Despite the widespread adoption of uniportal video-assisted thoracoscopic surgery (VATS), postoperative pain associated with this procedure remains a significant concern. Effective postoperative analgesia is essential for facilitating the recovery of patients undergoing thoracic surgery. Thoracic paravertebral block (TPVB) is widely recognized as an extremely effective method of analgesia in such surgeries. Our previous study has demonstrated that the diffusion of local anesthetic during nerve blocks is related to body position. Therefore, this study aimed to evaluate the impact of thoracic paravertebral nerve block in various body positions on the analgesic outcomes for patients undergoing single-port thoracoscopic lung resection. A randomized controlled trial was conducted to assess the impact of different body positions during thoracic paravertebral nerve blocks on the analgesic effect in patients undergoing single-port thoracoscopic partial lung resection. Patients scheduled for thoracoscopic lung resection will be included in this study. Participants (n = 200) will undergo thoracic paravertebral nerve block under ultrasound guidance. After the injection of the drug, they will be placed in either a supine position or a lateral position with the puncture side up. The NRS scores will be assessed at 1 h, 2 h, 8 h, 12 h, 24 h, and 48 h postoperatively. Postoperative opioid consumption, rescue analgesia time and frequency, patient satisfaction, incidence of adverse reactions, and length of hospital stay will also be recorded. This research project mainly aimed to investigate the impact of different perioperative positions for thoracic paravertebral nerve block on the analgesic effects in patients undergoing single-port thoracoscopic lung resection. The results may provide important implications for the development of effective analgesic strategies and robust clinical evidence to support the recovery of patients undergoing thoracic surgery. ClinicalTrials.gov NCT06789276. Registered on 10 January 2025.

BACKGROUND Monitoring nociception is extraordinarily challenging during general anesthesia. This study aimed to observe pupillary dilation reflex by ultrasound and determine whether ultrasonic pupillary parameters are correlated with sufentanil dose during the induction period of general anesthesia. MATERIAL AND METHODS We enrolled 93 patients undergoing general anesthesia. They were randomly divided into 3 groups - group P (saline), group S1 (0.2 μg/kg sufentanil), and group S2 (0.4 μg/kg sufentanil) - according to the sufentanil dose of induction. Patients were administered a tetanic stimulation 5 min after intravenous injection with sufentanil. Ultrasonic pupil diameters were recorded and measured at 4 time points: T0 (entering the room awake), T1 (after loss of consciousness), T2 (5 min after intravenous injection with sufentanil), and T3 (the moment at which pupil diameter was maximum after stimulation). Systolic blood pressure, diastolic blood pressure, heart rate, and BIS at T0~T3 were recorded. The process of pupillary dilation reflex was recorded in ultrasound views and videos to generate relevant clinical data, including pupillary dilation reflex amplitude, pupillary dilation reflex rate, whether pupillary dilation reflex was inhibited, pupillary dilation reflex latency, and pupillary dilation reflex duration. RESULTS Ultrasonic pupillary dilation reflex amplitude and pupillary dilation reflex rate were negatively correlated with sufentanil dose [Spearman r=-0.84 (95% CI, -0.88 to -0.77), p<0.01, Spearman r=-0.74, (95% CI, -0.82 to -0.64), p<0.01]. Only PD responded to stimulation within 30 s, whereas systolic blood pressure, diastolic blood pressure, and BIS did not respond to stimulation. CONCLUSIONS Ultrasound can be a useful method for observing pupillary dilation reflex, and sufentanil inhibits pupillary dilation reflex in a dose-dependent manner. Ultrasonic pupillary dilation reflex is sensitive to noxious stimulation.

The disruption of mitochondrial homeostasis in neurons accounts for the onset and progression of postoperative cognitive dysfunction (POCD). Echinacoside (ECH) can facilitate mitochondrial fusion to mediate neuroprotection, but its therapeutic efficacy is greatly limited by inefficient brain accumulation and neuronal delivery. Herein, ECH-encapsulated micelles are constructed from the copolymer containing the poly(carboxybetaine methacrylate) (PCBMA) block and phenylboronic acid (PBA)-modified poly(dimethylamino)ethyl methacrylate block, which mediates effective, brain-targeted delivery via intranasal administration. In POCD mice, the micelles efficiently penetrate nasal mucosa via the betaine structure in PCBMA that can be recognized by betaine-GABA transporter 1 (BGT-1) on nasal epithelial cells, followed by the accumulation into the hippocampus through the submucosal olfactory and trigeminal nerve pathways. Subsequently, the micelles are efficiently internalized by neurons via BGT-1-mediated endocytosis. The over-produced reactive oxygen species inside neurons trigger micelles dissociation and ECH release, thereby inducing mitochondrial fusion to enhance neuron survival, ameliorate cerebral microenvironment, and restore cognitive and memory functions. This study reports a non-invasive strategy to overcome the physiological barriers against cerebral drug delivery and renders profound implications for POCD treatment.

OBJECTIVE:To evaluate the effects of lung ultrasound (LUS) in assessing pulmonary ventilation status in patients with acute respiratory distress syndrome (ARDS). METHODS:A total of 35 ARDS patients aged 29-93 years, admitted to the Anesthesiology Intensive Care Unit and scheduled for chest computed tomography (CT), were retrospectively analyzed. Prior to the CT scan, arterial blood gas samples were collected, and LUS scores were obtained using a Sonostar portable ultrasound device. Based on the Berlin definition, patients were categorized into mild ARDS and moderate-to-severe ARDS groups. Lung density, lung volume, proportions of lung volume in different ventilation states, and LUS scores were compared between the groups. Spearman correlation analysis was used to evaluate the relationship between LUS scores and other parameters. RESULTS:Lung density, LUS scores, and the proportion of collapsed lung volume were significantly higher in the moderate-to-severe ARDS group than those in the mild ARDS group (all P < 0.05). In patients with moderate-to-severe ARDS, LUS scores showed a moderate correlation with the oxygenation index, lung density, and the proportion of collapsed lung volume. In mild ARDS patients, no significant correlation was observed between LUS scores and these parameters. CONCLUSION:LUS is an effective, non-invasive tool for evaluating pulmonary ventilation status in ARDS patients and is particularly reliable in assessing ventilation status in those with moderate-to-severe ARDS.

Acute lung injury (ALI) is a severe disease characterized by a pulmonary inflammatory response and oxidative stress. Triptolide has been demonstrated to have anti-inflammatory and antioxidant properties. Herein, we present triptolide-loaded mesenchymal stem cell-derived exosomes (MSC-Exos) as a multifunctional biomimetic delivery system (Tri-Exos) for targeting injured lung tissue. The therapeutic effect of Tri-Exos on ALI was evaluated by measuring inflammatory cytokines content, the expression of myeloperoxidase (MPO), the number of immune cells in bronchoalveolar lavage fluid, malondialdehyde (MDA) content, and superoxide dismutase (SOD) activity. Subsequently, immunohistochemistry and Western blotting were used to assess the expression levels of critical proteins in the nuclear factor erythroid 2-related factor 2 (Nrf-2) signaling pathway, autophagy pathway, apoptosis, and MAPK signaling pathway. The experimental results showed that LPS significantly increased pathological damage, secretion of inflammatory cytokines, and oxidative stress in lung tissue. However, treatment with Tri-Exos significantly alleviated this series of pathological changes. Tri-Exos significantly upregulated the expression of Nrf-2 signaling pathway-related proteins, autophagy, and apoptosis and inhibited the expression of MAPK signaling pathway-related proteins in the ALI model. Our study showed that Tri-Exos exerted a therapeutic effect on LPS-induced ALI by regulating the Nrf-2 signaling pathway-dependent autophagy and MAPK signaling pathway.

Ischemic heart disease invariably leads to devastating damage to human health. Nicotinamide ribose (NR), as one of the precursors of NAD+ synthesis, has been discovered to exert a protective role in various neurological and cardiovascular disorders. Our findings demonstrated that pretreatment with 200 mg/kg NR for 3 h significantly reduced myocardial infarct area, decreased levels of CK-MB and LDH in serum, and improved cardiac function in the rats during myocardial ischemia-reperfusion (I/R) injury. Meanwhile, 0.5 mM NR also effectively increased the viability and decreased the LDH release of H9c2 cells during OGD/R. We had provided evidence that NR pretreatment could decrease mitochondrial reactive oxygen species (mtROS) production and MDA content, and enhance SOD activity, thereby mitigating mitochondrial damage and inhibiting apoptosis during myocardial I/R injury. Further investigations revealed that NR increased NAD+ content and upregulated SIRT3 protein expression in myocardium. Through using of SIRT3 small interfering RNA and the SIRT3 deacetylase activity inhibitor 3-TYP, we had confirmed that the cardioprotective effect of NR on cardiomyocytes was largely dependent on the inhibition of mitochondrial oxidative stress via SIRT3-SOD2 axis. Overall, our study suggested that exogenous supplementation with NR mitigated mitochondrial damage and inhibited apoptosis during myocardial I/R injury by reducing mitochondrial oxidative stress via SIRT3-SOD2-mtROS pathway.

Objective: The aim of this research was to evaluate the effect of two different local anesthetic concentrations on rebound pain following Fascial Iliac Compartment Block (FICB) retreat in patients undergoing total knee arthroplasty (TKA). Method: 48 patients undergoing unilateral TKA under elective general anesthesia were randomly divided into two groups (n=24): the 0.1% ropivacaine group (Group A) and the 0.3% ropivacaine group (Group B). Before anesthesia, two groups of patients underwent a single ultrasound guided- FICB above the inguinal ligament, with 40 mL of 0.1% or 0.3% ropivacaine; all patients underwent perioperative multimodal analgesia. The first outcomes are incidence and degree of postoperative rebound pain; secondary outcomes are remedial analgesia rate within 48h postoperatively, opioid consumption from 0-24 h and 24-48 h postoperatively, NRS scores and muscle strength scores at rest and exercise at 24h and 48h postoperatively, and intravenous serum concentrations of interleukin-6 (IL-6) and tumor necrosis factor α(TNF-α) before surgery and at 24 and 48 h after surgery. Results: In group A, the incidence of postoperative rebound pain was lower (P<0.01), and the degree of rebound pain was milder (P<0.01). The remedial analgesia rate was lower within 48 h after surgery (P<0.05); opioid consumption was lower at 0-24 h after surgery (P<0.01); the postoperative NRS score at 24 h was lower (P<0.01), while the muscle strength score was higher (P<0.01); There was no statistically significant difference in intravenous serum concentrations of IL-6 and TNF-α before surgery, and at 24 and 48 h after surgery. Conclusion: The incidence of rebound pain after the resolution of FICB with low-concentration ropivacaine was lower, and low-concentration ropivacaine FICB was more suitable for multimodal analgesia in TKA patients.

This study aimed to explore the underlying mechanism of nebulized dexmedetomidine (DEX) in ameliorating ventilator-induced lung injury (VILI)-induced oxidative stress in rats. Forty 7 to 8-week-old Sprague-Dawley rats at the specific pathogen-free level were randomized into the control group, model group, nebulized dexmedetomidine (WH-YM) group, and dexmedetomidine intravenous infusion (JM-YM) group, each containing 10 rats. Except for the control group, rats in the other groups underwent mechanical ventilation (tidal volume, 40 mL/kg; respiratory rate, 70 breaths per minute; inspiratory-to-expiratory ratio, 1:2; fraction of inspired oxygen, 21%; positive end-expiratory pressure, 0 cmH2O). Nebulized DEX (6.3 µg/kg), and isodose intravenous DEX were given to rats of WH-YM and JM-YM groups prior to ventilation. Post 4-hour ventilation, rats were euthanized. Lung tissue wet-to-dry weight ratio, H&E staining for assessing diffuse alveolar damage (DAD), and expression levels of Nrf2 and Keap1 detected by qRT-PCR and Western blot were compared. Inflammatory markers TNF-α, IL-2, and IL-6, and oxidative stress indices malondialdehyde (MDA) and superoxide dismutase (SOD), were quantified in lung tissues and serum samples using commercial kits. Rats in the WH-YM and JM-YM groups demonstrated significant ameliorations in the wet-to-dry weight ratio and DAD score, decreased Keap1, TNF-α, IL-2, and IL-6 levels in lung tissues and serum samples, but increased Nrf2 and SOD level than those of controls. These changes were more pronounced in the WH-YM group than in the JM-YM group. DEX effectively alleviates VILI-induced oxidative stress and inflammation via the Keap1-Nrf2-ARE signaling pathway., especially in the nebulized administration.

Background: This study aimed to assess the potential function of Caveolin-1 (CAV-1) in mice with bone cancer pain. Method: Using a mice bone cancer pain model we explored the contribution of CAV-1 expression to bone cancer pain on the 14th day after surgery, mice in the tumor group were randomized and treated with increasing doses of the CAV-1 inhibitor, methyl-beta-cyclodextrin. Pain was assessed by monitoring the number of spontaneous flinches (NSF) and paw withdrawal mechanical threshold (PMWT)mechanical withdrawal threshold (MWT). The localization and expression of CAV-1 in mouse neurons was also determined. Additionally, the protein levels of CAV-1, extracellular signal regulated kinase (ERK) 1/2, cAMP response element-binding protein (CREB) were monitored in mouse spinal cord tissues by western blotting. Results: CAV-1 was remarkably upregulated in the spinal cord of the tumor group on the 4th day after surgery, then downregulated on day 10, and upregulated again at day 14. Such CAV-1 levels were maintained until day 28. In the tumor group, the expression of p-ERK1/2 and p-CERB were upregulated at day 14 after surgery. Intrathecal injection of methylbeta-cyclodextrin (MCD) downregulated p-ERK1/2 and p-CERB expression which correlated with alleviation of pain. Conclusion: Inhibition of CAV-1 in the spinal cord alleviates bone cancer pain in mice which correlates with inhibition of the ERK/CREB pathway.

Abstract Background and Aims : To analyze the factors affecting preoperative blood pressure fluctuations in patients undergoing elective surgical surgery. Methods and Results : In 776 elective surgical patients from January to October 2021, the changes of BP and base BP (1 day before the operation) were analyzed by more than 20%, divided into elevated BP group (n=328) and non-fluctuating group (n=448), and analyzed by multivariate logistic regression. Results 776 patients were included, including 335 men and 441 women; SBP increased 12.98±19.33mmHg 1 day before surgery and DBP increased 6.67±13.20mmHg 1 day before surgery. There were 328 patients with more than 20% fluctuation range, and the incidence of preoperative blood pressure increase reached 42.27%. After a multivariate logistic regression analysis, age, preoperative association with hypertension, and sleep duration at 1 day before surgery were independent risk factors for preoperative BP fluctuations. Older blood pressure is more likely to fluctuate (OR=1.021,95%CI: 1.007-1.035, P =0.0030); 1.785 times more frequently (OR=1.785,95%CI: 1.142 ~ 1.807, P =0.0114) before 1 day (OR=0.835,95%CI: 0.747~0.932, P =0.0014) by stepwise regression. Conclusion: The blood pressure in the operating room increased significantly from 1 day before surgery. Age, preoperative association with hypertension, and sleep duration of 1 day before surgery were independent risk factors affecting preoperative blood pressure fluctuations. And the older the age, the greater the fluctuation of blood pressure; the shorter the sleep time, the greater the difference of blood pressure.

Background Parental liver transplantation (PLT) improves long-term survival rates in paediatric hepatic failure patients; however, the mechanism of PLT-induced postoperative pulmonary complications (PPCs) is unclear. Methods A total of 133 paediatric patients undergoing PLT were included. Serum levels of NET components, including circulating free DNA (cfDNA), DNA-histone complex, and myeloperoxidase (MPO)-DNA complex, were detected. The occurrence of PPCs post-PLT, prolonged intensive care unit (ICU) stay and death within one year were recorded as the primary and secondary outcomes. Results The overall rate of PPCs in the hospital was 47.4%. High levels of serum cfDNA, DNA-histone complexes and MPO-DNA complexes were associated with an increased risk of PPCs (for cfDNA, OR 2.24; for DNA-histone complex, OR 1.64; and for MPO-DNA, OR 1.94), prolonged ICU stay (OR 1.98, 4.26 and 3.69, respectively), and death within one year (OR 1.53, 2.65 and 1.85, respectively). The area under the curve of NET components for the prediction of PPCs was 0.843 for cfDNA, 0.813 for DNA-histone complexes, and 0.906 for MPO-DNA complexes. During the one-year follow-up, the death rate was higher in patients with PPCs than in patients without PPCs (14.3% vs. 2.9%, P = 0.001). Conclusions High serum levels of NET components are associated with an increased incidence of PPCs and death within one year in paediatric patients undergoing PLT. Serum levels of NET components serve as a biomarker for post-PLT PPCs and a prognostic indicator.

目的 通过肺部超声技术评估个体化呼气末正压(PEEP)对全身麻醉腹腔镜胆囊手术患者肺部含气量的影响.方法 选取笔者医院择期行腹腔镜胆囊手术患者80例,年龄18～64岁,ASA分级Ⅰ ～Ⅱ级,BMI 18.5～28.0kg/m2,采用随机数字表法分为2组,即试验组(n=40)和对照组(n=40),试验组患者建立气腹5min后,PEEP从0cmH2O以每次增加2cmH2O开始递增,递增至20cmH2O,每次滴定过程持续1min,并记录当时的动态肺顺应性(Cdyn),将动态顺应性最大时的PEEP定为该患者的个体化PEEP,并持续到手术结束.对照组则以5cmH2O的恒定PEEP维持到手术结束.分别在术前(T1),拔除气管导管后30min(T2)以及术后20～30h(T3)对两组患者进行肺部超声图像的采集,并对两组患者肺部超声图像进行评分.结果 在T1时间点,试验组肺部超声评分(LUS)与对照组比较,差异无统计学意义(P>0.05),在T2、T3时间点两组LUS均较T1时间点增高(P<0.05),且试验组LUS小于对照组,差异有统计学意义(P<0.05).结论 行全身麻醉腹腔镜胆囊手术的患者术后会出现一定程度的肺含气量减少;个体化PEEP的使用,能够有效改善患者肺部含气量减少的程度,且效果优于5cmH2 O.

Objective . This study aims to observe the changes in pupil diameter (PD) after anesthesia with different doses of sufentanil with the ultrasound method and observe whether pupil contraction is correlated with hemodynamic changes and bispectral index (BIS) values. Methods . A total of 124 patients between the ages of 18–65 with ASA I–II undergoing general anesthesia for surgery were enrolled in the study. According to the sufentanil dose initially injected, they were randomly divided into groups P, S1, S2, and S3, with 31 cases in each group. Group P was injected with normal saline. Group S1 was injected with 0.2  μ g/kg of sufentanil. Group S2 was injected with 0.4  μ g/kg of sufentanil. Group S3 was injected with 0.6  μ g/kg of sufentanil. Following propofol administration and eye closure, the pupil diameter (PD) of the patients in the four groups was observed and measured by ultrasound after the loss of consciousness (T1) and within 3 min after the sufentanil injection at an interval of 30 s (30 s (T2), 1 min (T3), 1 min 30 s (T4), 2 min (T5), 2 min 30 s (T6), and 3 min (T7)). PD, systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and BIS values at T1–T7 were recorded. Results . The ultrasonic method was used to observe that different doses of sufentanil could make the patients’ pupils contract. During anesthesia induction, the changes in PD have a positive correlation with SBP, DBP, HR, and BIS values. Conclusion . Ultrasound can become a new noninvasive method to monitor pupil changes during general anesthesia, and ultrasonic observation of pupil changes has great potential for individualized analgesia management in the perioperative period.

目的 探讨术中限制性补液和非限制性补液对脊髓拴系综合征患儿术中各项指标的影响,为该手术的临床液体管理提供理论依据.方法 2020年08月—2022年02月于苏州大学附属儿童医院行后路脊髓拴系松解+椎管内脂肪瘤切除+硬脊膜修补术+椎管扩大术的100例先天性脊髓拴系患儿,根据术中补液的实际情况按照纳入排除标准得到:限制性补液组(补液差异率＜-10％,n=49)及非限制性补液组(补液差异率≥10％,n=23).结果 2组患儿术后乳酸水平、BE值差异无统计学意义(P＞0.05),限制性补液组患儿实际补液量、尿量、术后HCT低于25％的发生率明显小于非限制性补液组,差异具有统计学意义(P＜0.05).T2时限制性补液组平均动脉压大于非限制性补液组,心率低于非限制性补液组,差异具有统计学意义(P＜0.05).结论 限制性液体治疗更适合脊髓拴系综合征的患儿,既保证患儿术中血流动力学稳定和组织灌注,又有效降低了稀释性低HCT的发生率.

Background: ALI/ARDS is a severe lung injury leading to refractory respiratory failure, accounting for high morbidity and mortality. However, therapeutic approaches are rather limited. Targeting long non-coding RNA MALAT1 and microRNA miR-181a-5p might be potential option for ALI/ARDS intervention. Objective: We aimed to investigate the role of MALAT and miR-181a-5p in the pathogenesis of ALI/ARDS, and test the therapeutic effects of targeting MALAT and miR-181a-5p for ALI/ARDS intervention in vitro. Methods: MALAT1 and miR-181a-5p levels were measured in plasma from ALI/ARDS patients. In vitro human pulmonary microvascular endothelial cell (HPMEC) injury was induced by LPS treatment, and molecular targets of MALAT1 and miR-181a-5p were explored by molecular biology approaches, mainly focusing on cell apoptosis and vascular inflammation. Interaction between MALAT1 and miR-181a-5p was also detected. Finally, the effects of targeting MALAT1 and miR-181a-5p for ALI/ARDS intervention were validated in a rat ALI/ARDS model. Results: MALAT1 upregulation and miR-181a-5p downregulation were observed in ALI/ARDS patients. Transfection of mimic miR-181a-5p into HPMECs revealed decreased Fas and apoptosis, along with reduced inflammatory factors. Fas was proved to be a direct target of miR-181a-5p. Similar effects were also present upon MALAT1 knockdown. As for the interaction between MALAT1 and miR-181a-5p, MALAT1 knockdown increased miR-181a-5p expression. Knocking down of MALAT1 and miR-181a-5p could both improve the outcome in ALI/ARDS rats. Conclusion: MALAT1 antagonism or miR-181a-5p could both be potential therapeutic strategies for ALI/ARDS. Mechanistically, miR-181a-5p directly inhibits Fas and apoptosis, along with reduced inflammation. MALAT1 negatively regulates miR-181a-5p.

Background There is a growing interest in minimally invasive left atrial appendage closure therapies. However, for successful catheter surgery, it is necessary to achieve high-quality postoperative recovery. The aim of the study is to comparison of neuromuscular blockade and reversal using cisatricurium and neostigmine with rocuronium and sugamadex on the quality of recovery from general anaesthesia for percutaneous closure of left atria appendage. Methods Eighty-four patients who received percutaneous LAAC were randomly placed into two groups, general anesthesia and endotracheal intubation with either propofol-remifentanil-cisatracurium-neostigmine (group C) or propofol-remifentanil-rocuronium-sugammadex (group S). The QoR-40 questionnaire was used to assess recovery quality 6 h after surgery, and the time of spontaneous respiration, the time of consciousness recovery, the time of extubation, the duration in the postanaesthesia care unit (PACU), and the adverse events after awakening were collected. Results Compared with the group C, the group S demonstrated significantly higher individual QoR-40 dimension scores, a significantly shorter recovery time for spontaneous respiration and consciousness, time of extubation, and duration in the PACU, and a lower incidence of transient hypoxemia, agitation, nausea and vomiting and urinary retention. There was a non-significant trend for the length of stay in the hospital in both groups. Conclusions General anesthesia and endotracheal intubation with propofol-remifentanil-rocuronium-sugammadex provided better quality of recovery, shorter anaesthesia duration, and lower incidence of hypoxemia and agitation. Neuromuscular blockade and reversal using rocuronium and sugamadex is better than with cisatricurium and neostigmine on the quality of recovery from general anaesthesia for percutaneous closure of left atria appendage. Trial registration : chictr.org, ChiCTR2000031857. Registered on April 12, 2020.

目的 观察右美托咪定对妇科腹腔镜手术Trendelenburg体位患者视神经鞘直径(ONSD)的影响.方法 选取行腹腔镜全子宫切除术患者60例为研究对象,随机分为右美托咪定组(n=30)和对照组(n=30).右美托咪定组从麻醉诱导开始以0.4 μg/(kg·h)连续泵注右美托咪定,直至患者恢复平卧位并关闭气腹10 min后,对照组采用相同方式泵注0.9％氯化钠溶液.测量2组麻醉诱导前5 min(T0)及气腹头低位10 min(T1)、30 min(T2)、60 min(T3)和改回平卧位并关闭气腹后10min(T4)时ONSD、心率(HR)、平均动脉压(MAP).比较2组术后3 h内恶心呕吐和头痛的发生情况.结果 右美托咪定组在T1至T4共4个时点的ONSD均小于对照组,HR低于对照组,差异有统计学意义(P＜0.05).右美托咪定组术后3 h内恶心呕吐、头痛的发生率为20.00％、13.33％,分别低于对照组的46.67％、40.00％,差异有统计学意义(P＜0.05).结论 在妇科腹腔镜手术中应用右美托咪定可有效减缓Trendelenburg体位患者的ONSD增大,降低术后恶心呕吐和头痛的发生率.

OBJECTIVE:To determine the median effective concentration (EC50) of remifentanil to inhibit pupillary reflex dilation (PRD) induced by endotracheal intubation using a modified sequential test method.METHODS:In this prospective study, 34 patients undergoing elective surgery under general anesthesia were selected. The induction of anesthesia was started using propofol with an effect-site concentration (Ce(pro)) of 4.0 μg/mL. The effect-site concentration of remifentanil (Ce(Remi)) was set according to the modified sequential test method, with 0.42 ng/mL as the initial concentration for the first patient. The gradient ratio was 1.1. The Ce(Remi) of each patient was determined by whether the PRD of the previous patient disappeared during endotracheal intubation. If the PRD disappeared, a lower concentration was applied. Otherwise, a higher concentration was applied. The experiment ended after 9 crosses of PRD disappearance-presence and PRD presence-disappearance. The EC50 of remifentanil and 95% confidence interval (CI) were calculated using the Dixon and Massey's method. The Probit regression procedure was used to derive the EC50, 95% effective concentration (EC95) of remifentanil and their 95% CIs.RESULTS:The EC50 of remifentanil to inhibit PRD induced by endotracheal intubation was 4.41 ng/mL (95% CI, 4.32 to 4.49 ng/mL) and the EC95 was 5.24 ng/mL (95% CI, 4.78 to 7.68 ng/mL). In 34 patients, the time to reach the maximum change in heart rate, systolic blood pressure, mean arterial pressure and Bispectral index was 75.00 (60.00-98.00) s, 95.00 (75.00-133.00) s, 95.00 (75.00-135.00) s, and 100.00 (78.00-113.00) s, respectively, which was significantly longer than the time (42.00 (25.00-47.00) s) needed for pupillary diameter (P<0.05).CONCLUSION:The EC50 of remifentanil to inhibit PRD induced by endotracheal intubation was 4.41 ng/mL and the EC95 was 5.24 ng/mL. The time to reach the maximum pupillary diameter change was shorter than the time needed for heart rate, blood pressure, and Bispectral index. This prospective study was registered in the China Clinical Trials Registration Center (ChiCTR2100043771, https://www.chictr.org.cn).

Parkinson's disease (PD) is a neurodegenerative disorder characterized by a progressive degeneration in nigrostriatal dopamine pathway that is essential to control motor functions. Dexmedetomidine (DEX), a sedative and analgesic drug, is often used in patients with PD undergoing surgery. Although DEX seems to have promising future applications in neuroprotection, whether and how DEX alter the function of nigrostriatal circuit and its roles on motor deficits in PD remain unclear. Here we report that DEX attenuated motor deficits in a dose-dependent manner and protected the degeneration of dopaminergic neurons in MPTP-induced PD model mice. The DEX acted on the neurons in the nigrostriatal circuits, including activation of dopaminergic neurons and the reduction of the excitabilities of striatal neurons via dopamine D2 receptors. We further found that DEX prevented the increase in glutamatergic transmission of cholinergic interneurons (CINs) to alleviate motor dysfunction. It also decreased the intrinsic excitability and glutamatergic transmission of striatal D2 medium spiny neurons (D2-MSNs). Finally, D2 receptor antagonists prevented the restoration of DEX on motor deficits. These results demonstrate that DEX, a neuroprotective drug, restores the function of nigrostriatal neurons and improves the motor deficits, providing a potential neural mechanism of the effects of anesthetic drugs on PD progression.