Respiratory Physiology & Neurobiology最新文献

Diethelm Richter (1943-2025); a life in Respiratory Neurobiology. Diethelm Richter (1943-2025)；呼吸神经生物学的生活。

IF 1.6 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2026-02-21 DOI: 10.1016/j.resp.2026.104560

K Michael Spyer, Julian F R Paton

引用次数: 0

Passive Cigarette Smoke Induces Reversible Tracheal Hyperreactivity via Oxidative Stress and M₃ Receptor Desensitization in Rats. 被动香烟烟雾通过氧化应激和M₃受体脱敏诱导可逆性气管高反应性。

IF 1.6 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2026-02-17 DOI: 10.1016/j.resp.2026.104559

S A Salami, M O Allen, S O Muritala, B O Olabinjo, B A Murtala

Passive (second-hand) exposure to cigarette smoke contributes to airway dysfunction through oxidative stress, inflammation, and smooth muscle remodelling. This study investigated the effects of chronic passive cigarette smoke exposure on tracheal smooth muscle (TSM) contractility and oxidative stress biomarkers in adult male Wistar rats. Fifteen adult male Wistar rats were assigned to control, cigarette-exposed, or recovery groups. Rats underwent passive cigarette smoke exposure for 3 weeks, with the recovery group allowed an additional 3-week smoke-free period. The recovery group underwent the same exposure followed by a 3-week smoke-free period. Tracheal tissues were excised, mounted in an organ bath, and exposed to cumulative concentrations of phenylephrine, acetylcholine, potassium chloride, and calcium chloride. Contractile responses were also evaluated after pre-incubation with pharmacological modulators like atropine, salbutamol, nicorandil, acetovanillone, and L-NAME. Oxidative stress parameters, including malondialdehyde, superoxide dismutase (SOD), catalase, and glutathione, were quantified using spectrophotometric methods. Cigarette exposure significantly increased TSM contractile responses to phenylephrine, potassium chloride, and calcium chloride (p<0.05). However, acetylcholine-induced contraction was attenuated. Pre-incubation with acetovanillone restored acetylcholine responsiveness. Malondialdehyde levels were elevated, while SOD, catalase, and glutathione levels were significantly reduced in the cigarette group (p<0.05). Recovery reversed these oxidative changes and improved contractile responses. Three weeks of passive cigarette smoke exposure induced oxidative stress, enhanced tracheal smooth muscle contraction to phenylephrine, KCl, and CaCl₂, and reduced acetylcholine responsiveness. Recovery and acetovanillone treatment restored antioxidant activity, implicating oxidative stress-driven mechanisms in smoke-induced airway dysfunction.

被动（二手）暴露于香烟烟雾会通过氧化应激、炎症和平滑肌重塑导致气道功能障碍。本研究探讨了慢性被动香烟烟雾暴露对成年雄性Wistar大鼠气管平滑肌（TSM）收缩力和氧化应激生物标志物的影响。15只成年雄性Wistar大鼠被分为控制组、吸烟组和恢复组。大鼠接受被动香烟烟雾暴露3周，恢复组允许另外3周无烟期。恢复组接受同样的暴露，然后是3周的无烟期。切除气管组织，置于器官浴中，暴露于累积浓度的苯肾上腺素、乙酰胆碱、氯化钾和氯化钙中。在用阿托品、沙丁胺醇、尼可地尔、乙酰香草酮和L-NAME等药理学调节剂进行预培养后，还评估了收缩反应。氧化应激参数，包括丙二醛、超氧化物歧化酶（SOD）、过氧化氢酶和谷胱甘肽，用分光光度法定量。卷烟暴露显著增加了TSM对苯肾上腺素、氯化钾和氯化钙的收缩反应

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引用次数: 0

Deep inspirations prior to oscillometry for detecting lung alterations in a mouse model of asthma: Yea or nay? 在哮喘小鼠模型中，振荡法检测肺部变化前的深度启发：是还是不是？

IF 1.6 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2026-02-13 DOI: 10.1016/j.resp.2026.104551

Andrés Rojas-Ruiz, Jules Hugo Fournier, Cyndi Henry, Ynuk Bossé

Deep inspirations are avoided prior to oscillometry in humans because they transiently improve respiratory mechanics and thereby mask abnormalities in patients with lung diseases. In mice, oscillometry is measured under anesthesia and deep inspirations are contrastingly recommended since they optimize mechanical ventilation and reduce intersubject variability by recruiting closed airways. However, while modeling asthma, a lung disorder burdened by airway closure, deep inspirations may be counterproductive and mitigate differences between mice with and without experimental asthma. Herein, the effect of deep inspirations on respiratory mechanics was quantified in mice with and without experimental asthma. Male BALB/c and C57BL/6 mice were exposed once-daily to either saline or house-dust mite for 10 consecutive days. The day after the last exposure, respiratory mechanics were measured by oscillometry before and after two deep inspirations. In addition to decrease intersubject variability, deep inspirations improved respiratory mechanics in both mouse strains to a magnitude related to the initial level of impairment. Whether deep inspirations mask the detection of alterations caused by experimental asthma depended on the mouse strain. In fact, this question became irrelevant in BALB/c mice when it was discovered that all oscillometric readouts are unchanged by experimental asthma in this mouse strain. In C57BL/6 mice though, the worsening of respiratory mechanics caused by experimental asthma was largely abolished by deep inspirations. Deep inspirations are thus recommended in BALB/c mice since they reduce intersubject variability. However, their utility in C57BL/6 mice is debatable, since the reduced variability may be outweighed by a decreased effect size.

在人类进行振荡测量之前，应避免深吸气，因为深吸气可以短暂地改善呼吸力学，从而掩盖肺部疾病患者的异常。在小鼠中，振荡测量法是在麻醉下测量的，而深吸气则相反地被推荐，因为深吸气可以优化机械通气，并通过招募封闭气道减少受试者间的变异性。然而，在模拟哮喘（一种由气道关闭引起的肺部疾病）时，深度吸气可能适得其反，并减轻了患有和未患有实验性哮喘的小鼠之间的差异。在此，我们量化了深吸气对实验性哮喘和非实验性哮喘小鼠呼吸力学的影响。雄性BALB/c和C57BL/6小鼠每天1次暴露于生理盐水或屋尘螨，连续10天。最后一次暴露的第二天，用振荡法测量两次深吸气前后的呼吸力学。除了减少受试者间的可变性外，深吸气还将两种小鼠的呼吸力学改善到与初始损伤水平相关的程度。深吸气是否掩盖了由实验性哮喘引起的变化的检测取决于小鼠品系。事实上，这个问题在BALB/c小鼠中变得无关紧要，因为发现所有的振荡读数在实验哮喘小鼠中都没有改变。而在C57BL/6小鼠中，深吸气可基本消除实验性哮喘引起的呼吸力学恶化。因此，建议在BALB/c小鼠中进行深度启发，因为它们减少了受试者间的可变性。然而，它们在C57BL/6小鼠中的效用是有争议的，因为减少的变异性可能被减少的效应大小所抵消。

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引用次数: 0

Hypoxia-inducible factor mediates tissue-specific mitochondrial responses to acute hypoxia in mice but not in rats 缺氧诱导因子介导小鼠对急性缺氧的组织特异性线粒体反应，但在大鼠中没有。

IF 1.6 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2026-02-06 DOI: 10.1016/j.resp.2026.104549

Maud Demarest, Vincent Joseph

Oxygen availability is a key determinant of cellular homeostasis, and the mitochondrial response to hypoxia is essential for maintaining energy balance and limiting oxidative stress. The hypoxia-inducible factor (HIF) orchestrates transcriptional programs that adjust mitochondrial function by reducing respiration and electron transport to limit reactive oxygen species (ROS) production. We previously reported that mice exhibit greater tolerance to hypoxia than rats, showing HIF-1 stabilization associated with decrease metabolic response under acute hypoxia, and a mitochondrial shift from complex I– to complex II–supported respiration in the brain at high altitude. Here, we investigated the role of HIF in regulating mitochondrial oxygen consumption rates (OCR) in the cerebral cortex and liver of mice and rats exposed to acute hypoxia (10 % O₂, 6 h). To determine whether these effects were HIF-dependent, a group of animals were also treated with deferoxamine (a HIF stabilizer) under normoxia or with 2-methoxyestradiol (a HIF inhibitor) under hypoxia. We demonstrated that acute hypoxia significantly decreases OCR in the liver of mice, an effect that was partially reproduced by HIF stabilization and partly prevented by HIF inhibition, indicating a HIF-dependent mitochondrial response. In contrast, OCR remained unchanged in the cerebral cortex of mice and in both tissues of rats, indicating species- and tissue-specific regulation. These findings reveal that HIF activation under acute hypoxia selectively modulates liver mitochondrial function in mice but not in rats, supporting the view that interspecific differences in HIF-mediated metabolic regulation contribute to the superior hypoxic tolerance of mice.

氧气可用性是细胞稳态的关键决定因素，线粒体对缺氧的反应对于维持能量平衡和限制氧化应激至关重要。缺氧诱导因子（HIF）协调转录程序，通过减少呼吸和电子传递来调节线粒体功能，以限制活性氧（ROS）的产生。我们之前报道过，小鼠比大鼠表现出更强的缺氧耐受性，显示HIF-1稳定与急性缺氧下代谢反应降低有关，并且在高海拔地区大脑中线粒体从复合体I向复合体ii支持的呼吸转变。在这里，我们研究了HIF在急性缺氧（10% O₂，6h）小鼠和大鼠大脑皮层和肝脏线粒体耗氧量（OCR）调节中的作用。为了确定这些影响是否依赖于HIF，一组动物也在缺氧条件下接受去铁胺（一种HIF稳定剂）或2-甲氧基雌二醇（一种HIF抑制剂）治疗。我们证明，急性缺氧显著降低小鼠肝脏的OCR，这一效应部分由HIF稳定再现，部分由HIF抑制阻止，表明HIF依赖性线粒体反应。相比之下，OCR在小鼠的大脑皮层和大鼠的两个组织中保持不变，表明物种和组织特异性调节。这些发现表明，急性缺氧条件下HIF激活选择性地调节小鼠肝脏线粒体功能，但在大鼠中没有，支持了HIF介导的代谢调节的种间差异有助于小鼠卓越的缺氧耐受性的观点。

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引用次数: 0

Invasive cardiopulmonary exercise testing: Physiologic assessment of unexplained dyspnea and exercise intolerance 有创心肺运动试验：不明原因呼吸困难和运动不耐受的生理评估。

IF 1.6 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2026-02-02 DOI: 10.1016/j.resp.2026.104550

Emily A. Harris, Aaron B. Waxman

Unexplained dyspnea and exertional intolerance are common, burdensome clinical problems that may persist despite routine resting cardiopulmonary testing. Invasive cardiopulmonary exercise testing (iCPET) integrates breath-by-breath gas exchange with invasive hemodynamic and blood gas assessment during incremental exercise, enabling evaluation of physiologic abnormalities that may be unapparent at rest. This review summarizes practical considerations for iCPET performance (including upright cycle ergometry, catheter-based pressure measurements, direct Fick cardiac output, and symptom assessment using separate visual analog Modified Borg ratings for dyspnea and leg fatigue at peak exercise), and presents a structured approach to interpretation using pressure–flow relationships and age-related reference ranges. Emphasis is placed on how characteristic iCPET patterns inform mechanistic contributors to exertional dyspnea by identifying upstream physiologic triggers—such as abnormal rises in pulmonary arterial wedge pressure (exercise-HFpEF), abnormal pulmonary vascular pressure–flow responses (exercise-PAH), impaired preload augmentation associated with autonomic dysfunction, and impaired peripheral oxygen extraction consistent with mitochondrial myopathy. The review also highlights evolving applications in post-pulmonary embolism syndromes and acknowledges that exercise hemodynamic thresholds and protocols vary across centers, underscoring the need for broader standardization.

原因不明的呼吸困难和运动不耐受是常见的，尽管常规静息心肺测试，但可能持续存在的繁重临床问题。有创心肺运动试验（iCPET）将渐进式运动期间的呼吸气体交换与有创血流动力学和血气评估结合起来，能够评估休息时可能不明显的生理异常。本综述总结了iCPET性能的实际考虑因素（包括直立周期几何测量，导管压力测量，直接菲克心输出量，以及使用单独的视觉模拟修正博格评分来评估呼吸困难和运动高峰时的腿部疲劳），并提出了一种使用压力-流量关系和年龄相关参考范围进行解释的结构化方法。重点是通过识别上游生理触发因素，如肺动脉wedge压异常升高（运动- hfpef），肺血管压力-血流反应异常（运动- pah），与自主神经功能障碍相关的预负荷增强受损，以及与线粒体肌病一致的外周氧提取受损，iCPET特征模式如何告知运动性呼吸困难的机制因素。该综述还强调了在肺栓塞后综合征中的不断发展的应用，并承认运动血流动力学阈值和方案因中心而异，强调需要更广泛的标准化。

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引用次数: 0

Quantitative morphometric analysis of asthmatic mouse lungs using micro-CT: A preclinical imaging study 应用显微ct对哮喘小鼠肺的定量形态学分析：临床前影像学研究。

IF 1.6 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2026-01-29 DOI: 10.1016/j.resp.2026.104548

Hoang Bao Lam Nguyen , Juwan Kim , Ngan-Khanh Chau , Gyuri Kim , Hyunseop Kim , Kum Ju Chae , Sujeong Kim , Kyungrim Yi , Sori Kim , Ji-Seung Yoo , Sanghun Choi

Asthma is a heterogeneous disease comprising eosinophilic (EOS) and neutrophilic (NEU) phenotypes with distinct airway and parenchymal alterations. Using murine models, this study explored phenotype-specific structural and densitometric changes that are difficult to capture in human cohorts. Sixteen female C57BL/6NCrlOri mice were assigned to negative control (n = 5), EOS (n = 6), or NEU (n = 5) asthma groups. High-resolution micro-computed tomography (micro-CT) was used to quantify airway and parenchymal alterations. Morphometric parameters included bifurcation angle (

θ

), circularity (Cr), hydraulic diameter (D_h), wall thickness (WT), and luminal volume (LV). Voxel-wise parenchymal analysis, based on CT Hounsfield unit (HU) thresholds, classified regions as emphysema-like lung, ground-glass opacity (GGO), semi-consolidation, consolidation, and fibrosis. Compared with controls, asthmatic groups showed distinct but partially overlapping structural patterns. EOS demonstrated predominant alterations in distal airways and main bronchi, with increased Cr and D_h, accompanied by higher GGO and semi-consolidation. NEU caused widespread proximal airway dilation, reflected by greater LV, but showed minimal parenchymal changes. Tracheal Cr, D_h, and LV, correlated positively with GGO and semi-consolidation, suggesting a potential association between airway enlargement and parenchymal alterations. Besides, bronchoalveolar lavage (BAL) flow cytometry confirmed distinct inflammatory endotypes, with eosinophil enrichment in EOS mice and increased neutrophils and monocytes in NEU mice. Consistently, lung histopathology showed greater peribronchial inflammation and collagen-associated airway remodeling in NEU mice, whereas EOS mice exhibited moderate inflammatory infiltration with localized matrix deposition. Overall, quantitative micro-CT differentiates EOS and NEU asthma phenotypes by capturing airway and parenchymal features, supporting non-invasive preclinical phenotyping and phenotype-targeted therapy development.

哮喘是一种异质性疾病，包括嗜酸性粒细胞（EOS）和嗜中性粒细胞（NEU）表型，具有明显的气道和实质改变。使用小鼠模型，本研究探索了在人类队列中难以捕获的表型特异性结构和密度变化。16只雌性C57BL/6NCrlOri小鼠被分为阴性对照组（n=5）、EOS组（n=6）和NEU组（n=5）。高分辨率显微计算机断层扫描（micro-CT）用于量化气道和实质改变。形态学参数包括分岔角（θ）、圆度（Cr）、水力直径（Dh）、壁厚（WT）和管腔容积（LV）。基于CT Hounsfield单位（HU）阈值的体素级实质分析，将区域分为肺气肿样肺、磨玻璃样不透明（GGO）、半实变、实变和纤维化。与对照组相比，哮喘组表现出不同但部分重叠的结构模式。EOS主要表现为远端气道和主支气管的改变，Cr和Dh升高，伴有高GGO和半实变。NEU引起广泛的近端气道扩张，反映为更大的左室，但显示最小的实质改变。气管Cr、Dh和LV与GGO和半实变呈正相关，提示气道增大与实质改变之间存在潜在关联。此外，支气管肺泡灌洗（BAL）流式细胞术证实了不同的炎症内型，EOS小鼠中嗜酸性粒细胞富集，NEU小鼠中中性粒细胞和单核细胞增加。一致地，NEU小鼠的肺组织病理学显示更大的支气管周围炎症和胶原相关的气道重塑，而EOS小鼠表现为中度炎症浸润和局部基质沉积。总体而言，定量微ct通过捕捉气道和实质特征来区分EOS和NEU哮喘表型，支持非侵入性临床前表型和表型靶向治疗的发展。

{"title":"Quantitative morphometric analysis of asthmatic mouse lungs using micro-CT: A preclinical imaging study","authors":"Hoang Bao Lam Nguyen , Juwan Kim , Ngan-Khanh Chau , Gyuri Kim , Hyunseop Kim , Kum Ju Chae , Sujeong Kim , Kyungrim Yi , Sori Kim , Ji-Seung Yoo , Sanghun Choi","doi":"10.1016/j.resp.2026.104548","DOIUrl":"10.1016/j.resp.2026.104548","url":null,"abstract":"<div><div>Asthma is a heterogeneous disease comprising eosinophilic (EOS) and neutrophilic (NEU) phenotypes with distinct airway and parenchymal alterations. Using murine models, this study explored phenotype-specific structural and densitometric changes that are difficult to capture in human cohorts. Sixteen female C57BL/6NCrlOri mice were assigned to negative control (n = 5), EOS (n = 6), or NEU (n = 5) asthma groups. High-resolution micro-computed tomography (micro-CT) was used to quantify airway and parenchymal alterations. Morphometric parameters included bifurcation angle (<span><math><mi>θ</mi></math></span>), circularity (Cr), hydraulic diameter (D<sub>h</sub>), wall thickness (WT), and luminal volume (LV). Voxel-wise parenchymal analysis, based on CT Hounsfield unit (HU) thresholds, classified regions as emphysema-like lung, ground-glass opacity (GGO), semi-consolidation, consolidation, and fibrosis. Compared with controls, asthmatic groups showed distinct but partially overlapping structural patterns. EOS demonstrated predominant alterations in distal airways and main bronchi, with increased Cr and D<sub>h</sub>, accompanied by higher GGO and semi-consolidation. NEU caused widespread proximal airway dilation, reflected by greater LV, but showed minimal parenchymal changes. Tracheal Cr, D<sub>h</sub>, and LV, correlated positively with GGO and semi-consolidation, suggesting a potential association between airway enlargement and parenchymal alterations. Besides, bronchoalveolar lavage (BAL) flow cytometry confirmed distinct inflammatory endotypes, with eosinophil enrichment in EOS mice and increased neutrophils and monocytes in NEU mice. Consistently, lung histopathology showed greater peribronchial inflammation and collagen-associated airway remodeling in NEU mice, whereas EOS mice exhibited moderate inflammatory infiltration with localized matrix deposition. Overall, quantitative micro-CT differentiates EOS and NEU asthma phenotypes by capturing airway and parenchymal features, supporting non-invasive preclinical phenotyping and phenotype-targeted therapy development.</div></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":"341 ","pages":"Article 104548"},"PeriodicalIF":1.6,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146093898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Strain-specific metabolomic and inflammatory profiles in guinea pigs after LPS-induced inflammation: Comparative analysis of Dunkin-Hartley and Trik strains 豚鼠lps诱导炎症后的菌株特异性代谢组学和炎症谱：Dunkin-Hartley和Trik菌株的比较分析。

IF 1.6 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2026-01-28 DOI: 10.1016/j.resp.2026.104547

Juliana Hanusrichterova , Eva Baranovicova , Romana Barosova , Maros Kolomaznik , Pavol Mikolka , Petra Kosutova , Daniela Mokra , Juraj Mokry , Andrea Calkovska

Acute inflammation is a complex biological response triggered by various invading agents provoking distinct immune pathways. As inter-strain variability in guinea pigs can influence inflammatory responses, ultimately affecting disease progression, understanding these strain-specific differences can improve the reliability and translational relevance of guinea pig models for studying acute inflammation. In this study, two guinea pig strains, Trik coloured and Dunkin-Hartley albino, were subjected to bacterial endotoxin lipopolysaccharide (LPS) to induce acute systemic inflammation. Specific metabolite alterations in the blood plasma and bronchoalveolar lavage fluid (BALF) were identified using hydrogen-1 nuclear magnetic resonance (¹H NMR) spectroscopy. Distinct differences in the metabolomic profiles in the blood plasma indicated significant inter-strain variability in circulating metabolites during LPS-induced acute inflammation, including those involved in amino acid transamination, ammonia transfer, and immune responses. Metabolomic analysis of BALF from guinea pigs with LPS-induced inflammation revealed decreased levels of specific metabolites. Moreover, changes in blood and BALF white blood cell counts and body weight were evaluated after LPS exposure. In BALF, LPS caused a slight, non-significant increase in total cell count and a significant neutrophil increase in the Dunkin-Hartley strain. In blood, Trik strain showed a significant increase in total count of cells and a significant neutrophil decrease. LPS induced weight loss in both strains, more pronounced in Trik. The study points out strain-specific metabolomic changes in guinea pig LPS model, highlighting the importance of strain selection in inflammation research. While descriptive, these preliminary findings provide a basis for future work to explore inflammatory mechanisms of LPS and improve translation to human disease.

急性炎症是一种复杂的生物反应，由各种入侵因子引发不同的免疫途径。由于豚鼠的菌株间变异会影响炎症反应，最终影响疾病进展，了解这些菌株特异性差异可以提高豚鼠模型在研究急性炎症中的可靠性和翻译相关性。本研究采用细菌内毒素脂多糖（LPS）诱导豚鼠Trik - coloro和Dunkin-Hartley albino两株豚鼠急性全身性炎症。采用氢-1核磁共振（¹H NMR）谱法鉴定血浆和支气管肺泡灌洗液（BALF）中特异性代谢物的变化。血浆代谢组学谱的明显差异表明，在lps诱导的急性炎症期间，循环代谢物在品系间存在显著差异，包括那些涉及氨基酸转氨化、氨转移和免疫反应的代谢物。lps诱导炎症豚鼠的BALF代谢组学分析显示，特定代谢物水平下降。此外，还评估了LPS暴露后血液和半胱氨酸白细胞计数以及体重的变化。在BALF中，LPS引起Dunkin-Hartley菌株的总细胞计数轻微但不显著增加，中性粒细胞显著增加。在血液中，Trik菌株的细胞总数明显增加，中性粒细胞明显减少。LPS诱导两种菌株的体重减轻，在Trik中更为明显。该研究指出了豚鼠LPS模型中菌株特异性代谢组学的变化，突出了菌株选择在炎症研究中的重要性。虽然是描述性的，但这些初步发现为未来探索LPS的炎症机制和改善转化为人类疾病的工作提供了基础。

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引用次数: 0

Ventilatory limitation to exercise in patients with HFpEF and obesity: No room to breathe HFpEF和肥胖患者运动时的呼吸限制：没有呼吸空间

IF 1.6 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2026-01-27 DOI: 10.1016/j.resp.2026.104546

Tony G. Babb , Bryce N. Balmain , Andrew R. Tomlinson , Linda S. Hynan , Benjamin D. Levine , James P. MacNamara , Satyam Sarma

Background

Lowering pulmonary capillary wedge pressure (PCWP) by sublingual nitroglycerin (NTG) fails to increase exercise capacity in patients with heart failure with preserved ejection fraction (HFpEF). These findings beg the question as to the origin of exercise limitation. Our objective was to determine whether exercise tolerance could be ventilatory limited in older patients with HFpEF and obesity.

Methods

Patients with HFpEF and obesity (n = 42) underwent pulmonary artery and radial artery catheterizations. Cardiorespiratory responses, breathing mechanics, and arterial blood gases were measured at rest, 20 W, and at peak exercise before and after NTG.

Results

At rest, there was a drop in cardiac output and PaO₂ (p < 0.01) with subsequent increases in HR, a-

\bar{v}

O₂ difference, and A-aO₂ difference (p < 0.001) after NTG. At 20 W, there were increases in HR, a-

\bar{v}

O₂ difference, V̇_E/V̇CO₂, lactate, PaO₂, and A-aO₂ difference (p < 0.05). At peak exercise, there was an increase in V̇_E/V̇CO₂ and pH (p < 0.01), and a decrease in PaCO₂ (p < 0.001). However, before and after treatment, there was a qualitative decline in V̇_E/V̇CO₂ from 20 W to peak exercise suggesting these patients could not increase V̇_E further. There were no differences in breathing mechanics at rest, 20 W, or peak exercise after NTG.

Conclusions

We conclude that mechanical ventilatory constraints coupled with increased ventilatory inefficiency impose a ventilatory limitation to exercise in patients with HFpEF and obesity.

Clinical Trial Information

Clinical Trials number: NCT04068844

背景：舌下硝酸甘油（NTG）降低肺毛细血管楔压（PCWP）并不能增加具有保留射血分数（HFpEF）的心力衰竭患者的运动能力。这些发现引出了运动限制的起源问题。我们的目的是确定老年HFpEF和肥胖患者的运动耐量是否会受到通气限制。方法HFpEF合并肥胖患者（n = 42）行肺动脉和桡动脉插管。在静息、20 W和NTG前后的运动高峰时测量心肺反应、呼吸力学和动脉血气。结果静息时，NTG后心输出量和PaO2下降（p <； 0.01），HR、a-v¯O2差、a- ao2差升高（p < 0.001）。在20 W时，HR、a-v¯O2差异、V (E) /V （CO2）、乳酸、PaO2和A-aO2差异均增加（p < 0.05）。运动高峰时，V / E/V / CO2和pH升高（p < 0.01）， PaCO2降低（p < 0.001）。然而，在治疗前后，患者的V (E) /V （CO2）从20 W到运动峰值有质的下降，这表明这些患者不能进一步增加V (E)。在休息、20 W或NTG后的高峰运动时呼吸力学没有差异。我们得出结论，机械通气限制加上通气效率低下的增加对HFpEF和肥胖患者的运动施加了通气限制。临床试验信息临床试验编号：NCT04068844

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引用次数: 0

Tongue blade neuromuscular junction defects in old F344 rats 老龄F344大鼠舌叶神经肌肉连接缺损的研究。

IF 1.6 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2026-01-19 DOI: 10.1016/j.resp.2026.104545

John F. Kemp , Gary C. Sieck , Matthew J. Fogarty

Tongue-muscle associated behaviours (swallow, speech) are impaired in the elderly. In the Fischer 344 (F344) rat model of aging, hypoglossal motor neurons (MNs) and intrinsic tongue muscle weakness and atrophy are evident. Here we evaluated young (6-months) and old (24-months-old) F344 rat longitudinal muscles for neuromuscular junction (NMJ) innervation. In 140 µm free floating sections, presynaptic components were labelled with synaptophysin and neurofilament. Postsynaptic acetylcholine receptors were labelled with α-Bungarotoxin. NMJs were imaged using confocal microscopy with presynaptic invasion of the postsynaptic endplate quantified. We found marked denervation of female and male tongue NMJs in old age. Our findings are consistent with the significant role that tongue dysfunction has in aged tongue muscle dysfunction and hypoglossal MN death.

舌肌相关行为（吞咽、说话）在老年人中受损。在Fischer 344 （F344）衰老大鼠模型中，舌下运动神经元（MNs）和固有舌肌无力萎缩明显。在这里，我们评估了幼龄（6个月）和老年（24个月）F344大鼠纵向肌肉的神经肌肉接点（NMJ）神经支配。在140µm自由浮动切片上，用突触素和神经丝标记突触前成分。突触后乙酰胆碱受体用α-班加罗毒素标记。使用共聚焦显微镜对神经突触进行成像，并定量突触前终板的侵袭。我们发现老年女性和男性的舌头NMJs都有明显的去神经支配。我们的发现与舌功能障碍在老年舌肌功能障碍和舌下MN死亡中的重要作用是一致的。

引用次数: 0

Neurophysiologic tongue protrusion characteristics$ in obstructive sleep apnea: A comparative study 阻塞性睡眠呼吸暂停患者舌突神经生理特征的比较研究。

IF 1.6 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology

Pub Date : 2026-01-13 DOI: 10.1016/j.resp.2026.104544

Ron Oliven , Arie Oliven , Mostafa Somri , Emilia Hardak , Naveh Tov

The essential role of upper airway muscles in maintaining patency has led to the hypothesis that alterations in tongue muscle properties may contribute to the development of obstructive sleep apnea (OSA). Prior studies comparing the mechanical characteristics of tongue muscles in OSA patients and healthy controls have yielded inconsistent results. In this study, we evaluated tongue muscle mechanics using an objective, non-volitional method: surface electrical stimulation of the genioglossus (GG) muscle. Tongue protrusion force, whether generated volitionally or by electrical stimulation, was significantly lower in OSA patients. Stimulated force was consistently lower than volitional force across all participants; however, the two measures were strongly correlated (r = 0.62, p < 0.001). Tongue muscle fatigability in OSA patients did not differ significantly from controls during volitional testing or low-frequency stimulation but was increased during high-frequency stimulation. Twitch contraction and half-relaxation times, as well as high-to-low frequency force curves, were comparable between OSA and control subjects. These findings indicate that although tongue muscle fiber composition appears similar in OSA and control groups, maximal tongue protrusion force is reduced in OSA. Given the inconsistent results of prior studies, we suggest that the methodology of force assessment may be critical: different testing modes likely recruit distinct patterns of tongue muscle coordination and may uncover coordination deficits in OSA. Furthermore, the increased fatigability observed during high-frequency stimulation is consistent with the presence of tongue muscle neuropathy in this population.

上气道肌肉在维持气道通畅方面的重要作用使得舌肌特性的改变可能导致阻塞性睡眠呼吸暂停（OSA）的发生。先前的研究比较了OSA患者和健康对照者舌肌的力学特性，结果并不一致。在这项研究中，我们评估舌肌力学使用客观的，非意志的方法：颏舌肌（GG）的表面电刺激。在OSA患者中，无论是自愿还是电刺激产生的舌突力都明显降低。在所有参与者中，受刺激的力量始终低于意志力量；然而，这两种测量结果是强相关的（r = 0.62, p < 0.001）。在意志测试或低频刺激时，OSA患者的舌肌疲劳与对照组无显著差异，但在高频刺激时，舌肌疲劳有所增加。抽搐收缩和半松弛时间以及高低频力曲线在OSA和对照组之间具有可比性。这些发现表明，尽管OSA组和对照组的舌肌纤维组成相似，但OSA组的最大舌突力有所降低。鉴于之前的研究结果不一致，我们认为力评估的方法可能是至关重要的：不同的测试模式可能会招募不同的舌肌协调模式，并可能发现OSA的协调缺陷。此外，在高频刺激期间观察到的疲劳增加与该人群中舌肌神经病变的存在是一致的。

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