genes was increased abnormally after injury induced by complete cerebral ischemia and reperfusion, which suggests that Bcl-1 and Bax proteins are involved in apoptosis regulation in the injury induced by complete cerebral ischemia and reperfusion.