BACKGROUND:Postoperative cognitive dysfunction (POCD), a common neurological complication in elderly patients, significantly impairs recovery. Emerging evidence suggests the gut microbiota is involved in its pathogenesis. This study aimed to determine whether acupoint catgut embedding (ACE) could alleviate POCD by modulating the gut microbiota in aged mice after laparotomy. METHODS:Eighteen-month-old male C57BL/6J mice underwent laparotomy on day 8 (excluding the Sham group). The ACE group received ACE treatment, while the anesthesia and surgery group served as surgical controls. The fecal microbiota transplantation (FMT)-ACE and FMT-AS groups received FMT from corresponding donors. Additional groups received oral indole-3-propionic acid (IPA) or vehicle-treated surgery. Hippocampal inflammation and blood-brain barrier proteins were assessed on day 9; cognitive function and intestinal markers on day 15. RESULTS:Cognitive function was significantly improved in the ACE, FMT-ACE, and IPA groups. ACE and FMT-ACE treatments specifically elevated fecal g-Clostridia_UCG-014 abundance and serum IPA levels. These changes were accompanied by suppressed hippocampal toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling and proinflammatory cytokines [tumor necrosis factor alpha, interleukin (IL)-1β], together with elevated tight junction proteins (occludin, claudin-5). Furthermore, colonic aryl hydrocarbon receptor (AhR) and IL-22 were upregulated, while serum lipopolysaccharide and diamine oxidase were reduced. Accordingly, IPA treatment mirrored the key anti-inflammatory and barrier-protective effects. CONCLUSION:ACE alleviates POCD probably by modulating gut microbiota, specifically increasing g-Clostridia_UCG-014 abundance and metabolite IPA. These effects are potentially mediated by dual pathways: (a) suppression of neuroinflammation via TLR4/NF-κB signaling, and (b) enhancement of gut barrier integrity via AhR/IL-22 axis. Our findings highlight the therapeutic potential of ACE in targeting the gut-brain axis for POCD management.

Stroke induces cardiac dysfunction, which increases poststroke mortality and morbidity. An imbalance in the autonomic nervous system resulting from brain injury may serve as the underlying mechanism. The present study investigated whether transcutaneous auricular vagus nerve stimulation (taVNS) attenuates poststroke cardiac dysfunction by activating the parasympathetic nervous system. Adult male mice were subjected to transient middle cerebral artery occlusion (MCAO) and reperfusion surgery. The mice in the treatment group received repeated taVNS starting 60 min after the onset of cerebral ischemia. To assess whether the effects of taVNS were associated with parasympathetic activity, the MCAO mice in the atropine group received intraperitoneal injections of atropine to inhibit parasympathetic activity prior to taVNS. taVNS significantly increased the left ventricular ejection fraction (EF), attenuated myocardial apoptosis, reduced myocardial hypertrophy, and reduced fibrosis following stroke. The beneficial effects of taVNS on cardiac dysfunction were abolished by atropine administration. Heart rate variability (HRV) analysis and western blot analysis revealed that taVNS increased parasympathetic activity but decreased sympathetic dominance in mice with MCAO. Furthermore, the cardioprotective effects of taVNS were associated with muscarinic acetylcholine receptor activation, PI3K-Akt pathway modulation, and eNOS regulation in the heart. Therefore, taVNS alleviates cardiac dysfunction after stroke and is associated with activation of the parasympathetic nervous system.

Intestinal ischemia/reperfusion is a prevalent pathological process that can result in intestinal dysfunction, bacterial translocation, energy metabolism disturbances, and subsequent harm to distal tissues and organs via the circulatory system. Acute lung injury frequently arises as a complication of intestinal ischemia/reperfusion, exhibiting early onset and a grim prognosis. Without appropriate preventative measures and efficacious interventions, this condition may progress to acute respiratory distress syndrome and elevate mortality rates. Nonetheless, the precise mechanisms and efficacious treatments remain elusive. This paper synthesizes recent research models and pertinent injury evaluation criteria within the realm of acute lung injury induced by intestinal ischemia/reperfusion. The objective is to investigate the roles of pathophysiological mechanisms like oxidative stress, inflammatory response, apoptosis, ferroptosis, and pyroptosis; and to assess the strengths and limitations of current therapeutic approaches for acute lung injury stemming from intestinal ischemia/reperfusion. The goal is to elucidate potential targets for enhancing recovery rates, identify suitable treatment modalities, and offer insights for translating fundamental research into clinical applications.

Sepsis-associated lung injury often coexists with intestinal dysfunction. Butyrate, an essential gut microbiota metabolite, participates in gut-lung crosstalk and has immunoregulatory effects. This study aims to investigate the effect and mechanism of sodium butyrate (NaB) on lung injury. Sepsis-associated lung injury was established in mice by cecal ligation and puncture (CLP). Mice in treatment groups received NaB gavage after surgery. The survival rate, the oxygenation index and the lung wet-to-dry weight (W/D) ratio were calculated respectively. Pulmonary and intestinal histologic changes were observed. The total protein concentration in bronchoalveolar lavage fluid (BALF) was measured, and inflammatory factors in serum and BALF were examined. Diamine oxidase (DAO), lipopolysaccharide (LPS), and surfactant-associated protein D (SP-D) levels in serum and amphiregulin in lung tissue were assessed. Intercellular junction protein expression in the lung and intestinal tissues were examined. Changes in immune cells were analyzed. NaB treatment improved the survival rate, the oxygenation index and the histologic changes. NaB decreased the W/D ratio, total protein concentration, and the levels of proinflammatory cytokines, as well as SP-D, DAO and LPS, while increased the levels of anti-inflammatory cytokines and amphiregulin. The intercellular junction protein expression were improved by NaB. Furthermore, the CD4+/CD8+ T-cell ratio and the proportion of CD4+Foxp3+ regulatory T cells (Tregs) were increased by NaB. Our data suggested that NaB gavage effectively improved the survival rate and mitigated lung injury in CLP mice. The possible mechanism was that NaB augmented CD4+Foxp3+ Tregs and enhanced the barrier function of the gut and the lung.

Abstract Background Diabetes mellitus (DM) can aggravate lung ischemia-reperfusion (I/R) injury and is a significant risk factor for recipient mortality after lung transplantation. Metformin protects against I/R injury in a variety of organs. However, the effect of metformin on diabetic lung I/R injury remains unclear. Therefore, this study aimed to observe the effect and mechanism of metformin on lung I/R injury following lung transplantation in type 2 diabetic rats. Methods Sprague–Dawley rats were randomly divided into the following six groups: the control + sham group (CS group), the control + I/R group (CIR group), the DM + sham group (DS group), the DM + I/R group (DIR group), the DM + I/R + metformin group (DIRM group) and the DM + I/R + metformin + Compound C group (DIRMC group). Control and diabetic rats underwent the sham operation or left lung transplantation operation. Lung function, alveolar capillary permeability, inflammatory response, oxidative stress, necroptosis and the p-AMPK/AMPK ratio were determined after 24 h of reperfusion. Results Compared with the CIR group, the DIR group exhibited decreased lung function, increased alveolar capillary permeability, inflammatory responses, oxidative stress and necroptosis, but decreased the p-AMPK/AMPK ratio. Metformin improved the function of lung grafts, decreased alveolar capillary permeability, inflammatory responses, oxidative stress and necroptosis, and increased the p-AMPK/AMPK ratio. In contrast, the protective effects of metformin were abrogated by Compound C. Conclusions Metformin attenuates lung I/R injury and necroptosis through AMPK pathway in type 2 diabetic lung transplant recipient rats.

Immunosuppression due to ischemic stroke is a pivotal factor that can increase the incidence of infectious diseases and mortality after stroke. Electroacupuncture (EA) has been confirmed to improve the prognosis of ischemic stroke model through the parasympathetic nervous system (PNS). The role of EA in regulating immunosuppression after ischemic stroke through PNS is unclear. Using ischemic stroke model, the experiment found that EA exerted the effects in improving survival rate, and neurological deficits, reducing infarct volume, proportion of neuronal apoptosis, and systemic inflammation. Importantly, mice received EA showed a significantly higher in weight, cell number, and α7nAChR levels of spleen, suggesting the improvement of immunosuppression; EA also activated dorsal motor nucleus of the vagus which was the main source of vagus, the main component of the PNS. However, none of these changes were found in mice that did not receive EA. Taken together, EA improves the prognosis of ischemic stroke by activating PNS and regulating spleen immune function in mice.

Ischemic stroke is a cerebrovascular lesion caused by local ischemia and hypoxia. Diabetes mellitus (DM) is a chronic inflammatory disease that disturbs immune homeostasis and predisposes patients to ischemic stroke. The mechanism by which DM exacerbates stroke remains unclear, although it may involve disturbances in immune homeostasis. Regulatory T cells (Tregs) play a regulatory role in many diseases, but the mechanism of Tregs in diabetes complicated by stroke remains unclear. Sodium butyrate is a short-chain fatty acid that increases Treg levels. This study examined the role of sodium butyrate in the prognosis of neurological function in diabetic stroke and the mechanism by which Tregs are amplified in the bilateral cerebral hemispheres. We evaluated the brain infarct volume, observed 48-h neuronal injury and 28-day behavioral changes, and calculated the 28-day survival rate in mice. We also measured Treg levels in peripheral blood and brain tissue, recorded changes in the blood‒brain barrier and water channel proteins and neurotrophic changes in mice, measured cytokine levels and peripheral B-cell distribution in bilateral hemispheres and peripheral blood, and examined the polarization of microglia and the distribution of peripheral T-cell subpopulations in bilateral hemispheres. Diabetes significantly exacerbated the poor prognosis and neurological deficits in mice with stroke, and sodium butyrate significantly improved infarct volume, prognosis, and neurological function and showed different mechanisms in brain tissue and peripheral blood. The potential regulatory mechanism in brain tissue involved modulating Tregs/TGF-β/microglia to suppress neuroinflammation, while that in peripheral blood involved improving the systemic inflammatory response through Tregs/TGF-β/T cells.

为了加强住院医师规范化培训力度,提高住院医师的临床胜任力,医学模拟教学应运而生.传统教学中单一技能的培训不能满足住院医师临床胜任力培养的需求,为了培养麻醉学住院医师的岗位胜任力,哈尔滨医科大学附属第二医院麻醉模拟平台开发了基于情景的规范化操作培训课程.该课程以Miller金字塔原理作为理论依据,将临床技能培训和情景模拟教学相结合,要求学员除掌握理论知识和操作技能外,还要重视在真实工作环境中的实际表现.单一的临床技能培训可以规范学员的操作习惯,情景模拟教学使学员身临其境,直观地感受和体会真正的临床工作情景,完整地体验临床工作流程,培训学员操作前评估和访视患者、识别和处理操作相关的并发症,帮助学员树立临床工作流程化、整体化的观念,避免重操作轻评估、重技术轻人文的临床思维和工作习惯,从而保障医疗安全.

临床麻醉学课程是麻醉学专业学生临床主干课程之一,其任务是通过理论教学和临床实习使学生掌握临床麻醉学有关的基本理论、基本知识和基本技能.针对传统临床麻醉学课程线下单一灌输式课堂教学方式的弊端,及与课程内容相关医学生思想政治工作疏离与缺失的问题,研究如何将传统课堂教学方式转变为符合新时代教育教学发展的线上线下混合式教学的授课方式,并深入挖掘课程思政元素,将其导入和融合到课程之中,使经历了多次教材更新和近三十年历史沿革的临床麻醉学课程历久弥新,是作为国家一流本科专业建设点的哈尔滨医科大学麻醉学本科专业的历史使命.

Objective:To investigate the effect of orexin-A (OA) on cognitive function of neonatal rats after brain injury caused by hyperoxia and related molecular mechanisms.Methods:STotally, 63 clean Sprague-Dawley rats with body weight of 40 to 50 g were randomly divided into three groups according to the random number table method: hyperoxic group (HO group, n=21), given high concentration of oxygen (>80%) and intraperitoneal injection of 0.5 ml phosphate buffer saline (PBS) for 7 consecutive days; OA group [hyperoxia+ intraperitoneal injection of 30 μg/kg OA (diluted with PBS to 0.5 ml) for 7 consecutive days, n=21]; control group (group C, n=21) given air inhalation and intraperitoneal injection of 0.5 ml PBS for consecutive 7 days. Morris water maze test was performed on the first day after the successful establishment of the model. After 6 consecutive days, the wet/dry weight ratio (W/D) of the hippocampus was determined. The mRNA expression levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and cold-induced RNA binding protein (CIRP) in the hippocampus were detected by Real-time polymerase chain reaction (PCR). The protein expression of IL-1β, TNF-α and CIRP in the hippocampus was detected by Western blotting. The intergroup ratio of behavioral performance indicators was analyzed by repeated measurement design, and the intergroup ratio of other indicators was analyzed by one-way ANOVA. Results:The residence time in the quadrant of the platform [(17.2±4.4), (25.9±3.6) s] and the average swimming speed [(11.69±0.83), (13.92±0.98) cm/s] in HO and OA groups were significantly lower than those in group C ( F=74.600, 283.000, P<0.05). In HO and OA groups, the escape latency [(48.4±8.6), (38.6±8.1), (33.9±7.4), (19.6±5.7), (22.9±5.5), (41.3±6.4), (33.4±5.5), (27.5±4.7), (15.5±4.5), (16.4±4.3) s], W/D [(5.94±0.36), (5.27±0.33)] of the hippocampus, the mRNA expression level of hippocampal CIRP (3.35±0.63, 1.96±0.30), TNF-α (2.89±0.45, 1.34±0.37) and IL-1β (2.66±0.53, 1.73±0.45) mRNA and the expression of proteins [(0.86±0.23), (0.61±0.19), (0.82±0.26), (0.57±0.22), (0.78±0.18), (0.52±0.15) pg/ml] were significantly higher than those in group C ( F=14.200, 15.620, 14.480, 5.273, 30.280, 57.840, 72.590, 66.660, 32.210, 32.710, 23.520, 47.010, P<0.05). The retention time in platform quadrant and average swimming speed in OA group were significantly increased as compared with those in HO group ( F=74.600, 283.000, P<0.05). The escape latency, hippocampal W/D ratio, the expression of hippocampal IL-1β, TNF-α and CIRP mRNA and proteins in OA group were significantly reduced as compared with those in HO group ( F=14.200, 15.620, 14.480, 5.273, 30.280, 57.840, 72.590, 66.660, 32.210, 32.710, 23.520, 47.010, P<0.05). Conclusion:OA may decrease the expression levels of CIRP, TNF-α and IL-1β in the hippocampus to reduce brain damage caused by hyperoxia in neonatal rats.

近年来,随着医学专业学位研究生教育改革深入推进,我国逐步确立了住院医师规范化培训与专业学位硕士(专硕)研究生教育并轨的新型培养模式.新模式下,应用型医疗人才输出加快,各种医疗教育资源得到充分利用,但"重临床,轻科研"的培养特点使专硕科研创新能力训练不足,研究生教育出现"本科化"趋势.麻醉学逐渐从临床麻醉向围术期医学跨越发展,麻醉科在疾病诊断、治疗和预防中的作用日趋关键.麻醉学专硕是我国麻醉学科重要的接班人,但他们工作任务重,风险高,往往更加容易忽视自身科研能力的训练.因此,如何能够聚焦麻醉学专硕的缺陷点和潜力点改进教学模型并强化课外科研训练,一直是麻醉学专硕教育领域的关注点及难点.文章总结并探讨科研研讨模式(seminar)的基础上引入BOPPPS+PAL理念,能够使学生主动学习和被动学习有机结合,进一步提高学习积极性和学习效率,以期为麻醉学专硕乃至整个临床医学专硕教学方式改革提供新方法.

国际标准化组织( ISO )颁布的《质量管理体系——业绩改进指南》( ISO 9004 )指出, 质量管理不仅要着眼于产品和服务的质量, 也需关注实现质量目标的方法和路径.这一质量管理理念不仅适用于产品,也同样适用于医疗行为.然而医疗行为不同于产品, 它是一个动态的、多方参与的过程.因此,医疗行为质量控制工作的开展必须确保建立一个知识共享、具有协调和组织能力的系统, 同时要营建一个鼓励并追求质量改进的意识和文化体系.因地域辽阔,医院数量较多,分布较分散,众多医院麻醉科的信息化建设基础较薄弱, 黑龙江省麻醉质控工作的开展难度较大.黑龙江省麻醉质控中心从本省实际情况出发,通过开展实地调查、基线调研、推动信息化建设、加强质控专项培训等多种方法, 推进全省麻醉质控工作的开展及临床麻醉现状的改进.

Propofol exhibits neuroprotective effects mediated by the inhibition of excitatory amino acid (EAA) neurotransmitter release and potentiation of inhibitory amino acid (IAA) neurotransmitters. To our knowledge, this is the first study to investigate the effects of propofol on the EAA and IAA balance in neurogenic pulmonary edema (NPE).

BACKGROUND: The process of brain death induces acute lung injury in donors and aggravates ischemia-reperfusion injury (IRI) in grafts. Hydrogen, a new anti-oxidant, attenuates IRI in several organ transplant models. We examined whether 2% inhaled hydrogen would show favorable effects on lung grafts from brain-dead donor rats.METHODS: Brain-dead donor rats inhaled mixed gases with either 50% oxygen and 50% nitrogen or mixed gases with 2% hydrogen, 50% oxygen and 48% nitrogen for 2 hours. The recipients inhaled the same gas as the donors and were euthanized 2 hours after lung transplantation.RESULTS: Hydrogen improved PaO2/FIO2 and PVO2/FIO2 from the arterial and pulmonary venous blood in recipients and decreased the lung injury score in grafts from brain-dead donors. Hydrogen decreased the amount of IL-8 and TNF-alpha in serum, inhibited the activity of malondialdehyde and myeloperoxidase, and increased the activity of superoxide dismutase in the lung grafts from brain-dead donors. Furthermore, hydrogen decreased the apoptotic index of the cells and inhibited the protein expression of intercellular adhesion molecule-1 and caspase-3 in lung grafts from brain-dead donors.CONCLUSIONS: Hydrogen can exert protective effects on lung grafts from brain-dead donors through anti-inflammatory, anti-oxidant and anti-apoptotic mechanisms J Heart Lung Transplant 2013;32:251-258 (c) 2013 International Society for Heart and Lung Transplantation. All rights reserved.

Objective To evaluate the relationship between the concentration of pentane in the exhaled air and degree of the lung injury in non-heart-beating (NHB) rabbits.Methods Twenty-four healthy male Japanese white rabbits weighing 2.4-3.0 kg were randomly divided into 4 groups ( n =6 each):A,B,C and D groups.The NHB model was established by exsanguination through the femoral artery.The exhaled gases were collected and lung tissues were removed at 0,30,60 and 120 min after cardiac arrest in A,B,C and D groups respectively.The concentration of pentane in the exhaled gases was detected immediately using the gas chromatography-mass spectrography.The wet to dry (W/D) lung weight ratio and content of malondialdehyde (MDA) in lung tissues were measured.The lung injury score (LIS) was recorded.The maximal volume ( Vmax ) of the lung was recorded when the airway pressure reached 30 cm H2O.Results Compared with groups A and B,the exhaled pentane concentration was significantly increased in group C,and the W/D ratio,content of MDA and LIS were significantly increased,while Vmax was significantly decreased in group D ( P ＜ 0.05).Compared with group C,W/D ratio and LIS were significantly increased in group D ( P ＜ 0.05 ).Conclusion The concentration of exhaled pentane can not reflect the degree of the lung injury in NHB rabbits.