Respiratory Physiology & Neurobiology最新文献_第10页

Breath-hold diving as a tool to harness a beneficial increase in cardiac vagal tone 屏气潜水作为一种工具，利用有益的增加心脏迷走神经张力。

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2025-05-01 Epub Date: 2025-03-15 DOI: 10.1016/j.resp.2025.104416

Pierrick Martinez , Mathias Dutschmann , Vincent Epercieux , Géraud Gourjon , Fabrice Joulia

Here we review central mechanisms that mediate the diving bradycardia and propose that breath-hold diving (BH-D) is a powerful therapeutic tool to improve cardiac vagal tone (CVT). Physiological fluctuations in CVT are known as the respiratory heart rate variability (respirHRV) and involve two respiratory-related brainstem mechanisms. During inspiration pre-Bötzinger complex (pre-BötC) neurons inhibit cardiac vagal motor neurons to increase heart rate and subsequently cardiac vagal disinhibition and a decrease in heart rate is associated with a Kölliker-Fuse (KF) nucleus-mediated partial glottal constriction during early expiration. Both KF and pre-BötC receive direct descending cortical inputs that could mediate volitional glottal closure as critical anatomical framework to volitionally target brainstem circuits that generate CVT during BH-D. Accordingly we show that volitional and reflex glottal closure during BH-D appropriates the respirHRV core network to mediate the diving bradycardia via converging trigeminal afferents inputs from the nose and forehead. Additional sensory inputs linked to prolonged BH-D after regular training further increase CVT during the acute dive and can yield a long-term increase in CVT. Centrally, evidence of Hebbian plasticity within respirHRV/BH-D core circuit further support the notion that regular BH-D exercise can yield a permanent increase in CVT specifically via a sensitization of synapse involved in the generation of the respirHRV. Contrary to other regular physical activity, BH-D reportedly does not cause structural remodeling of the heart and therefore we suggest that regular BH-D exercise could be employed as a save and non-invasive approach to treat sympathetic hyperactivity, particularly in elderly patients with cardio-vascular predispositions.

在这里，我们回顾了介导潜水性心动过缓的中枢机制，并提出屏气潜水（BH-D）是改善心脏迷走神经张力（CVT）的有力治疗工具。CVT的生理波动被称为呼吸性心率变异性（呼吸性心率变异性），涉及两种与呼吸相关的脑干机制。吸气时pre-Bötzinger复合体（pre-BötC）神经元抑制心脏迷走神经运动神经元增加心率，随后心脏迷走神经解除抑制，心率降低与呼气早期Kölliker-Fuse （KF）核介导的部分声门收缩有关。KF和pre-BötC都接受直接下行皮质输入，这可能介导意志声门关闭，作为在BH-D期间产生CVT的意志目标脑干回路的关键解剖框架。因此，我们表明，在BH-D期间，意志和反射性声门关闭使呼吸hrv核心网络通过来自鼻子和前额的会聚三叉神经传入输入来调节潜水性心动过缓。在常规训练后，与长时间的BH-D相关的额外感觉输入进一步增加了急性潜水期间的CVT，并可能导致CVT的长期增加。总之，在呼吸hrv /BH-D核心回路中Hebbian可塑性的证据进一步支持了这样一种观点，即定期的BH-D锻炼可以产生永久性的CVT增加，特别是通过参与呼吸hrv产生的突触的敏化。与其他常规的身体活动相反，据报道，BH-D运动不会引起心脏结构重塑，因此我们建议，定期的BH-D运动可以作为一种拯救和非侵入性的方法来治疗交感神经亢进，特别是对于有心血管易感性的老年患者。

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引用次数: 0

Altered breathing pattern of lowlanders sleeping at high altitude: Novel insights from home sleep apnoea tests procedures 低地人在高海拔地区睡眠的呼吸模式改变：来自家庭睡眠呼吸暂停测试程序的新见解。

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2025-05-01 Epub Date: 2025-03-06 DOI: 10.1016/j.resp.2025.104415

Pierpaolo Prosperi , Antonella Spacone , Alberto Taverna , Riccardo Rua , Sofia Bonan , Giorgia Rapacchiale , Danilo Bondi , Camillo Di Giulio , Giuseppe Miserocchi , Vittore Verratti

Lowlanders sojourning at high altitude often experience sleep disturbances, which are driven by blood gases alterations and manifest as stress-related patterns, including frequent awakenings, apnoeas, reduction in sleep duration and possibly with the occurrence of periodic breathing. This study demonstrated clinical evidence of sleep disturbances at high altitude by using portable device during a Himalayan expedition. The home sleep apnoea test was conducted on 10 participants taking part in the "Lobuche Peak - Pyramid Exploration & Physiology". The longitudinal design included five assessments, before the expedition, at pre-expedition at Kathmandu (≈1400 m), at a peak altitude of ≈ 5000 m, upon return to Kathmandu and one month after return in Italy. Total sleep time was below 7 h of duration at the highest altitude in all participants. Nocturnal SpO₂ dropped below daytime measurement and was greatly reduced at high altitude; conversely, heart rate increased. All participants experienced an increase in apnea-hypopnea index at high altitude, with seven out of 10 falling in moderate-to-severe grade. Periodic breathing pattern was clearly observed in two participants, of whom one developed acute mountain sickness and one did not. All the impairments were fully reversible once back at low altitude. Translationally, our findings underscore the importance of conducting home sleep apnoea tests at living altitude. Sleep-disordered breathing arises from a complex pattern that can be due to a wide range of responses, and the overall functions revealed by home sleep apnoea testing during a field expedition have the potential to increase the safety of high altitude sojourners, while advancing our knowledge of hypoxia as the red line linking respiratory and environmental physiology.

居住在高海拔地区的低地人经常会遇到睡眠障碍，这是由血气变化引起的，表现为与压力相关的模式，包括频繁醒来、呼吸暂停、睡眠时间缩短以及可能出现的周期性呼吸。本研究通过在喜马拉雅山探险期间使用便携式设备，展示了高海拔地区睡眠障碍的临床证据。对参加“罗布切峰-金字塔探索与生理学”的10名参与者进行了家庭睡眠呼吸暂停测试。纵向设计包括5次评估，分别在考察前、考察前在加德满都（约1400米）、高峰海拔约5000米、返回加德满都时和返回意大利一个月后。在海拔最高的地方，所有参与者的总睡眠时间都低于7小时。夜间SpO2低于白天测量值，在高海拔地区显著降低；相反，心率增加了。在高海拔地区，所有参与者的呼吸暂停低通气指数都有所上升，10人中有7人的呼吸暂停低通气指数呈中度至重度下降。两名参与者明显观察到周期性呼吸模式，其中一人出现急性高原反应，一人没有。一旦回到低空，所有的损伤都是完全可逆的。因此，我们的发现强调了在生活海拔进行家庭睡眠呼吸暂停测试的重要性。睡眠呼吸障碍是由一个复杂的模式引起的，可能是由于广泛的反应，在野外探险期间通过家庭睡眠呼吸暂停测试揭示的整体功能有可能提高高海拔旅行者的安全性，同时推进我们对缺氧的认识，将其作为连接呼吸和环境生理学的红线。

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引用次数: 0

A computational fluid dynamics analysis of BiPAP pressure settings on airway biomechanics using a CT-based respiratory tract model 基于ct呼吸道模型的BiPAP压力设置对气道生物力学的计算流体动力学分析。

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2025-04-01 Epub Date: 2025-01-16 DOI: 10.1016/j.resp.2025.104397

Xinlei Huang , Goutam Saha , Akshoy Ranjan Paul , Adele Tahan , Suvash C. Saha

Central and Obstructive Sleep Apnea (CSA and OSA), Chronic Obstructive Pulmonary Disease (COPD), and Obesity Hypoventilation Syndrome (OHS) disrupt breathing patterns, posing significant health risks and reducing the quality of life. Bilevel Positive Airway Pressure (BiPAP) therapy offers adjustable inhalation and exhalation pressures, potentially enhancing treatment adaptability for the above diseases. This is the first-ever study that employs Computational Fluid Dynamics (CFD) to examine the biomechanical impacts of BiPAP under four settings: Inspiratory Positive Airway Pressure (IPAP)/Expiratory Positive Airway Pressure (EPAP) of 12/8, 16/6, and 18/8 cmH₂O, compared to a without-BiPAP scenario of zero-gauge pressure. Utilizing a computed-tomography-based respiratory tract model from the nasal cavity extending to the 13th generation, we analyzed parameters such as static pressure, shear stress, and airway wall normal force across different airway regions. Our results indicate that BiPAP, particularly at higher IPAP settings, effectively increases static pressure, thereby improving airway patency and potentially reducing the risk of airway collapse in both CSA and OSA. Lower EPAP, on the other hand, helps reduce the work of breathing during exhalation, which is particularly useful for patients who have difficulty exhaling against higher pressures or need to exhale CO₂ more effectively. This comparative analysis confirms that BiPAP not only maintains open airways but does so with an adjustable approach that can be used for the specific needs of patients with various respiratory dysfunctions, thereby offering a versatile and effective treatment option.

中枢性和阻塞性睡眠呼吸暂停（CSA和OSA）、慢性阻塞性肺疾病（COPD）和肥胖低通气综合征（OHS）会扰乱呼吸模式，造成重大健康风险并降低生活质量。双水平气道正压（BiPAP）治疗提供可调节的吸入和呼出压力，潜在地增强了对上述疾病的治疗适应性。这是首次使用计算流体动力学（CFD）来检查BiPAP在四种设置下的生物力学影响的研究：吸气气道正压(IPAP)/呼气气道正压（EPAP）为12/8、16/6和18/8 cmH2O，与无BiPAP零表压的情况相比。利用从鼻腔延伸到第13代的基于计算机断层扫描的呼吸道模型，我们分析了不同气道区域的静压、剪切应力和气道壁法向力等参数。我们的研究结果表明，BiPAP，特别是在较高的IPAP设置下，有效地增加静压，从而改善气道通畅，并潜在地降低CSA和OSA患者气道塌陷的风险。另一方面，较低的EPAP有助于减少呼气过程中的呼吸功，这对于在较高压力下呼吸困难或需要更有效地呼出二氧化碳的患者特别有用。这一对比分析证实BiPAP不仅维持气道畅通，而且采用可调节的方法，可用于各种呼吸功能障碍患者的特定需求，从而提供了一种多功能和有效的治疗选择。

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引用次数: 0

End-tidal CO2 and ventilation: Novel markers for assessing performance levels in elite long-distance runners 潮末二氧化碳和通风：评估优秀长跑运动员表现水平的新指标。

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2025-04-01 Epub Date: 2024-12-31 DOI: 10.1016/j.resp.2024.104389

Akihiro Sakamoto , Yohei Matsumoto , Hisashi Naito , Chin Moi Chow

Well-trained individuals, compared to less well-trained individuals, exhibit a lower minute ventilation (V̇_E) and higher end-tidal partial pressure of CO₂ (P_ETCO₂) at a given work rate. This study investigated whether such breathing adaptations seen in well-trained individuals also applied to elite long-distance runners. Forty-one long-distance runners were categorized into high (Long-High, consisting of Tokyo-Hakone College Ekiden [relay marathon] runners and Olympic athletes, n = 23), or low performance-level group (Long-Low, n = 18) according to their race times. Ten middle-distance runners (Middle) also participated in a comparison group. All subjects performed an incremental exercise test on a motorized treadmill until exhaustion. Maximum V̇O₂ and velocity were greater for the Long groups than the Middle group, however these measures were not distinguishable between the Long-High and the Long-Low groups. By contrast, V̇_E and P_ETCO₂ were able to identify the Long-High group. Submaximal V̇_E were lowest, whilst P_ETCO₂ especially at high running velocities were highest for the Long-High group. This study confirms that breathing patterns with lower V̇_E and higher P_ETCO₂ are relevant adaptation markers for assessing endurance race performance in elite long-distance runners.

在给定的工作速率下，训练良好的个体比训练不佳的个体表现出更低的分钟通气量（V (E)）和更高的CO2末潮分压（PETCO2）。这项研究调查了在训练有素的人身上看到的这种呼吸适应是否也适用于优秀的长跑运动员。41名长跑运动员根据成绩分为高水平组（Long-High，由东京箱根大学马拉松接力选手和奥运会运动员组成，n=23）和低水平组（Long-Low, n=18）。10名中长跑运动员（Middle）也参加了一个对照组。所有受试者在电动跑步机上进行增量运动测试，直到精疲力竭。长组的最大V / O2和速度大于中组，但这些指标在长高组和长低组之间没有区别。相比之下，V (E)和PETCO2能够识别Long-High组。长-高组的次最大V / E最低，而PETCO2在高跑速时最高。本研究证实，低V / E和高PETCO2的呼吸模式是评估优秀长跑运动员耐力赛表现的相关适应指标。

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引用次数: 0

Breathlessness dimensions should be evaluated in relation to the level of exertion: A clinical study 评估呼吸困难程度时应考虑用力程度：一项临床研究。

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2025-04-01 Epub Date: 2025-01-25 DOI: 10.1016/j.resp.2025.104398

Viktor Elmberg , Gufran Ali , David Gustafsson , Dennis Jensen , Magnus Ekström

Background/aim

Exertional breathlessness is a dominating symptom in cardiorespiratory disease, limiting exercise capacity. Multidimensional measurement has been proposed to capture breathlessness, but it is unknown whether it is useful to differentiate people with abnormal vs normal exertional breathlessness intensity.

Methods

This was a secondary analysis of a randomized controlled trial of outpatients aged ≥ 18 years performing a symptom-limited cycle incremental exercise test (IET). Breathlessness sensations at end of IET were identified using the multidimensional dyspnea profile (MDP) 30-min post-exercise and compared between people with abnormally high breathlessness (Borg 0–10 rating > upper limit of normal [ULN]) and people within normal ranges (≤ ULN) in relation to the percentage of predicted peak power output defined by normative reference equations.

Results

Of 92 participants, 20 (22 %) had abnormally high breathlessness. Compared with those with normal breathlessness (n = 72 [78 %]), the abnormal group reported higher symptom intensity at peak exercise (7.9 ± 1.7 vs 6.3 ± 1.4 Borg units; p < 0.001) and had lower peak power output 129 ± 52 W vs 167 ± 55 W; p < 0.001). Differences between those with normal, and abnormal exertional breathlessness regarding MDP ratings were not statistically significant (all p > 0.05): overall unpleasantness, 4.1 ± 2.3 vs 4.7 ± 1.6; immediate perception, 10.9 ± 2.8 vs 11.5 ± 1.8; and emotional response, 4.1 ± 7.6 vs 3.2 ± 7.5. MDP ratings had no relation to peak power output.

Conclusion

Breathlessness dimensions are similar at the peak of a standardized IET and cannot differentiate between people with normal and abnormally high exertional breathlessness.

背景/目的：运动性呼吸困难是心肺疾病的主要症状，限制了运动能力。多维度测量已被提议用于捕捉呼吸困难，但目前尚不清楚它是否有助于区分异常和正常呼吸困难强度的人。方法：这是一项对年龄≥18岁的门诊患者进行症状限制周期增量运动试验（IET）的随机对照试验的二次分析。使用运动后30分钟的多维呼吸困难谱（MDP）识别IET结束时的呼吸困难感觉，并比较异常高呼吸困难（Borg 0-10评级>正常上限[ULN]）和正常范围内（≤ULN）的人（与规范参考方程定义的预测峰值功率输出百分比有关）。结果：在92名参与者中，20名（22%）有异常的高度呼吸困难。与正常呼吸困难组（n=72[78%]）相比，异常组在运动高峰时的症状强度更高(7.9±1.7比6.3±1.4 Borg单位；P0.05)：总体不愉快，4.1±2.3 vs 4.7±1.6；即时感知：10.9±2.8 vs 11.5±1.8；情绪反应，4.1±7.6 vs 3.2±7.5。MDP额定值与峰值输出功率无关。结论：在标准化IET峰值时，呼吸困难的维度相似，无法区分正常和异常高的运动性呼吸困难。

{"title":"Breathlessness dimensions should be evaluated in relation to the level of exertion: A clinical study","authors":"Viktor Elmberg , Gufran Ali , David Gustafsson , Dennis Jensen , Magnus Ekström","doi":"10.1016/j.resp.2025.104398","DOIUrl":"10.1016/j.resp.2025.104398","url":null,"abstract":"<div><h3>Background/aim</h3><div>Exertional breathlessness is a dominating symptom in cardiorespiratory disease, limiting exercise capacity. Multidimensional measurement has been proposed to capture breathlessness, but it is unknown whether it is useful to differentiate people with abnormal vs normal exertional breathlessness intensity.</div></div><div><h3>Methods</h3><div>This was a secondary analysis of a randomized controlled trial of outpatients aged ≥ 18 years performing a symptom-limited cycle incremental exercise test (IET). Breathlessness sensations at end of IET were identified using the multidimensional dyspnea profile (MDP) 30-min post-exercise and compared between people with abnormally high breathlessness (Borg 0–10 rating > upper limit of normal [ULN]) and people within normal ranges (≤ ULN) in relation to the percentage of predicted peak power output defined by normative reference equations.</div></div><div><h3>Results</h3><div>Of 92 participants, 20 (22 %) had abnormally high breathlessness. Compared with those with normal breathlessness (n = 72 [78 %]), the abnormal group reported higher symptom intensity at peak exercise (7.9 ± 1.7 vs 6.3 ± 1.4 Borg units; p < 0.001) and had lower peak power output 129 ± 52 W vs 167 ± 55 W; p < 0.001). Differences between those with normal, and abnormal exertional breathlessness regarding MDP ratings were not statistically significant (all p > 0.05): overall unpleasantness, 4.1 ± 2.3 vs 4.7 ± 1.6; immediate perception, 10.9 ± 2.8 vs 11.5 ± 1.8; and emotional response, 4.1 ± 7.6 vs 3.2 ± 7.5. MDP ratings had no relation to peak power output.</div></div><div><h3>Conclusion</h3><div>Breathlessness dimensions are similar at the peak of a standardized IET and cannot differentiate between people with normal and abnormally high exertional breathlessness.</div></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":"333 ","pages":"Article 104398"},"PeriodicalIF":1.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effectiveness of selective NaV1.7 blocker PF-05089771 in reducing cough associated with allergic rhinitis in guinea pigs 选择性NaV1.7阻滞剂PF-05089771减轻豚鼠变应性鼻炎相关咳嗽的有效性

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2025-04-01 Epub Date: 2024-12-25 DOI: 10.1016/j.resp.2024.104387

Janka Jakusova , Tomas Buday , Daniela Mokra , Romana Barosova , Juliana Hanusrichterova , Marian Adamkov , Veronika Mestanova , Jana Plevkova , Mariana Brozmanova

Background

Allergic rhinitis (AR) is a common cause of chronic cough, linked to dysregulated airway C- and Aδ-fibres through inflammatory mediators. Despite the limited efficacy of current antitussive therapies, recent studies show that the Na_V1.7 inhibitor can block cough in naïve guinea pigs. This study aimed to analyse the effect of the Na_V1.7 blocker PF-05089771 on cough in guinea pigs with AR.

Methods

Dunkin Hartley guinea pigs were sensitised and challenged with ovalbumin (OVA). Cough was induced using citric acid aerosol (0.4 M) before nasal challenge (NCH), and then one hour after the 1st, 3rd, and 6th NCH. The OVA-inhibitor group was pre-treated with inhaled Na_V1.7 blocker (PF-05089771, 100 μM) before tussigen inhalation.

Results

Chronic AR increased cough response to citric acid in both males and females. Pre-treatment with Na_V1.7 blocker significantly inhibited cough reflex by ≈ 75 % in males and ≈ 80 % in females without affecting respiratory rate.

Conclusion

Na_V1.7 blocker inhalation effectively inhibits cough in guinea pigs with AR.

背景：变应性鼻炎（AR）是慢性咳嗽的常见原因，通过炎症介质与气道C-和a -纤维失调有关。尽管目前的止咳疗法疗效有限，但最近的研究表明，NaV1.7抑制剂可以阻断naïve豚鼠的咳嗽。本研究旨在分析NaV1.7阻滞剂PF-05089771对ar豚鼠咳嗽的影响。方法：Dunkin Hartley豚鼠致敏，卵清蛋白（OVA）攻毒。用柠檬酸气雾剂（0.4M）在灌鼻前及灌鼻后1、3、6 h诱导咳嗽。OVA-inhibitor组在吸入性牙周菌前吸入NaV1.7阻断剂（PF-05089771, 100μM）进行预处理。结果：慢性AR增加了男性和女性对柠檬酸的咳嗽反应。在不影响呼吸频率的情况下，NaV1.7阻滞剂对男性咳嗽反射的抑制率约为75%，对女性咳嗽反射的抑制率约为80%。结论：吸入NaV1.7阻滞剂可有效抑制豚鼠急性呼吸道变应性咳嗽。

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引用次数: 0

Effect of imatinib on lipopolysaccharide‑induced acute lung injury and endothelial dysfunction through the P38 MAPK and NF-κB signaling pathways in vivo and in vitro 伊马替尼通过体内和体外P38 MAPK和NF-κB信号通路对脂多糖诱导的急性肺损伤和内皮功能障碍的影响

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2025-04-01 Epub Date: 2024-12-25 DOI: 10.1016/j.resp.2024.104388

Yaru Liu , Duanyang Li , Tianyi Zhang , Keruo Wang , Xue Liang , Xiaolong Zong , Hong Yang , Zhenyu Li

Background

The primary purpose of this study was to demonstrate the preventive effects of imatinib (IMA) on lipopolysaccharide (LPS)-induced inflammation in a mouse model of acute lung injury (ALI) and human umbilical vascular endothelial cells.

Methods

LPS stimulation for 24 h induced ALI and cell inflammation. The pathological results of the lungs were evaluated using the wet/dry weight ratio, pulmonary vascular permeability measurements, and myeloperoxidase immunohistochemistry. The expression of pro-inflammatory mediators was analyzed using RT-PCR and enzyme-linked immunosorbent assay. Protein levels were analyzed using western blotting. The structure of cell junctions was detected using immunofluorescence.

Results

IMA improved LPS-induced pulmonary pathological damage and reduced the lung wet/dry weight ratio and myeloperoxidase expression in the lung tissue. IMA decreased bronchoalveolar lavage fluid inflammatory cell count and the release of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and monocyte chemotactic protein 1 (MCP-1) in the blood. Pretreatment of human umbilical vascular endothelial cells with IMA significantly attenuated LPS-induced actin stress fiber formation and vascular endothelial-cadherin disruption. In addition, IMA downregulated the mRNA abundances of vascular cell adhesion molecule 1, intercellular adhesion molecule 1, IL-1β, IL-6, and tumor necrosis factor-α(TNF-α) expression. The phosphorylation of p65, nuclear factor-kappa B inhibitor alpha (IκBα), p38, extracellular signal-regulated kinase, and Jun N-terminal kinase induced by LPS were attenuated after IMA treatment in vivo and in vitro.

Conclusions

IMA modulates the nuclear factor-kappa B and mitogen-activated protein kinase signaling pathways and the production of pro-inflammatory cytokines to prevent cellular damage due to LPS infection. These results indicate that IMA may be a potential modulator of LPS-induced ALI.

背景：本研究的主要目的是证明伊马替尼（IMA）对小鼠急性肺损伤（ALI）模型和人脐血管内皮细胞中脂多糖（LPS）诱导的炎症的预防作用。方法：LPS刺激24h诱导ALI和细胞炎症。采用干湿比、肺血管通透性测量和髓过氧化物酶免疫组化评价肺病理结果。采用RT-PCR和酶联免疫吸附法分析促炎介质的表达。western blotting分析蛋白水平。免疫荧光法检测细胞连接结构。结果：IMA改善了lps诱导的肺病理损伤，降低了肺干湿比和肺组织中髓过氧化物酶的表达。IMA降低支气管肺泡灌洗液炎症细胞计数和血液中肿瘤坏死因子-α (TNF-α)、白细胞介素(IL)-6和单核细胞趋化蛋白1 （MCP-1）的释放。IMA预处理人脐血管内皮细胞可显著减弱lps诱导的肌动蛋白应激纤维形成和血管内皮-钙粘蛋白破坏。IMA还下调了血管细胞粘附分子1、细胞间粘附分子1、IL-1β、IL-6 mRNA丰度和肿瘤坏死因子-α(TNF-α)表达。IMA在体内和体外处理后，LPS诱导的p65、核因子- κB抑制剂α (IκBα)、p38、细胞外信号调节激酶和Jun n -末端激酶的磷酸化均减弱。结论：IMA可调节核因子κ B和丝裂原活化蛋白激酶信号通路及促炎细胞因子的产生，预防LPS感染引起的细胞损伤。这些结果表明，IMA可能是lps诱导的ALI的潜在调节剂。

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引用次数: 0

Characteristics of brain network after cardiopulmonary phase synchronization enhancement 心肺相同步增强后脑网络的特征。

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2025-04-01 Epub Date: 2025-01-13 DOI: 10.1016/j.resp.2025.104396

Yumiao Ren , Lin Xie , Xiaoni Wang , Jianbao Zhang

The central neural mechanism plays an important role in cardiopulmonary coupling. How the brain stem affects the cardiopulmonary coupling is relatively clear, but there are few studies on the cerebral cortex activity of cardiopulmonary coupling. We aim to study the response of the cerebral cortex for cardiopulmonary phase synchronization enhancement. The method of brain network was used and Pearson correlation analysis performed on the global attributes and phase synchronization time (CRPST) in the spontaneous, 2/2 and 4/4 breathing modes. Furthermore, calculated the phase lag index (PLI) among 21 lead EEG signals, and then analyzed the correlation between PLI and the parameters of cardiovascular and respiratory systems. Our results show that the global brain network characteristic parameters are significantly different in the three breath modes in the α (8–14 Hz) band. The global efficiency and feature path length are significantly positively correlated with the phase synchronization and PLI indexes are widely related to CRPST and respiratory depth in the spontaneous breathing mode, while the brain network parameters and PLI indexes are not correlated with CRPST and PLI mainly positively correlated with respiratory rate in the controlled breathing modes. The differences of brain networks in the three modes are mainly caused by the physiological factors of cardiopulmonary coupling. These show that enhanced cardiopulmonary phase synchronization with controlled breathing based on heartbeat has a significant effect on the cardiopulmonary system and maybe provide some ideas for regulating cardiopulmonary function in the future.

中枢神经机制在心肺耦合中起着重要作用。脑干如何影响心肺耦合是比较清楚的，但关于心肺耦合的大脑皮层活动的研究很少。我们的目的是研究大脑皮层对心肺相同步增强的反应。采用脑网络方法，对自发性、2/2和4/4呼吸模式的全局属性和相位同步时间（CRPST）进行Pearson相关分析。计算21个脑电图导联信号的相位滞后指数（PLI），分析PLI与心血管和呼吸系统参数的相关性。结果表明，在α（8-14 Hz）波段，三种呼吸模式下的脑网络特征参数存在显著差异。在自主呼吸模式下，整体效率和特征路径长度与相同步显著正相关，PLI指数与CRPST和呼吸深度广泛相关，而在控制呼吸模式下，脑网络参数和PLI指数与CRPST不相关，PLI主要与呼吸频率呈正相关。三种模式脑网络的差异主要是由心肺耦合的生理因素引起的。以上结果表明，基于心跳控制呼吸的增强心肺相同步对心肺系统有重要影响，可能为今后心肺功能的调节提供一些思路。

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引用次数: 0

Modelling the distribution of the oxygen-haemoglobin dissociation curve in vivo: An observational study 模拟体内氧-血红蛋白解离曲线的分布：一项观察性研究

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2025-04-01 Epub Date: 2025-02-03 DOI: 10.1016/j.resp.2025.104400

Colin J. Crooks , Joe West , Joanne R. Morling , Mark Simmonds , Irene Juurlink , Steve Briggs , Simon Cruickshank , Susan Hammond-Pears , Dominick Shaw , Timothy R. Card , Andrew W. Fogarty

Few studies have explored the variability of the oxygen-haemoglobin dissociation curve in vivo.

96,428 blood gas measurements were obtained (80,376 arterial, 6959 venous) from a cohort of 7656 patients who were admitted to a large UK teaching hospital between 1 February 2020 and 31 December 2021 for a Covid-19 related admission with a positive PCR. There was consistent variation of the distribution of the oxygen-haemoglobin curve across most oxygen saturation strata with typical values at 91–92 % saturation (mean 8.1kPa, standard deviation sd 0.6 kPa or 60.8 mmHg sd 4.5 mmHg), with the exception of the highest strata of oxygen saturation of 99–100 % (mean 17.7 kPa, sd 8.1kPa or 132 mmHg sd 60.8).

The higher oxygen partial pressures at higher oxygen saturations are a concern in view of the increased mortality observed in RCTs of higher oxygen saturation targets. However, the observational study design precludes any attribution of causality.

很少有研究探索体内氧-血红蛋白解离曲线的变异性。从2020年2月1日至2021年12月31日期间入住英国一家大型教学医院的7656名患者中获得了96,428项血气测量（80,376项动脉测量，6959项静脉测量），这些患者入院时与Covid-19相关，PCR阳性。氧-血红蛋白曲线分布在大多数氧饱和度地层中具有一致的变化，典型值为91-92 %饱和度（平均8.1kPa，标准差sd 0.6 kPa或60.8 mmHg sd 4.5 mmHg），但氧饱和度最高的地层为99-100 %（平均17.7 kPa，标准差8.1kPa或132 mmHg sd 60.8）。考虑到在高氧饱和度目标的随机对照试验中观察到的死亡率增加，高氧饱和度下的高氧分压是一个值得关注的问题。然而，观察性研究的设计排除了任何因果关系的归因。

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引用次数: 0

Respiratory plasticity induced by chronic hyperoxia in juvenile and adult rats 慢性高氧诱导幼年和成年大鼠的呼吸可塑性。

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2025-04-01 Epub Date: 2024-12-26 DOI: 10.1016/j.resp.2024.104386

Ryan W. Bavis , Matthew D. Danielson , Gemma Dufour , Julia Hanus , Ashley E. Pratt , Kristina E. Tobin

Chronic hyperoxia during early postnatal development depresses breathing when neonatal rats are returned to room air and causes long-lasting attenuation of the hypoxic ventilatory response (HVR). In contrast, little is known about the control of breathing of juvenile or adult mammals after chronic exposure to moderate hyperoxia later in life. Therefore, Sprague-Dawley rats were exposed to 60 % O₂ for 7 days (juveniles) or for 4 and 14 days (adults) and ventilation was measured by whole-body plethysmography immediately after the exposure or following a longer period of recovery in room air. Hyperoxia-treated juvenile rats appeared to hypoventilate when returned to room air (11–13 % lower ventilation and CO₂ convection requirement relative to age-matched controls), but chronic hyperoxia did not alter normoxic ventilation in adult rats. In contrast, pre-treatment with chronic hyperoxia augmented the HVR in both juvenile rats (+41 %) and adult rats (+28–50 %). The hypercapnic ventilatory response (7 % CO₂) also tended to be augmented in adult rats after 14 days of hyperoxia, but this effect was not significant after accounting for variation in metabolic rate (i.e, CO₂ convection requirement). These findings confirm that chronic hyperoxia elicits age-specific respiratory plasticity in rats. These age-dependent differences are not caused by a lack of plasticity in adult-exposed rats; rather, there are qualitative differences in the plasticity that is expressed after chronic hyperoxia in neonates, juveniles, and adults as well as differences in its persistence.

出生后早期发育期间的慢性高氧会抑制新生大鼠的呼吸，并导致低氧通气反应（HVR）的长期衰减。相比之下，对于幼年或成年哺乳动物在生命后期长期暴露于中度高氧环境后对呼吸的控制知之甚少。因此，Sprague-Dawley大鼠暴露于60% O2环境7天（幼鼠）或4天和14天（成年鼠），暴露后立即或在室内空气中恢复较长时间后通过全身容积描记仪测量通气量。高氧处理的幼年大鼠在返回室内空气时出现低通气（与年龄匹配的对照组相比，通气量和二氧化碳对流需求降低11-13%），但慢性高氧不会改变成年大鼠的正常通气量。相比之下，慢性高氧预处理使幼年大鼠（+41%）和成年大鼠（+28-50%）的HVR增加。高氧14天后，成年大鼠的高碳酸血症通气反应（7% CO2）也趋于增强，但考虑到代谢率（即CO2对流需求）的变化后，这种影响并不显著。这些发现证实了慢性高氧引起大鼠年龄特异性呼吸可塑性。这些年龄依赖性差异不是由于成年暴露的大鼠缺乏可塑性造成的；相反，在新生儿、幼崽和成虫中，慢性高氧后表达的可塑性存在质的差异，其持久性也存在差异。

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