eSpira FM System肺功能检测系统是用于检测与肺功能相关的全部生理数据的大型系统，可对麻醉动物进行一系列成组实验的数据自动分析检测，包括用力肺活量相关数据的测试。
· 广泛应用于COPD、肺间质疾病、肺纤维化等疾病临床前研究；
· 与人肺功能检测相类似，eSpira™系统提供与人类肺功能指标一致的各种生理指标参数；
· 该系统可用于小鼠、大鼠/豚鼠以及其他大型动物；
· 系统高度自动化并提供丰富的图标供分析研究使用；
主要检测参数：
· 用力呼气量Forced Expiratory Volume (FEV)
· 肺总量 Total Lung Capacity
· 用力肺活量Forced Vital Capacity
· 最大呼气流量Peak Expiratory Flow
· 最大呼气中段流量Maximum Mid Expiratory Flow
· 准静态压力容积曲线Quasistatic Pressure Volume Curves
· 功能残气量FRC
· 阻力/顺应性Resistance/Compliance
· Explanations and more parameters
型号：FM
产品主要特点：
· 适用于各种实验动物：小鼠、大鼠、豚鼠、犬、灵长类动物；
· 经典的肺量测定法（spirometry）检测肺功能；
· 综合的肺功能分析；
· COPD及肺间质疾病研究的必备工具；
· 在数分钟内测定FEV(x)、FEF(x)、FVC、FRC、FEVpef、MMEF等参数；
· 气道阻力和肺顺应性直接生理数据检测；
· 软件自动生成可直接打印的数据报告；
上图为利用eSpira™系统在慢性哮喘小鼠模型上获取的数据。小鼠通过卵清蛋白(OVA)激发致敏，对照组只注射明矾和缓冲液。在最后一次激发24小时后进行肺功能检测。 如图，FVC降低了49%，FEV50降低了46%。数据表明eSpira™系统用于小鼠哮喘模型，可以有效的检测肺功能的改变。
通过 ePacq（EMMS Post Acquisition）分析软件应用程序为数据审查和呈现提供了完整的解决方案。ePacq 使研究人员可以即时访问使用 EMMS eDacq 记录的数据，以表格和图形格式显示数据。
ePacq 显示分析的原始数据
ePacq 可用于将大型数据集压缩成更易于管理的东西。这种数据压缩的传统技术将涉及编写冗长的 Excel 表格。这种方法既费时又容易出错。ePacq 通过提供快速简便的实验数据总结消除了这些问题。
· 特定时间段内的个体受试者数据
· 治疗组统计，包括平均值、最大值、最小值、标准差、SEM
· 研究统计数据，所有治疗组的平均数据。
ePacq 显示分析的协议数据
如需无创方式检测小动物的肺功能参数，可选择：
全身体积描记系统（无创型肺功能测量系统）
如需检测小动物的气道阻力，可选择：
小动物气道阻力和肺顺应性检测系统
参考文献：
[1]. Yoon, S., et al., Comparative study of lung toxicity of E-cigarette ingredients to investigate E-cigarette or vaping product associated lung injury. Journal of Hazardous Materials, 2023. 445: p. 130454.
[2]. Wang, J., et al., Macrophage-derived GPNMB trapped by fibrotic extracellular matrix promotes pulmonary fibrosis. Communications Biology, 2023. 6(1): p. 136.
[3]. Han, L., et al., Tracking the response to Pseudomonas aeruginosa infection in ozone-induced chronic obstructive pulmonary disease mouse models. Biomedicine & Pharmacotherapy, 2022. 150: p. 112980.
[4]. Zhang, Y., et al., Adipose-derived mesenchymal stem cells suppress ozone-mediated airway inflammation in a mouse model of chronic obstructive pulmonary disease. Molecular Immunology, 2022. 151: p. 95-102.
[5]. Yu, J., et al., Astragaloside trigger autophagy: Implication a potential therapeutic strategy for pulmonary fibrosis. Biomedicine & Pharmacotherapy, 2022. 154: p. 113603.
[6]. Wang, M., et al., Blockade of phosphotyrosine pathways suggesting SH2 superbinder as a novel therapy for pulmonary fibrosis. Theranostics, 2022. 12(10): p. 4513.
[7]. Kim, H., et al., Comprehensive Targeted Metabolomic Study in the Lung, Plasma, and Urine of PPE/LPS-Induced COPD Mice Model. International Journal of Molecular Sciences, 2022. 23(5): p. 2748.
[8]. Chen, D., et al., Fine particulate matter and lung function among burning-exposed deepwater horizon oil spill workers. Environmental Health Perspectives, 2022. 130(2): p. 027001.
[9]. Li, Q., et al., Inhibition of ROCK ameliorates pulmonary fibrosis by suppressing M2 macrophage polarisation through phosphorylation of STAT3. Clinical and Translational Medicine, 2022. 12(10): p. e1036.
[10]. Seitz, A.M., et al., Forces at the Anterior Meniscus Attachments Strongly Increase Under Dynamic Knee Joint Loading. The American Journal of Sports Medicine, 2021. 49(4): p. 994-1004.
如需对大小鼠肺部进行定量给药，可以选择：大小鼠气管内定量给药装置
有两种型号可供选择：大鼠型气管内定量给药套装，小鼠型气管内定量给药套装
气管内定量给药装置的主要特色：
参考文献：
[1]. McGonigal, R., et al., Schwann cell nodal membrane disruption triggers bystander axonal degeneration in a Guillain-Barré syndrome mouse model. The Journal of clinical investigation, 2022. 132(14).
[2]. Aguilar, K., et al., Microglial response promotes neurodegeneration in the Ndufs4 KO mouse model of Leigh syndrome. Glia, 2022. 70(11): p. 2032-2044.
[3]. Li, J., et al., ActRIIB: ALK4-Fc alleviates muscle dysfunction and comorbidities in murine models of neuromuscular disorders. The Journal of Clinical Investigation, 2021. 131(4).
[4]. Saunders, S.P., et al., Dysregulated skin barrier function in Tmem79 mutant mice promotes IL‐17A‐dependent spontaneous skin and lung inflammation. Allergy, 2020. 75(12): p. 3216-3227.
[5]. Uchiyama, M., et al., O2-dependent protein internalization underlies astrocytic sensing of acute hypoxia by restricting multimodal TRPA1 channel responses. Current Biology, 2020. 30(17): p. 3378-3396. e7.
[6]. Bolea, I., et al., Defined neuronal populations drive fatal phenotype in a mouse model of Leigh syndrome. Elife, 2019. 8: p. e47163.
[7]. Kerscher, B., et al., BET bromodomain inhibitor iBET151 impedes human ILC2 activation and prevents experimental allergic lung inflammation. Frontiers in immunology, 2019. 10: p. 678.
[8]. Li, X., et al., Mesenchymal stem cells alleviate oxidative stress–induced mitochondrial dysfunction in the airways. Journal of Allergy and Clinical Immunology, 2018. 141(5): p. 1634-1645. e5.
[9]. Saunders, S.P., et al., Spontaneous atopic dermatitis is mediated by innate immunity, with the secondary lung inflammation of the atopic march requiring adaptive immunity. Journal of Allergy and Clinical Immunology, 2016. 137(2): p. 482-491.
[10]. McGonigal, R., et al., C1q-targeted inhibition of the classical complement pathway prevents injury in a novel mouse model of acute motor axonal neuropathy. Acta neuropathologica communications, 2016. 4(1): p. 1-16.
[11]. Wiegman, C.H., et al., Oxidative stress–induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease. Journal of Allergy and Clinical Immunology, 2015. 136(3): p. 769-780.
