Background. Postoperative cognitive dysfunction (POCD) refers to disorders affecting orientation, attention, perception, consciousness, and judgment that develop after geriatric orthopedic surgery. Cerebral blood oxygen saturation detection is a way to diagnose cerebral oxygen supply during operation. At present, more and more applications are used for early diagnosis of postoperative cognitive function. Therefore, the present study is to analyze the relationship between postoperative cognitive dysfunction and cerebral blood oxygen saturation in elderly orthopedic patients. Methods. This study enrolled 90 elderly patients undergoing orthopedic surgery in our hospital. According to the postoperative cognitive dysfunction, they were divided into POCD group ( N = 45 ) and no-POCD ( N = 45 ) group. The cognitive and psychological function and cerebral blood oxygen saturation were analyzed before and 3 months after the operation. Finally, the indicators of cognitive psychological function and the indicators of cerebral blood oxygen saturation are correlated and analyzed. Results. Compared with the normal group, patients with cognitive dysfunction at 3 months after surgery time below preoperative rScO2, time below a 10% decrease from preoperative rScO2, CDL preoperative, minimum rScO2 value, and maximum rScO2 value have significant changes. The results of the correlation analysis found that there is also a significant correlation between the postoperative cognitive and psychological function of the patient and the cerebral blood oxygen saturation at 3 weeks after the operation. Conclusion. In elderly orthopedic patients, there is a significant relationship between cerebral blood oxygen saturation detection and cognitive function 3 months after surgery.

This study aimed to investigate the role of sevoflurane on anti-oxidant effects in sepsis-induced multiple organ failure. Western blot and quantitative RT-PCR were used to measure the expression of Nrf2 and its downstream genes. The DCFH-DA fluorescence probe assay was performed to assess the intracellular levels in HUVECs and LMVECs. Electrophoretic mobility shift assay was used to assess the DNA binding activities of Nrf2. Better survival, reduced expression of inflammatory cytokines, and improved pathological infiltration in the lungs and kidneys were observed in septic rats treated with sevoflurane. SOD activity increased and Nrf2-ARE signaling pathway was activated following sevoflurane treatment. The protective effect was lost in sepsis-induced acute lung injury (ALI) following inhibition of Nrf2 by intratracheal delivery of siRNA-Nrf2. In vitro experiments, we found the sevoflurane could suppress ROS production after stimulation with LPS and the application of sevoflurane augments the DNA-binding activity of Nrf2 in HUVECs and LMVECs. However, knockdown of Nrf2 by siRNA-Nrf2, the Protein kinase C (PKC) inhibitor, and the Nrf2 inhibitor ML385 could partially recover ROS production, inhibit the activity of SOD, and repress the expression of anti-oxidant genes following sevoflurane treatment. Sevoflurane could have protective effects in ALI and septic multiple organ disorders (MODs).

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