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Abstract Background Postoperative cognitive dysfunction (POCD) is a common complication after anesthesia/surgery, especially among elderly patients, and poses a significant threat to their postoperative quality of life and overall well-being. While it is widely accepted that elderly patients may experience POCD following anesthesia/surgery, the exact mechanism behind this phenomenon remains unclear. Several studies have indicated that the interaction between silent mating type information regulation 2 homologue 1 (SIRT1) and brain-derived neurotrophic factor (BDNF) is crucial in controlling cognitive function and is strongly linked to neurodegenerative disorders. Hence, this research aims to explore how SIRT1/BDNF impacts cognitive decline caused by anesthesia/surgery in aged mice. Methods Open field test (OFT) was used to determine whether anesthesia/surgery affected the motor ability of mice, while the postoperative cognitive function of 18 months old mice was evaluated with Novel object recognition test (NORT), Object location test (OLT) and Fear condition test (FC). The expressions of SIRT1 and other molecules were analyzed by western blot and immunofluorescence staining. The hippocampal synaptic plasticity was detected by Golgi staining and Long-term potentiation (LTP). The effects of SIRT1 and BDNF overexpression as well as chemogenetic activation of glutamatergic neurons in hippocampal CA1 region of 18 months old vesicular glutamate transporter 1 (VGLUT1) mice on POCD were further investigated. Results The research results revealed that older mice exhibited cognitive impairment following intramedullary fixation of tibial fracture. Additionally, a notable decrease in the expression of SIRT1/BDNF and neuronal excitability in hippocampal CA1 glutamatergic neurons was observed. By increasing levels of SIRT1/BDNF or enhancing glutamatergic neuron excitability in the CA1 region, it was possible to effectively mitigate synaptic plasticity impairment and ameliorate postoperative cognitive dysfunction. Conclusions The decline in SIRT1/BDNF levels leading to changes in synaptic plasticity and neuronal excitability in older mice could be a significant factor contributing to cognitive impairment after anesthesia/surgery. Graphical Abstract

BackgroundCardiac paraganglioma (CPGL) accounts for 1–3% of cardiac tumors and is usually benign. In total, 35–50% of CPGL lesions secrete catecholamines, causing hypertension, excessive sweating, palpitations, headache, and other symptoms. Preoperative imaging evaluation is important to determine the location of the cardiac mass, its blood supply vessels, and the relationship with surrounding structures. Multimodal imaging techniques combine with morphological and functional information to provide powerful methods for preoperative diagnosis and lesion localization. Furthermore, they can assist to reduce the incidence of intraoperative and postoperative complications and improve patient prognosis.Case ReportA 67-year-old woman suffered from paroxysmal palpitations with a heart rate of 110 beats per minute 1 month ago. Urine catecholamine and methoxyepinephrine levels were significantly increased. The patient had a 5-year history of hypertension with a maximum blood pressure of 160/100 mmHg. Computed tomography (CT) examination found a soft tissue mass in the right atrium with heterogeneous and significant enhancement, whose blood supply was from the left ileal branch artery. The patient then underwent cardiac magnetic resonance (CMR). The lesion showed inhomogeneous iso signals on the T1-weighted image (T1WI), slightly high signals on the T2 fat-suppression image, inhomogeneous high signals on the diffusion-weighted imaging (DWI), and apparent diffusion coefficient (ADC) images. The mass exhibited heterogeneous and significant enhancement on the first perfusion and delayed scans after intravenous contrast injection. However, abnormal signals were surprisingly found in the patient’s right lung, and the possibility of metastatic lesions could not be excluded. The patient underwent F-18 fluorodeoxyglucose-positron emission tomography/computed tomography (18F-FDG PET/CT) to rule out metastatic lesions. A fluorodeoxyglucose (FDG)-avid soft tissue mass was shown in the right atrium, with the maximum standardized uptake value (SUVmax) at about 15.2, as well as a pathological intake of brown fat throughout the body. Combined with clinical symptoms, CPGL was considered without significant sign of metastasis in 18F-FDG PET/CT. Finally, the patient underwent surgical resection and the post-operative pathology confirmed a CPGL.ConclusionThe combination of 18F-FDG PET/CT with the CMR containing different image acquisition sequences provides a powerful aid for preoperative non-invasive diagnosis, localization, and staging of CPGL, which helps to reduce intraoperative and postoperative complications and improve patient prognosis.

Anxiety disorders are the most common psychiatric diseases, and perioperative factors often increase the incidence of anxiety. However, the mechanism and treatment for perioperative anxiety, especially anesthesia/surgery-induced postoperative anxiety, are largely unknown. Sirtuin 3 (SIRT3) which located in the mitochondria is the NAD-dependent deacetylase protein. SIRT3 mediated oxidative stress is associated with several neuropsychiatric diseases. In addition, hyperpolarization-activated cyclic nucleotide-gated 1 (HCN1) channel is also reported involved in anxiety symptoms. The purpose was to assess the role of SIRT3 on postoperative anxiety like behavior in C57/BL6 mice. We found that SIRT3 level reduced and HCN1 expression level increased in mice medial prefrontal cortex (mPFC) as well as anxiety like behavior postoperatively. In interventional research, SIRT3 adeno-associated virus vector or control vector was injected into the mPFC brain region. Enzyme-linked immunosorbent assay, immunofluorescence staining, and western blotting were employed to detect oxidative stress reactions and HCN1 channel activity. SIRT3 overexpression attenuated postoperative anxiety in mice. Superoxide dismutase 2 (SOD2) acetylation levels, SOD2 oxidative stress activity, mitochondrial membrane potential levels, and HCN1 channels were also inhibited by SIRT3 overexpression. Furthermore, the HCN1 channel inhibitor ZD7288 significantly protected against anesthesia/surgery-induced anxiety, but without SIRT3/ac-SOD2 expression or oxidative stress changes. Our results suggest that SIRT3 may achieve antianxiety effects through regulation of SOD2 acetylation-mediated oxidative stress and HCN1 channels in the mPFC, further strengthening the therapeutic potential of targeting SIRT3 for anesthesia/surgery-induced anxiety-like behavior.