BACKGROUND:Perioperative hypothermia may lead to coagulation function for patients undergoing total knee arthroplasty,and an increase in blood loss.OBJECTIVE:To compare the influence of temperature protection with non-temperature protection on coagulation function in patients undergoing total knee arthroplasty.METHODS:Forty ASA Ⅰ-Ⅱ patients scheduled for total knee arthroplasty were randomly divided into temperature protection and non-temperature protection groups (n=20 per group).The patients in the temperature protection group underwent heat-preservation including preheating room temperature,actively blanket warmer,were infused or flushed with fluids of 37 ℃ by heating apparatus;the patients in the non-temperature protection group received full-body-covered cotton quilt only.The nasopharyngeal temperature were detected at postoperative 10 minutes,intraoperative 1 hour and postoperative 1 hour,and 1.25 mL of venous blood were collected to detect the fibrin formation time,blood clot formation time,and maximum amplitude using thrombelastography.Additionally,the intraoperative blood loss and volume of drainage at postoperative 24 hours were recorded.RESULTS AND CONCLUSION:(1) The nasopharyngeal temperature in the non-temperature protection group was significantly lower than that in the temperature protection group at postoperative 1 hour (P ＜ 0.05).(2) The intraoperative blood loss and volume of drainage at postoperative 24 hours in the temperature protection group were significantly less than those in the non-temperature protection group (P ＜ 0.05).(3) Compared with the temperature protection group,fibrin formation time and blood clot formation time at intraoperative and postoperative 1 hour were significantly lengthened,and maximum amplitude at postoperative 1 hour was significantly shortened in the non-temperature protection group (P ＜ 0.05).(4) These findings show that intraoperative hypothermia can weaken platelet function,inhibit coagulation factor activity,and increase the amount of blood loss and drainage.In the meanwhile,heat-preservation is able to reduce the loss of body heat,improve coagulation function and reduce blood loss for patients undergoing knee replacement.

BACKGROUND: Transcutaneous electrical acupoint stimulation (TEAS) exerts good analgesic effect, but its effectiveness and safety in analgesia after total knee arthroplasty have not been reported.OBJECTIVE: To evaluate the analgesic effect of TEAS at the auricular Shenmen (H 7) point in patients undergoing total knee arthroplasty.METHODS: Forty ASA Ⅰ-Ⅲ patients scheduled for total knee arthroplasty under general anesthesia combined with femoral nerve block were enrolled and randomly divided into experimental and control groups (n=20 per group). The patients in the experimental group received TEAS at auricular Shenmen (H 7) point before anesthesia, 8, 16, 36, and 56 hours postoperatively for 30 minutes. The patients in the control group received same method with the experimental group, but without electrical stimulation. Ultrasound-guided continuous femoral nerve blockade was performed before induction, followed by tracheal tube was inserted and the patients were mechanically ventilated. The patients received patient-controlled continuous femoral nerve analgesia after surgery for 72 hours. The Visual Analogue Scale scores and the quadriceps maximum voluntary isometric contraction were recorded at postoperative 6, 12, 24, 48 and 72 hours. The consumption of ropivacaine and tramadol hydrochloride was recorded. Additionally, the incidence of adverse reactions was recorded.RESULTS AND CONCLUSION: (1) The Visual Analogue Scale scores in the experimental group were significantly lower than those in the control group at postoperative 48 and 72 hours (P < 0.05). (2) The quadriceps maximum voluntary isometric contraction in the control group was significantly lower than that in the experimental group at each time point (P < 0.05). (3) The consumption of ropivacaine in the control group ((495.7±39.4) mL) was significantly more than that in the experimental group ((394.5±27.1) mL) (P < 0.05). Seven cases in the control group and one case in the experimental group received the injection of tramadol hydrochloride (P < 0.05). (4) Nausea and vomiting occurred in six cases in the control group and one case in the experimental group, and dizziness only occurred in four cases in the control group (P < 0.05). (5) To conclude, TEAS at the auricular Shenmen (H 7) point can improve the pain after total knee arthroplasty, reduce the consumption of ropivacaine and tramadol hydrochloride, and maintain quadriceps strength.

Objective:To evaluate the role of silent information regulator 1 (SIRT1)/nuclear factor E2 related factor 2 (Nrf2) signaling pathway in sleep deprivation-induced cognitive dysfunction in rats.Methods:Thirty-six adult male Sprague-Dawley rats, aged 54-56 weeks, weighing 600-750 g, were divided into 3 groups ( n=12 each) using a random number table method: control group (group C), sleep deprivation group (group SD) and sleep deprivation+ SIRT1 agonist Srt1720 group (group SD+ Srt). Sleep deprivation model was established by modified multi-platform water environment method.Srt1720 10 mg/kg was injected intraperitoneally every 12 h starting from 24 h before establishing the model in group SD+ Srt, while the equal volume of 0.9% normal saline was injected intraperitoneally in C and SD groups.After the end of sleep deprivation, Morris water maze test was performed to evaluate the cognitive function.Animals were then sacrificed, and their hippocampi were removed for determination of neuronal degeneration rate in hippocampal CA1 region (using HE staining), the apoptosis rate in hippocampal CA1 (using TUNEL assay ), the expression of SIRT1 and Nrf2 in hippocampal CA1 (by immunohistochemistry) and the contents of reactive oxygen species (ROS) and superoxide dismutase (SOD) (by microplate method). Results:Compared with group C, the escape latency was significantly prolonged, the time of staying at the platform quadrant was shortened, and the frequency of crossing the platform was decreased on 2-4 days, the apoptotic rate and neuronal degeneration rate were increased, the expression of SIRT1 and Nrf2 was down-regulated, ROC content was increased, and SOD content was decreased in SD and SD+ Srt groups ( P<0.05). Compared with group SD, the escape latency was significantly shortened, the time of staying at the platform quadrant was prolonged, and the frequency of crossing the platform was increased on 3 and 4 days, the apoptotic rate and neuronal degeneration rate were decreased, the expression of SIRT1 and Nrf2 was up-regulated, ROC content was decreased, and SOD content was increased in group SD+ Srt ( P<0.05). Conclusions:Sleep deprivation can induce oxidative stress response in hippocampus by inhibiting the activation of SIRT1/Nrf2 signaling pathway, leading to cognitive dysfunction in rats.

Objective:To evaluate the effect of edaravone on mitochondrial function during ketamine-induced apoptosis in PC12 cells.Methods:Nerve growth factor (NGF)-induced differentiating PC-12 cells were divided into 3 groups ( n=30 each) using a random number table method: control group (group C), ketamine group (group K) and edaravone plus ketamine group (group EK). Cells in group C were commonly cultured.In group K, PC12 cells were incubated with PBS and 100 μmol/L ketamine at 7 days after differentiation.In group EK, cells were incubated with 10 μmol/L edaravone and 100 μmol/L ketamine.The cell viability, caspase-3/7 activity, reactive oxygen species (ROS) activity, adenosine triphosphate (ATP) content and NADH/NAD + ratio were determined using analysis kits at 24 h of incubation.The cell apoptosis was observed by TUNEL assay and apoptosis rate was calculated. Results:Compared with group C, the cell viability, caspase-3/7 activity, NADH/NAD + ratio and apoptosis rate were significantly increased, and ROS activity and ATP content were decreased in group K ( P<0.05). Compared with group K, the cell viability, caspase-3/7 activity, NADH/NAD + ratio and apoptosis rate were significantly decreased, and ROS activity and ATP content were increased in group EK ( P<0.05). Conclusion:The mechanism by which edaravone inhibits ketamine-induced apoptosis in PC12 cells is related to improving mitochondrial function.