Sleep disruption (SD) is increasingly recognized as a systemic stressor that worsens inflammatory disease, yet how it reshapes lung immunity remains poorly defined. To address this, we combined an ovalbumin (OVA)-induced allergic airway inflammation model with sleep disruption paradigms, together with transcriptomic profiling, in vivo pharmacological interventions, and in vitro RAW264.7 macrophage-like cells. In an OVA-induced allergic airway inflammation model, SD markedly increased methacholine responsiveness, aggravated peribronchial inflammation and mucus metaplasia, and promoted a more severe inflammatory airway phenotype. These changes were accompanied by enhanced pulmonary catecholaminergic signaling, reflected by increased tyrosine hydroxylase immunoreactivity and elevated norepinephrine levels. Mechanistically, SD induced mitochondrial dysfunction in the lung, characterized by ultrastructural injury, increased mitochondrial reactive oxygen species, and accumulation of cytosolic mtDNA, together with activation of the cGAS-STING pathway. Cell-type localization analysis showed that activated STING signaling was predominantly associated with F4/80-positive pulmonary macrophages, whereas overlap with Ly6G-positive neutrophils was limited. In vivo, chemical sympathectomy with 6-hydroxydopamine attenuated airway hyperresponsiveness and reduced pulmonary STING pathway activation. In RAW 264.7 cells, norepinephrine (NE) amplified lipopolysaccharide (LPS)-induced inflammatory responses, promoted mitochondrial oxidative stress, increased cytosolic mtDNA accumulation, and enhanced IRF3 activation, effects that were attenuated by adrenergic blockade and STING inhibition. Together, these findings support a model in which sleep disruption increases catecholaminergic exposure in allergic lungs, thereby driving macrophage mitochondrial stress and mtDNA-cGAS-STING dependent inflammatory amplification. This work identifies a brain-to-lung neuroimmune mechanism linking sleep loss to worsened airway disease and highlights sympathetic-macrophage signaling as a potential mechanism-informed therapeutic target. Sleep disruption enhances sympathetic nervous system activity, leading to increased norepinephrine (NE) release to the lung. NE acts on pulmonary macrophages, likely through adrenergic signaling pathways, inducing mitochondrial oxidative stress and structural disruption. This is characterized by elevated mitochondrial ROS, which promotes the release and cytosolic accumulation of mitochondrial DNA (mtDNA). The released mtDNA activates the cGAS-STING signaling pathway, leading to TBK1-IRF3 activation and downstream inflammatory gene expression, ultimately contributing to enhanced airway inflammation, mucus hypersecretion, and airway hyperresponsiveness under allergen challenge. Created in BioRender. Haotian, C. (2026) https://BioRender.com/xywyr61.

Asthma is frequently accompanied by anxiety disorders, yet the mechanisms linking asthma to neuropsychiatric symptoms remain poorly defined. Here, we investigated the contribution of the pulmonary microbiota and its metabolites to anxiety-like behavior in an ovalbumin-induced asthma mouse model. Behavioral testing and resting-state functional magnetic resonance imaging revealed anxiety-like phenotypes and altered hippocampal function in a subset of asthmatic mice that were susceptible to anxiety-like behavior. These mice exhibited hippocampal neuroinflammation and neuronal damage, accompanied by dysbiosis of the pulmonary microbiota. Intratracheal transplantation of lung microbiota from anxiety-susceptible donors induced similar behavioral changes in recipient mice, indicating a causal role of the pulmonary microbiota. Untargeted metabolomics identified formononetin as a candidate metabolite positively correlated with the relative abundance of Acidobacteria. Intratracheal administration of formononetin alleviated anxiety-like behaviors, reduced hippocampal inflammation and injury, and restored hippocampal BDNF/TrkB signaling. However, these effects were abolished by the TrkB antagonist ANA-12. Transcriptomic and immunofluorescence analyses suggested that formononetin acts through modulation of hippocampal microglia. In vitro and small RNA sequencing analyses further demonstrated that formononetin promotes BDNF production by downregulating miR-1912-3p, thereby relieving its translational repression in microglia. Together, these findings reveal a lung-brain axis in which a pulmonary microbiota-associated metabolite modulates microglial function to alleviate asthma-related anxiety.

Airway epithelial dysfunction is a hallmark of asthma, contributing to chronic inflammation and structural remodeling. Recent research suggests the role of post-translational modifications in regulating epithelial immune responses. However, the role of specific deubiquitinating enzymes (DUBs) remains unclear. In this study, we identified OTU deubiquitinase 7a (OTUD7a) as a gene that is significantly downregulated in a murine model of allergic asthma. Transcriptomic analysis of two independent datasets (GSE71822 and GSE9383) consistently revealed the suppression of OTUD7a in asthmatic lungs. Furthermore, immunofluorescence analysis suggested that OTUD7a was detected in CC10-positive bronchiolar epithelial cells, non-ciliated epithelial cells known for their anti-inflammatory functions. To explore the molecular associations of OTUD7a, we established a club cell line overexpressing Flag-tagged OTUD7a and performed co-immunoprecipitation-mass spectrometry (Co-IP/MS). We identified 1135 candidate interacting proteins. In parallel, LC-MS/MS-based ubiquitinome profiling in ovalbumin (OVA)-induced asthmatic lungs revealed widespread changes in protein ubiquitination, with more than 3000 differentially modified ubiquitination sites. These changes were enriched in pathways associated with immune signaling, cytoskeletal dynamics, and epithelial barrier function. Collectively, our findings suggest that OTUD7a, as a DUB detected in CC10-positive bronchiolar epithelial cells, is markedly decreased in asthma and they present a comprehensive landscape of ubiquitination changes in allergic airway inflammation. Therefore, our study offers new insight into post-translational regulation in the pathogenesis of asthma.

Objective:To explore the feasibility of establishing a mouse stellate ganglion (SG) regulation model through infrared polarized light (IPL) irradiation of the SG, and preliminarily evaluate its effects on SG function and related physiological indicators. Surgery, and IPL groups, with 8 mice in each group. A ZZIR-ID therapeutic device was used to directly irradiate bilateral SG regions of IPL group mice, with wavelength 980 nm, power density 1000 mW/cm2, 10 min per session (5 min per side), every other day for 6 times. The control group received no treatment, while the. Results:Compared with the control and Sham surgery groups, the incidence of Horner's syndrome in the IPL group increased significantly (P < 0.05), manifesting as bilateral ptosis and enophthalmos, lasting about 2 h. Immediately after treatment, eye temperature in the IPL group increased significantly compared to pre-treatment (P < 0.05). Heart rate in the IPL group decreased significantly 30 min post-treatment compared to pre-treatment (P < 0.01), lasting 1-2 h. There was no statistically significant difference in weight changes between groups (P > 0.05). In all treated mice, the characteristic signs of Horner's syndrome developed within minutes of starting IPL exposure, reached their peak intensity between 1.5 and 2.5 h, and resolved completely within 3-4 h of the 10-min irradiation session. Conclusion:IPL irradiation of SG can effectively induce Horner's syndrome in mice, elevate eye temperature, and reduce heart rate. These findings suggest IPL as a potential method for modulating SG activity in preclinical models.

Airway hyperresponsiveness (AHR) is often associated with mood disorders such as anxiety and depression which makes the airway symptoms more complicated and refractory. However, the underlying mechanisms remain unclear. This study investigated whether this was related to the activation of microglia in the hippocampus. Female Balb/c mice were randomly assigned into an AHR model induced by ovalbumin (OVA) and an anxiety model induced by chronic restraint stress (CRS). Anxiety-like behavior was assessed by open field test, elevated plus maze and tail suspension test. Airway resistance following methacholine inhalation was measured by using the FlexiVent apparatus. Hematoxylin and eosin, periodic acid-Schiff as well as Masson trichrome were performed to evaluate inflammatory cell infiltration in the lung tissue. In addition, the status of microglia in the hippocampus was evaluated by immunofluorescence, while the activation of inflammation signaling pathway was assessed by Western blots. Compared with the Control group, mice in OVA and CRS groups exhibited higher airway resistance, spent less time in the center area of the open field and the open arms of the elevated plus maze, and showed increased immobility time in the tail suspension test. Microglia in hippocampus exhibited pronounced morphological alterations, increased expression of activation markers Iba1 and CD86, and upregulation of the NLRP3 inflammasome pathway. Minocycline treatment significantly reduced the airway resistance and anxiety-like behavior in OVA mice, while also inhibiting activation of the NLRP3 inflammasome pathway. This study provides evidence for the comorbidity between AHR and anxiety, potentially mediated by hippocampal microglial activation and the NLRP3/Caspase-1/IL-1β pathway. These findings enhance our understanding of the underlying mechanisms, and offer potential targets for treating AHR-related anxiety.

Asthma is a chronic inflammatory respiratory disease that seriously affects patients’ quality of life. Although various pharmacological treatments are currently available, some patients still have poor responses, highlighting the urgent need for new intervention strategies. In recent years, stellate ganglion irradiation (SGI), as an emerging neuromodulation technique, has shown unique therapeutic advantages in various inflammatory diseases. However, the mechanism by which SGI alleviates asthma remains unclear. Silent information regulator 1 (SIRT1), an NAD+-dependent histone deacetylase, plays a key role in regulating cellular inflammatory responses by inhibiting NF-κB and other inflammatory signaling pathways. Given the involvement of SIRT1 and NF-κB imbalance in the pathogenesis of asthmatic airway inflammation, we hypothesize that SGI may alleviate asthmatic inflammation by activating SIRT1 and inhibiting NF-κB activation. To test this hypothesis, we used an ovalbumin (OVA)-induced mouse model of asthma to comprehensively evaluate the effects of SGI on asthma pathophysiology and explore the mediating role of the SIRT1-NF-κB pathway. We found that compared with the asthma group, SGI treatment significantly improved the general symptoms of mice, reduced airway hyperresponsiveness, alleviated inflammatory cell infiltration and cytokine levels in bronchoalveolar lavage fluid (BALF), and ameliorated lung histopathological changes. Mechanistic studies showed that SIRT1 expression was downregulated and the NF-κB pathway was activated in the lung tissues of asthmatic mice, while SGI treatment upregulated SIRT1 expression and inhibited NF-κB activity. In conclusion, this study reveals for the first time that SGI alleviates asthmatic airway inflammation through the SIRT1-NF-κB pathway, providing a new approach for the adjuvant treatment of asthma.

Background According to the Chinese Society of Anesthesiology, it is recommended that patients with difficult airways be documented and notified, which will provide healthcare professionals with a direct reference when managing airways. However, compliance with this initiative remains unclear. This study was conducted to investigate the current status and need for difficult airway notification at Plastic Surgery Hospital and to explore the factors contributing to noncompliance. Methods Anesthesiologists, surgeons, and patients in Plastic Surgery Hospital were administered separate questionnaires regarding notification of difficult airway management. Participants were surveyed regarding their attitudes and current practices regarding difficult airway notification. In addition, questions were asked regarding the barriers that contribute to noncompliance. Results A total of 632 valid responses were obtained and analyzed, giving a response rate of 99.21%. 399 patients (89.46%) felt it was very important for anesthesiologists to inform them about their difficult airway, and 91.03% felt it was very important for them to receive a letter of their airway assessment. However, twenty-two anesthesiologists (64.7%) reported verbally informing less than 50% of patients about their difficult airway after surgery, and only four anesthesiologists informed all patients they encountered. Most surgeons (91.22%) and anesthesiologists (91.18%) believe that it is vital to inform patients verbally, while 114 surgeons (77.03%) and 31 anesthesiologists (91.18%) believe that it is essential to complete a difficult airway notification alert. Among the factors causing noncompliance, 17 (34.69%) believed that absence of mandatory rules, 9 (18.37%) believed that increased workload, and 8 (16.33%) believed that notification methods were lacking. Conclusions The compliance to difficult airway notification remains low in Plastic Surgery Hospital despite the high incidence of difficult airways. Although anesthesiologists, surgeons, and patients are strongly in favor of it. Among the barriers to compliance were the absence of a well-developed notification system and a means of notification such as an alert form for difficult airways. This may spur the anesthesiology society to publish the notification system.

Objective To explore the feasibility of establishing a mouse stellate ganglion (SG) regulation model through infrared polarized light (IPL) irradiation of the SG, and preliminarily evaluate its effects on SG function and related physiological indicators. Methods BALB/c mice were randomly divided into control, Sham surgery, and IPL groups, with 8 mice in each group. A ZZIR-ID therapeutic device was used to directly irradiate bilateral SG regions of IPL group mice, with wavelength 980 nm, power density 1000 mW/cm2, 15 minutes each time, every other day for 6 times. The control group received no treatment, while the Sham surgery group received IPL irradiation on the top of the head. Horner's syndrome manifestations were observed and eye temperature was measured before and immediately after treatment. Heart rate changes were continuously recorded. Results Compared with the control and Sham surgery groups, the incidence of Horner's syndrome in the IPL group increased significantly (P < 0.05), manifesting as bilateral ptosis and enophthalmos, lasting about 2 hours. Immediately after treatment, eye temperature in the IPL group increased significantly compared to pre-treatment (P < 0.05). Heart rate in the IPL group decreased significantly 30 minutes post-treatment compared to pre-treatment (P < 0.01), lasting 1–2 hours. There was no statistically significant difference in weight changes between groups (P > 0.05). Conclusion IPL irradiation of SG can effectively induce Horner's syndrome in mice, elevate eye temperature, reduce heart rate, and exert certain anti-inflammatory immunomodulatory effects. This provides experimental evidence for IPL as a novel method to establish SG regulation models.

Purpose:Esketamine have anesthetic and analgesic properties. This study aimed to observe the enhancing effect of subanesthetic doses of esketamine (0.15-0.3 mg/kg/h) with dexmedetomidine and remifentanil during anesthesia for liposuction surgery. Patients and Methods:A total of 155 subjects were randomized with a 1:1 ratio to Group E (esketamine-dexmedetomidine/remifentanil, n=78) or Group C (saline-dexmedetomidine/remifentanil group, n=77). The primary outcome was satisfaction of patient and surgical team with the procedure. The secondary outcomes were the postoperative Athens Insomnia Scale (AIS) and Hospital Anxiety and Depression Scale (HADS) scores, hemodynamic and respiratory changes, drug consumption, adverse event rates, and predictors associated with patient satisfaction. Results:Patient and surgical team satisfaction with the procedure was significantly higher in Group E than in Group C (4.7 ± 0.6 vs 4.2 ± 0.7, P < 0.001; 4.7 ± 0.5 vs 4.4 ± 0.7, P = 0.005). The postoperative AIS (4 [1, 6] vs 5 [2, 9], P = 0.012) and HADS-A (1 [0, 3] vs 2 [0, 6], P = 0.012) scores were significantly lower in Group E than in Group C. Hemodynamic and respiratory parameters were more stable in Group E than in Group C, with the lower opioids consumption of sufentanil (0 [0, 4] vs 5 [2.5, 7.7], P < 0.001) and remifentanil (700 [480, 900] vs 800 [500, 1200], P = 0.023) in Group E compared to Group C. On ordinal logistics regression, postoperative sleep quality (OR, 0.70; 95% CI, 0.62-0.79), anxiety level (OR, 0.77; 95% CI, 0.62-0.95) and recovery time in post-anesthesia care unit (PACU) (OR, 0.69; 95% CI, 0.56-0.98) were identified as significant predictors associated with patient satisfaction. Conclusion:A subanesthetic dose of esketamine (0.15-0.3 mg/kg/h) as an adjuvant can improves the sedative and analgesic effects of dexmedetomidine and remifentanil during anesthesia for liposuction surgery. Clinical Trial Registration:ChiCTR2400080363.

Blood‑oxygenation-level-dependent (BOLD) functional MRI (fMRI) has provided a wealth of information about brain function and neural networks. However, the BOLD signal is based on vascular responses secondary to neural activity. Therefore, alterations in the vascular function could confound the task-evoked fMRI findings, and also affect functional connectivity mapping in resting-state fMRI. Cerebrovascular reactivity (CVR), referring to the ability of the cerebral blood vessels to dilate or constrict in response to stimulus, is an important indicator of cerebrovascular health. Conventional CVR mapping techniques require breathing maneuvers or drug challenges, which could be cumbersome in clinical settings and impractical in some patient cohorts. Recently, CVR mapping techniques using resting-state fMRI data have been developed. This chapter describes current evidence and literature on how CVR influences resting-state fMRI measurements, and how CVR can be extracted from resting-state fMRI data and utilized in clinical patients.

对于术前评估为困难气道的患者应当采用清醒镇静表面麻醉下实施气管插管.实施清醒气管插管的关键技术是完善的气道局部麻醉.清醒气管插管是麻醉科医师必须掌握的技能之一.本文通过回顾近十年的文献,旨为麻醉科医师提供清醒气管插管气道局部麻醉技术相关理论参考.

Purpose: The use of ketamine, an anesthetic, as a treatment for asthma has been investigated in numerous studies. However, how ketamine affects asthma is unclear. The present study examined the effects of ketamine on a murine model of mixed-granulocytic asthma, and the role of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway.Methods: The murine model of mixed-granulocytic asthma was established using ovalbumin (OVA) for sensitization and the combination of OVA and lipopolysaccharides (LPS) for challenge. The main characteristics of asthma, oxidative stress biomarkers, and the expression of the Nrf2 pathway were examined. ML385 was administered to verify the role of the Nrf2 pathway.Results: Mice in the OVA +LPS group developed asthmatic characteristics, including airway hyperresponsiveness, mixed-granulocytic airway inflammation, mucus overproduction, as well as increased levels of oxidative stress and impaired apoptosis of inflammatory cells. Among the three concentrations, ketamine at 75mg/kg effectively attenuated these asthmatic symptoms, activated the Nrf2 pathway, decreased oxidative stress, and induced apoptosis of eosinophils and neutrophils in bronchoalveolar lavage fluid (BALF) with a reducing level of myeloid cell leukemia 1(Mcl-1). ML385 (an Nrf2 inhibitor) eliminated the protective effects of ketamine on the mixed-granulocytic asthma model.Conclusion: The study concluded that ketamine reduced oxidative stress and attenuated asthmatic symptoms (neutrophilic airway inflammation) by activating the Nrf2-Keap1 pathway, with 75 mg/kg ketamine showing the best results. Ketamine administration also increased neutrophil and eosinophil apoptosis in BALF, which may contribute to the resolution of inflammation. The use of ketamine as a treatment for asthma may therefore be beneficial.

Dexmedetomidine (DEX) suppresses inflammatory responses and protects against organ injury. The aim of the present study was to investigate the effect of DEX on airway hyperresponsiveness (AHR) and allergic airway inflammation, as well as its underlying mechanism of action in a murine model of ovalburnin (OVA)-induced asthma. A total of 30 female BALB/c mice were divided into 6 groups (n=5 mice/group): Control, OVA, OVA + DEX (20, 30 or 50 mu g/kg) and OVA + TAK-242 [a toll-like receptor 4 (TLR4) inhibitor]. The mice were intraperitoneally injected with 20, 30 or 50 mu g/kg DEX 1 h before OVA challenge. AHR to inhaled methacholine (Mch) was measured, and the mice were sacrificed 24 h after the last challenge. AHR following Mch inhalation was measured using the FlexiVent apparatus. Hematoxylin and eosin, periodic acid-Schiff and Wright-Giemsa staining was performed to evaluate inflammatory cell infiltration in the lung tissue. The levels of IL-4, IL-5 and IL-13 in the bronchoalveolar lavage fluid were analyzed using ELISA, and their mRNA expression levels in the lung tissue were examined using reverse transcription-quantitative PCR. The protein expression of TLR4, NF-kappa B and phosphorylated (p) NF-kappa B in the lung tissue was also detected using immunohistochemistry. In the murine OVA-induced asthma model, DEX decreased AHR following Mch inhalation and reduced the infiltration of inflammatory cells. IL-4, IL-5 and IL-13 levels in the bronchoalveolar lavage fluid were significantly lower following DEX treatment. Furthermore, DEX treatment inhibited the expression of TLR4, NF-kappa B and p-NF-kappa B in the lung tissue and exhibited a similar effect to TAK-242 treatment. In conclusion, DEX may attenuate AHR and allergic airway inflammation by inhibiting the TLR4/NF-kappa B pathway. These results suggested that DEX may represent a potential anti-inflammatory agent for the treatment and management of patients with asthma.

Background: Asthma is a disease that affects health worldwide. It is characterised by inflammation and airway hyperreactivity. Because airway hyperreactivity can occur in other diseases, perioperative airway hyperreactivity is more insidious and widespread than in asthma and has serious implications that need to be addressed urgently. The use of dexmedetomidine in acute asthma and lung protection has been reported, but the exact mechanism is unclear. Objective: To investigate the effectiveness and mechanisms associated with dexmedetomidine in airway hyperresponsiveness. Methods: Forty BALB/c female mice were randomly divided into five groups: group K (blank group), group A (asthma group), group HD (asthma + dexmedetomidine treatment group), group TH (asthma + yohimbine group) and group HT (asthma + dexmedetomidine + yohimbine group), and the airway resistance of group K, group A and group HD were analysed by invasive airway resistance assay, ELISA assay, immunohistochemistry and q-PCR, respectively. Airway resistance; IL-4 and IgE levels in serum and BLAF; and IL-4, IL-13, Muc5AC, NFκB, TLR2, TLR4 and TSLP1 protein levels in lung tissues of the 5 groups were analysed by invasive airway resistance assay, ELISA, immunohistochemistry and qPCR. Results: Compared with group A, there were statistical differences in airway resistance ( P < 0.05); LIL-4 and IgE ( P < 0.05) in serum and BLAF; and Muc5AC, TLR4 and NFκB protein contents ( P < 0.05) in lung tissues in the HD group. Conclusion: 1. Dexmedetomidine can attenuate airway hyperresponsiveness in the OVA asthma model; 2. Dexmedetomidine reduced the production of IL-4 and IgE by down-regulating the TLR4/NF-κB signaling pathway, thereby reducing the lung inflammatory response and airway hyperresponsiveness in the OVA-induced asthma model.

目的:探究低剂量右美托咪定复合丙泊酚联合舒芬太尼用于面部整形手术的临床效果.方法:前瞻性选择2018年8月-2019年10月在中国医学科学院北京协和医学院整形外科医院就诊后接受面部整形手术的患者60例.将全部患者根据随机数字表法分为对照组以及观察组,每组30例.对照组使用丙泊酚联合舒芬太尼进行麻醉,观察组使用右美托咪定+丙泊酚联合舒芬太尼进行麻醉.对比两组血流动力学指标[麻醉诱导前,麻醉后15min,手术开始,手术完成时的平均动脉压(MAP)、心率(HR)、动脉血氧分压(SpO2)],术后苏醒时间,术后清醒时间,视觉模拟评分(Visual analog scale,VAS),镇静评分(Ramsay评分),术中体动次数和舒芬太尼追加使用剂量,麻醉恢复室内不良反应发生率以及手术医生、麻醉医生、患者的满意度.结果:两组麻醉诱导前、麻醉后15min、手术开始、手术完成时的MAP、HR、SpO2比较差异均不具有统计学意义(P>0.05).观察组的术后苏醒时间、术后清醒时间均短于对照组,差异有统计学意义(P<0.05).观察组术后的VAS评分、镇静评分高于对照组,差异有统计学意义(P<0.05).观察组术中体动次数和舒芬太尼追加使用剂量均低于对照组,差异有统计学意义(P<0.05).两组在麻醉恢复室内不良反应发生率比较差异不具有统计学意义(P>0.05).且两组手术医生、麻醉医生、患者满意度比较差异不具有统计学意义(P>0.05).结论:接受面部整形手术的患者,采用低剂量右美托咪定复合丙泊酚的麻醉方法,可保证手术过程中血流动力学的稳定,并有助于缩短术后清醒时间,改善术后的镇静效果,并且安全性良好.

SaCo(safe comfortable)可视喉罩是一种新型的国产可视喉罩,喉罩内置的摄像头可以持续观察喉罩的置入、留置、拔除的全部过程,为喉罩的安全使用提供方便.小耳畸形患儿有不同程度的半侧颜面短小或者小颌畸形,此类患儿咽腔容积小,困难气管插管的发生率较高[1-2].大量的临床观察已经证实,经喉罩和插管型喉罩可以快速完成气管插管,是目前解决困难插管最有效方法之一[3-4].由于普通喉罩没有可视功能,气管插管时需要联合使用可视插管软镜,增加了操作的步骤和设备需求,在一定程度上限制该方法的广泛使用.本研究观察小耳畸形患儿经SaCo可视喉罩实施气管插管的安全性,为患儿的气管插管和困难插管提供一种新的选择.

lntracellular calcium ion is the key secondary messenger system of the cellular processes in airway smooth muscle cells(ASMc). The treatment and regulation of Ca(2+)in airway smooth muscle (ASM) is, in part, to associated with many airway diseases such as asthma, COPD and pulmonary fibrosis. The mechanism of contraction and relaxation of ASM is a concerned aspect in airway diseases. This review emphasizes established and recent discoveries whice show the research progress of Ca(2+)on cell contraction and relaxation in ASM in recent years, to provide theoretical support and new targets for clinical prevention and treatment of perioperative bronchospasm and variousrespiratory related diseases.

近年来,随着困难气道管理工具的研发和推广应用,困难气道管理指南的制定以及对气道管理培训的重视和积极开展,困难气道的发生率显著降低[1-10].尽管如此,由于迄今仍缺乏公认的、健全的能够准确预测困难气道的评估体系,未预料的困难气道时有发生,如果未及时给予恰当处理,将导致患者缺氧性脑损伤,甚至死亡[3,11].此外,众多文献明确指出,气道评估不完善以及预防体系不健全是导致气道管理失败和气道相关不良事件增加的主要原因[10,12-14].

Therefore, health care workers must raise the awareness of "silent lung" during perioperative period, especially for patients with a history of bronchial asthma or recent history of upper respiratory tract infection. By the through preoperative assessment and preparation, the rational use of drugs in order to prevent and control airway hyperresponsiveness, selecting the appropriate airway management tools, and enhancing anesthesia management of perioperative period, all those measures are effective to prevent the occurrence of "silent lung". Meanwhile, health care workers should have the ability to quickly identify and diagnose "silent lung"occurred during perioperative period, give timely and effective treatment, so as to ensure the patients′safety as possible as they can.

近年来,随着多种困难气道管理工具的研发、推广应用以及对气道管理培训的重视和完善,困难气管插管发生率显著降低[1]. 然而,导致气道管理失败和气道相关不良事件发生的主要原因仍然是气道评估不完善和预防体系不健全[1-3]. 为了完善术前气道评估,并保证困难气道患者再次手术安全,除了相关病史、体格检查以及影像学等辅助检查之外,记录了既往困难气道管理相关情况的困难气道告知书将会给气道管理相关医护人员提供直接、有价值的参考[4].2017年中华医学会麻醉学分会发布的困难气道管理指南指出,术后应将困难气道处理情况记录并告知患者[5]. 目前,美国、加拿大已经建立了规范的困难气道告知体系,并且困难气道告知书已经得到广泛应用. 本文总结归纳了美国、加拿大困难气道告知书的书写内容[6] ,以及困难气道告知书在困难气道管理中的具体应用,旨在为探索创建国内困难气道告知书的书写模式和建立困难气道告知体系提供借鉴.