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Objective: The role of inflammation in cognitive alterations in a post-operative setting is still not fully understood. Surgical interventions can cause systemic inflammations which eventually can induce neuroinflammation. However, the main causes of functional changes after surgery are still elusive. In this study, we investigated the role of CD38, a TNFα-inducible NADH+ cyclase and hydrolase. We assume that CD38 overexpression impairs mitochondrial ATP synthesis. Within the hippocampus, the resulting cellular death could lead to cognitive impairment. Methods: Seventy-nine Wistar-HAN rats were subjected for three hours either to partial hepatectomy under sevoflurane anaesthesia ('surgery'), sevoflurane anaesthesia alone ('anaesthesia') or control. Rats were randomly selected to determine levels of CD38, TNFα, IL-6, and ATP, for GFAP immunohistochemistry and for Morris Water Maze testing. Results: Plasma TNFα and IL-6 levels were significantly higher in the surgery group in the immediate post-operative phase. GFAP expression and hippocampal CD38 concentration were significantly elevated 24 h after the intervention in the surgery group as compared to anaesthesia alone and controls. ATP levels did not differ significantly between the three groups. No treatment differences in spatial cognition parameters were found. Conclusions: Surgery in the form of partial hepatectomy activated the peripheral immune system and induced hippocampal glial activation and a CD38 increase. These changes, however, were not associated with rats' cognitive impairment ≥24 h after surgery. [ABSTRACT FROM AUTHOR]