Special thanks to all volunteers who participated in the original study. The work of L. Eichhorn was supported through a scholarship of the Else-Kr&#246;ner-Fresenius Foundation. The authors would like to thank Springer, Part of Springer Science+Business Media, for copyright clearance (License Number 3894660871180) and the kind permission of reusing previously published data.

道德守则 在涉及人类受试者的研究进行的所有程序均符合1964年赫尔辛基宣言的道德标准和其后来的修正。这项研究的设计得到了德国波恩大学医院的伦理委员会。 注:请确保受试者处于良好的健康状态，不含任何抗高血压药物和至少24小时的免费如咖啡因或等于物质儿茶酚胺诱导剂。 1.被检者的制备<ol><li>清洁用70％酒精前额皮肤脱脂前NIRS电极定位在皮肤上。 </li><li>上方放置眉和矢状沟（轨迹额极2）的权额头上的近红外光谱电极来测量脑（=中心）组织氧合。 </li><li>评估信号的稳定性。该RSO 2 -信号应该是恒定的（7; 3％）为至少5分钟。 </li><li>用于测量与NIRS（近红外光谱组织 -电极）外围组织氧合，放置一个电极的股四头肌（或者在前臂）的中间的上方。不要将电极之上的静脉丛或动脉。 </li><li>将心电电极在头发上免费的胸部。心电图导联都标有不同的字母。在胸大肌上胸大肌左侧的上左下肋缘的medioclavicular线，"F"的第五肋间中间胸肋头，"C"的胸肋头大的权利，"L"地方"R"，" N"上右下肋缘。 </li><li>在同一肢体和侧面，其中NIRS 组织 -电极置于指尖末梢测量脉搏血氧饱和度（SPO 2）。 </li><li>测量无创血压（NIBP），通过使用血压袖带。用对侧肢体，使外周脉搏肟待测量etry。为了得到高时间分辨率血压效果，请选择用于测量一分钟的间隔。通过触摸屏幕，然后选择"设置"选择无创血压。 </li><li>呼吸暂停前至少20分钟，建立的静脉内行成的过程中和呼吸暂停后绘制在各个时间点的血液样本的右侧或左侧臂内侧肘静脉。 <ol><li>清洁用70％酒精皮肤。 </li><li>使用止血带，以帮助更加突出的静脉。 </li><li>使用皮肤消毒，避免感染和经皮肤进针。 </li><li>减少在导管毂血液回闪后的插入角度。推导管插入静脉。 </li><li>取出针和冲洗导管用无菌生理盐水（氯化钠0.9％）。 </li></ol></li></ol> 2，数据收集<ol><li>校准所有监视器的内部时钟，以同步供以后处理的测量。 <ol><li>氯ICK在桌面上右下角的时钟图标，然后在弹出的窗口中点击"更改日期和时间设置"。 </li><li>按下NIRS设置菜单按钮设计，并通过菜单更改日期和时间。 </li></ol></li><li>要存储离线分析生理数据，将显示器设备插入扩展坞，并通过网线连接到计算机。确保对接站的IP地址和子网掩码是正确的网络设置，以获得一个连接。为了得到这个信息，请联系设备供应商。 </li><li>使用监控设备特定的软件保存在电脑上的测量。点击"开始"，开始记录和测量结束后，将结果保存。 注:在某些设备，数据必须在测量过程中实时保存。 注意: 对于故障的排除采取以下步骤的保养要点:如果NIRS 组织 SIG的变异NALS太高，重新评估电极（避免直接在电极更大的静脉丛或动脉）的位置。近红外光谱脑信号的高变异性，也可以为潜水员的过度减少部分CO 2的间接标记。指示受呼吸慢，低潮量和重新评估的信号。受试者被允许最终窒息之前采取3很深的启示。避免包括这个时期到基线值的评估。最大吸气后的第30秒被变量值表征。不要用它们进行分析。 </li></ol> 3.呼吸暂停<ol><li>有受试者在卧位，以免血液循环，由于血管收缩应力引起的变化休息至少15分钟。有科目呼吸正常，以避免过度的影响，造成血管收缩。限制呼吸频率≤15次/ min。 </li><li>抽血样本S代表基线分析。丢弃前5毫升血液抽取，避免测量不确定度。每个静脉采血用无菌生理盐水，以防止凝血后冲洗导管。 </li><li>确保监测值是不可见的主题，以避免视觉影响他们的呼吸暂停的表现。 </li><li>检查每个设备功能和信号质量。确保电极不能通过在呼吸暂停的端测试受试者的不自主运动中除去。 </li><li>有明确的协议的结论。给最后2分钟的倒计时口头。受试者应该在这个准备时间正常呼吸。到最后一口气3深灵感此前是允许的。让拍摄对象表示通过手指标志的最后吸入。呼吸暂停应尽可能长地进行。 注:最后一口气的结束表明呼吸暂停的开始。呼吸暂停的端部被定义为呼吸暂停后的第一启示。 </li><li>马克重要的事件（ 即，开始了次呼吸暂停结束）以电子方式按"事件标记按钮"的NIRS设备上避免更多的时间分析不准确。 注:胸部和腹部非自愿隔膜活动引起的变动都在呼吸暂停下半年共同并注明斗争阶段。 </li><li>在不同的时间点取决于研究的目的绘制血样。 </li><li>离心血液样品在1500×g离心10分钟。取上清，并将其存储在-80℃下以供将来分析。 </li></ol> 4.处理数据<ol><li>从监控设备处理数据: <ol><li>打开电脑，然后按上保存的文件"启动"来分析数据。 </li><li>点击"审核"来获得访问趋势监测和在菜单中选择子网掩码"选项"，然后选择"工具"。时间间隔可以通过"走势区间"如果有必要进行修改。 </li><li>选择面具"趋势"和SAV即打开文件"趋势"，在做进一步处理电子表格程序。 </li></ol></li><li>从近红外光谱设备处理数据: <ol><li>在电脑上打开软件，并通过 WIFI连接NIRS设备。 </li><li>从近红外光谱设备的数据传送到计算机。 </li><li>保存为CSV格式的数据。 </li><li>在进一步的处理电子表格程序打开文件。 </li></ol></li></ol> 5.分析值<ol><li>创建两个数据集的电子表格来比较值。识别至少30秒其中，NIRS值和血氧饱和度是不变的（±3％）的时间间隔。取这些值的平均值来定义基线水平。 注:心率是众所周知的显着变化之前，呼吸暂停。为了进行进一步的分析，基线心脏速率在时间点30秒的呼吸暂停开始后所定义。 </li><li>找到单调减少的开始点在RSO 2和血氧饱和度</sub&gt;通过寻找相比基线水平值&gt; 2％的减少呼吸暂停期间。这个时间点被定义为"开始去饱和"。 </li><li>识别在呼吸暂停的端部作为呼吸暂停终止后的值单调增加的RSO 2和血氧饱和度增加的起点。这点被定义为"开始重新饱和的"。 </li><li>计算"呼吸暂停启动"和"开始饱和度"和"呼吸暂停结束"和"开始重新饱和"为NIRS 脑 ，NIRS 组织 血氧饱和度之间的时间差之间的时间差。保存在单独的电子表格以秒为单位的每个差异。 </li><li> 可选:计算在第二和呼吸暂停的最后一分钟的每一个参与者的心脏心率变异。这可能会在此压力阶段揭示交感神经/副交感神经的平衡信息。 </li></ol> 6.统计处理<ol><li>比较血氧饱和度的，NIRS 脑和NIRS 组织价值观"饱和的开始"之间的时间差。试验的测量差高斯分布（ 例如，使用夏皮罗-威尔克常态试验样品50大小小）。 </li><li>如果测量差的分布是正态分布显著不同，使用Wilcoxon符号秩检验。如果可以假设正态分布，可以考虑使用配对t检验。 </li></ol>

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<li>Eichhorn, L., Erdfelder, F., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/pubmed?term=((Influence+of+Apnea-induced+Hypoxia+on+Catecholamine+Release+and+Cardiovascular+Dynamics%5BTitle%5D)+AND+%22Int+J+Sports+Med%22%5BJournal%5D)">Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics.</a> Int J Sports Med. , (2016).</li>
</ol>

The authors have nothing to disclose.

总呼吸暂停时间主要是由肺尺寸和每分钟的氧气消耗，并通过一个个人承受造成增加的pCO 2或减小PO 2的呼吸反射能力的影响。呼吸暂停潜水员培训，以最大限度地发挥他们的屏气时间，用于在最大吸气这样做。因此，时间直到缺氧是个体之间可检测的不同，并取决于受试者的身体状况和训练状态，甚至可能通过他们的日常状态和意愿而改变承受呼吸反射。可以通过协议步骤的详细...

临床相关的急性缺氧和高碳酸血症伴大多见于阻塞性睡眠呼吸暂停综合征（OSAS），急性呼吸道阻塞或心肺复苏过程中。在OSAS等低氧条件的领域主要局限包括有关动物研究的病理生理学和人体模型是不存在1有限转让知识。模仿人体缺氧，缺氧的气体混合物迄今已使用2 - 7。然而，这些条件都比较有代表性的高海拔环境比，其中缺氧，在一般情况下，伴随的高碳酸血症的临床情况的。为了监测心脏骤停和复苏过程中的组织氧合，动物研究已经完成8探讨生理代偿机制。 窒息潜水员能够压低呼吸冲动运动员健康是受低动脉血氧饱和度9和增加的pCO 2 10,11诱发。我们以模仿急性缺氧和高碳酸血症相伴12临床情况调查呼吸暂停潜水员。该模型可用于评价临床设置，提高患者的OSAS或病理呼吸病症的病理生理学的了解，并揭示了新的可能性在呼吸暂停的情况下，研究的潜在计数器平衡机制。此外，不同的技术来检测缺氧人类可以在动态缺氧的情况下，可行性和准确性被测试存在于紧急情况下（ 即 ，气道阻塞，喉或无法插管，可以不透风的情况），或者以模拟在患者间歇性缺氧OSAS患者。 非侵入性的技术来检测缺氧在人中是有限的。外围脉搏血氧饱和度（SPO 2）预好客的认可工具TAL和医院设置，检测缺氧13。该方法是基于血红蛋白的光吸收。然而， 血氧饱和度测量被限制为外周动脉氧合并且不能在无脉性电活动（PEA）或集中最小循环14的情况下使用。与此相反，近红外光谱法可用于在实时的PEA中出血性休克或蛛网膜下腔出血15中，以评估脑组织氧饱和度（RSO 2）， - 19。它的使用在不断增加20和方法论研究显示血氧饱和度和RSO 2 3,4之间的正相关关系。 在这项研究中，我们提供了一个模型来模拟人类的临床相关缺氧并给出了一个一步一步的方法来比较外围脉搏血氧饱和度和NIRS在德和再饱和的情况下。通过在的情况下进行分析生理数据pnea，我们的反平衡机制的认识得以提高。

<table><tbody><tr><td>SpO&lt;sub&gt;2&lt;/sub&gt;</td><td>Dr&amp;auml;ger Medical AG&amp;amp;CO.KG</td><td>SHP ACC MCABLE-Masimo Set</td><td>peripheral SpO&lt;sub&gt;2&lt;/sub&gt;-Monitoring</td></tr><tr><td>Non Invasive Blood Pressure (NIBP)</td><td>Dr&amp;auml;ger Medical AG&amp;amp;CO.KG</td><td>NIBP cuff M+,&amp;nbsp; MP00916&amp;nbsp;</td><td></td></tr><tr><td>Electrocardiographic (ECG) &amp;nbsp;</td><td>Dr&amp;auml;ger Medical AG&amp;amp;CO.KG</td><td>Infinity M540 Monitor</td><td>ECG monitoring</td></tr><tr><td>Docking station</td><td>Dr&amp;auml;ger Medical AG&amp;amp;CO.KG</td><td>M500 Docking Station</td><td>connection of M540 to laptop</td></tr><tr><td>NIRS</td><td>NONIN Medical&amp;rsquo;s EQUANOX</td><td>Model 7600 Regional Oximeter System</td><td>measuring of cerebral and&amp;nbsp; tissue oxygenation</td></tr><tr><td>NIRS diodes</td><td>EQUANOX Advance Sensor</td><td>Model 8004CA</td><td>suited for measuring cerebral and somatic oxygen-saturation</td></tr><tr><td>&lt;strong&gt;Laptop&amp;nbsp;&lt;/strong&gt;</td><td></td><td></td><td></td></tr><tr><td>DataGrabber</td><td>Dr&amp;auml;ger Medical AG&amp;amp;CO.KG</td><td>DataGrabber v2005.10.16</td><td>software to synchronize M540 with laptop</td></tr><tr><td>eVision</td><td>Nonin Medical. Inc.</td><td>Version 1.3.0.0</td><td>software to synchronize NONIN with laptop</td></tr></tbody></table>

a model to simulate clinically relevant hypoxia in humans

In case of apnea, arterial partial pressure of oxygen (pO2) decreases, while partial pressure of carbon dioxide (pCO2) increases. To avoid damage to hypoxia sensitive organs such as the brain, compensatory circulatory mechanisms help to maintain an adequate oxygen supply. This is mainly achieved by increased cerebral blood flow. Intermittent hypoxia is a commonly seen phenomenon in patients with obstructive sleep apnea. Acute airway obstruction can also result in hypoxia and hypercapnia. Until now, no adequate model has been established to simulate these dynamics in humans. Previous investigations focusing on human hypoxia used inhaled hypoxic gas mixtures. However, the resulting hypoxia was combined with hyperventilation and is therefore more representative of high altitude environments than of apnea. Furthermore, the transferability of previously performed animal experiments to humans is limited and the pathophysiological background of apnea induced physiological changes is poorly understood. In this study, healthy human apneic divers were utilized to mimic clinically relevant hypoxia and hypercapnia during apnea. Additionally, pulse-oximetry and Near Infrared Spectroscopy (NIRS) were used to evaluate changes in cerebral and peripheral oxygen saturation before, during, and after apnea.

图1显示血氧饱和度和NIRS值（NIRS 脑和NIRS 组织 ）的同步录音暂停期间，一个病人。总的呼吸暂停时间为363秒。继呼吸暂停NIRS和血氧饱和度值约140秒保持稳定。通过外围血氧饱和度，而238秒后，被检出脑近红外光谱的减少204秒后，检测血氧饱和度的下降。最小测量血氧饱和度以下呼吸暂停为58?...

Watch this Scientific Journal Video about A Model to Simulate Clinically Relevant Hypoxia in Humans at JoVE.com

A Model to Simulate Clinically Relevant Hypoxia in Humans

在人类缺氧模拟通常也被因吸入低氧气体混合物进行。在这项研究中，呼吸暂停潜水员被用来模拟人类动态缺氧。另外，在去饱和和再饱和动力学的生理变化与非侵入性工具，例如近红外光谱法（NIRS）和外围氧合饱和度（ 血氧饱和度）来评价。

一个模型来模拟人类临床相关性缺氧

In case of apnea, arterial partial pressure of oxygen (pO2) decreases, while partial pressure of carbon dioxide (pCO2) increases. To avoid damage to ...

a-model-to-simulate-clinically-relevant-hypoxia-in-humans

Research

JoVE Journal

Medicine

8.8K 次观看.  University Hospital of Bonn. 在人类缺氧模拟通常也被因吸入低氧气体混合物进行。在这项研究中，呼吸暂停潜水员被用来模拟人类动态缺氧。另外，在去饱和和再饱和动力学的生理变化与非侵入性工具，例如近红外光谱法（NIRS）和外围氧合饱和度（ 血氧饱和度）来评价。 

视频: A Model to Simulate Clinically Relevant Hypoxia in Humans

In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis

Hypoxia has been implicated in the metastasis of Ewing sarcoma (ES) by clinical observations and in vitro data, yet direct evidence for its pro-metastatic effect is lacking and the exact mechanisms of its action are unclear. Here, we report an animal model that allows for direct testing of the effects of tumor hypoxia on ES dissemination and investigation into the underlying pathways involved. This approach combines two well-established experimental strategies, orthotopic xenografting of ES cells and femoral artery ligation (FAL), which induces hindlimb ischemia. Human ES cells were injected into the gastrocnemius muscles of SCID/beige mice and the primary tumors were allowed to grow to a size of 250 mm3. At this stage either the tumors were excised (control group) or the animals were subjected to FAL to create tumor hypoxia, followed by tumor excision 3 days later. The efficiency of FAL was confirmed by a significant increase in binding of hypoxyprobe-1 in the tumor tissue, severe tumor necrosis and complete inhibition of primary tumor growth. Importantly, despite these direct effects of ischemia, an enhanced dissemination of tumor cells from the hypoxic tumors was observed. This experimental strategy enables comparative analysis of the metastatic properties of primary tumors of the same size, yet significantly different levels of hypoxia. It also provides a new platform to further assess the mechanistic basis for the hypoxia-induced alterations that occur during metastatic tumor progression in vivo. In addition, while this model was established using ES cells, we anticipate that this experimental strategy can be used to test the effect of hypoxia in other sarcomas, as well as tumors orthotopically implanted in sites with a well-defined blood supply route.

In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis

This manuscript describes the development of an animal model that allows for the direct testing of the effects of tumor hypoxia on metastasis and the deciphering the mechanisms of its action. Although the experiments described here focus on Ewing sarcoma, a similar approach can be applied to other tumor types.

体内模型对缺氧对肿瘤转移的影响测试

Hypoxia has been implicated in the metastasis of Ewing sarcoma (ES) by clinical observations and in vitro data, yet direct evidence for its pro-metastatic ...

科研

癌症研究

Delivery of In Vivo Acute Intermittent Hypoxia in Neonatal Rodents to Prime Subventricular Zone-derived Neural Progenitor Cell Cultures

Extended culture of neural stem/progenitor cells facilitates in vitro analyses to understand their biology while enabling expansion of cell populations to adequate numbers prior to transplantation. Identifying approaches to refine this process, to augment the production of all CNS cell types (i.e., neurons), and to possibly contribute to therapeutic cell therapy protocols is a high research priority. This report describes an easily applied in vivo &#8220;pre-conditioning&#8221; stimulus which can be delivered to awake, non-anesthetized animals. Thus, it is a non-invasive and non-stressful procedure. Specifically described are the procedures for exposing mouse or rat pups (aged postnatal day 1-8) to a brief (40-80 min) period of intermittent hypoxia (AIH). The procedures included in this video protocol include calibration of the whole-body plethysmography chamber in which pups are placed during AIH and the technical details of AIH exposure. The efficacy of this approach to elicit tissue-level changes in the awake animal is demonstrated through the enhancement of subsequent in vitro expansion and neuronal differentiation in cells harvested from the subventricular zone (SVZ). These results support the notion that tissue level changes across multiple systems could be observed following AIH, and support the continued optimization and establishment of AIH as a priming or conditioning modality for therapeutic cell populations.

Delivery of In Vivo Acute Intermittent Hypoxia in Neonatal Rodents to Prime Subventricular Zone-derived Neural Progenitor Cell Cultures

This article describes the methodology for administering short periods of intermittent hypoxia to postnatal day 1-8 mouse or rat pups. This approach effectively elicits a robust tissue level &#8220;priming effect&#8221; on cultured neural progenitor cells that are harvested within 30 min of hypoxia exposure.

交付<em&gt;在体内</em&gt;急性间歇性缺氧新生儿鼠害总理下区源性神经祖细胞培养

Extended culture of neural stem/progenitor cells facilitates in vitro analyses to understand their biology while enabling expansion of cell populations to ...

发育生物学

A Swine Model of Neonatal Asphyxia

Annually more than 1 million neonates die worldwide as related to asphyxia. Asphyxiated neonates commonly have multi-organ failure including hypotension, perfusion deficit, hypoxic-ischemic encephalopathy, pulmonary hypertension, vasculopathic enterocolitis, renal failure and thrombo-embolic complications. Animal models are developed to help us understand the patho-physiology and pharmacology of neonatal asphyxia. In comparison to rodents and newborn lambs, the newborn piglet has been proven to be a valuable model. The newborn piglet has several advantages including similar development as that of 36-38 weeks human fetus with comparable body systems, large body size (&tilde;1.5-2 kg at birth) that allows the instrumentation and monitoring of the animal and controls the confounding variables of hypoxia and hemodynamic derangements.
We here describe an experimental protocol to simulate neonatal asphyxia and allow us to examine the systemic and regional hemodynamic changes during the asphyxiating and reoxygenation process as well as the respective effects of interventions. Further, the model has the advantage of studying multi-organ failure or dysfunction simultaneously and the interaction with various body systems. The experimental model is a non-survival procedure that involves the surgical instrumentation of newborn piglets (1-3 day-old and 1.5-2.5 kg weight, mixed breed) to allow the establishment of mechanical ventilation, vascular (arterial and central venous) access and the placement of catheters and flow probes (Transonic Inc.) for the continuously monitoring of intra-vascular pressure and blood flow across different arteries including main pulmonary, common carotid, superior mesenteric and left renal arteries. Using these surgically instrumented piglets, after stabilization for 30-60 minutes as defined by Z&lt;10% variation in hemodynamic parameters and normal blood gases, we commence an experimental protocol of severe hypoxemia which is induced via normocapnic alveolar hypoxia. The piglet is ventilated with 10-15% oxygen by increasing the inhaled concentration of nitrogen gas for 2h, aiming for arterial oxygen saturations of 30-40%. This degree of hypoxemia will produce clinical asphyxia with severe metabolic acidosis, systemic hypotension and cardiogenic shock with hypoperfusion to vital organs. The hypoxia is followed by reoxygenation with 100% oxygen for 0.5h and then 21% oxygen for 3.5h. Pharmacologic interventions can be introduced in due course and their effects investigated in a blinded, block-randomized fashion.

Large animal models have good translational values in the examination of physiology and pharmacology of neonatal asphyxia. Using newborn piglets, we develop an experimental protocol to simulate neonatal asphyxia which has advantages of studying the systemic and regional hemodynamics, oxygen transport with biochemical and pathologic pathways and correlations.

新生儿窒息了猪模型

Annually more than 1 million neonates die worldwide as related to asphyxia. Asphyxiated neonates commonly have multi-organ failure including hypotension, ...

医学

Detection of Microregional Hypoxia in Mouse Cerebral Cortex by Two-photon Imaging of Endogenous NADH Fluorescence

The brain's ability to function at high levels of metabolic demand depends on continuous oxygen supply through blood flow and tissue oxygen diffusion. Here we present a visualized experimental and methodological protocol to directly visualize microregional tissue hypoxia and to infer perivascular oxygen gradients in the mouse cortex. It is based on the non-linear relationship between nicotinamide adenine dinucleotide (NADH) endogenous fluorescence intensity and oxygen partial pressure in the tissue, where observed tissue NADH fluorescence abruptly increases at tissue oxygen levels below 10 mmHg1. We use two-photon excitation at 740 nm which allows for concurrent excitation of intrinsic NADH tissue fluorescence and blood plasma contrasted with Texas-Red dextran. The advantages of this method over existing approaches include the following: it takes advantage of an intrinsic tissue signal and can be performed using standard two-photon in vivo imaging equipment; it permits continuous monitoring in the whole field of view with a depth resolution of ~50 &mu;m. We demonstrate that brain tissue areas furthest from cerebral blood vessels correspond to vulnerable watershed areas which are the first to become functionally hypoxic following a decline in vascular oxygen supply. This method allows one to image microregional cortical oxygenation and is therefore useful for examining the role of inadequate or restricted tissue oxygen supply in neurovascular diseases and stroke.

Here we describe a method to directly visualize microregional tissue hypoxia in the mouse cortex in vivo. It is based on concurrent two-photon imaging of nicotinamide adenine dinucleotide (NADH) and the cortical microcirculation. This method is useful for high resolution analysis of tissue oxygen supply.

检测内源NADH的荧光双光子成像的小鼠大脑皮层Microregional缺氧

The brain's ability to function at high levels of metabolic demand depends on continuous oxygen supply through blood flow and tissue oxygen diffusion. ...

神经科学

Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice

Exercise training is an important strategy for maintaining health and preventing many chronic diseases. It is the first line of treatment recommended by international guidelines for patients suffering from cardiovascular diseases, more specifically, lower extremity artery diseases, where the patients' walking capacity is considerably altered, affecting their quality of life. 
Traditionally, both low continuous exercise and interval training have been used. Recently, supramaximal training has also been shown to improve athletes' performances via vascular adaptations, amongst other mechanisms. The combination of this type of training with hypoxia could bring an additional and/or synergic effect, which could be of interest for certain pathologies. Here, we describe how to perform supramaximal intensity training sessions in hypoxia on healthy mice at 150% of their maximal speed, using a motorized treadmill and a hypoxic box. We also show how to dissect the mouse in order to retrieve organs of interest, particularly the pulmonary artery, the abdominal aorta, and the iliac artery. Finally, we show how to perform ex vivo vascular function assessment on the retrieved vessels, using isometric tension studies.

High-intensity training in hypoxia is a protocol that has been proven to induce vascular adaptations potentially beneficial in some patients and to improve athletes&#39; repeated sprint ability. Here, we test the feasibility of training mice using that protocol and identify those vascular adaptations using ex vivo vascular function assessment.

小鼠低血压运动的下位强度及血管功能评估

Exercise training is an important strategy for maintaining health and preventing many chronic diseases. It is the first line of treatment recommended by ...

行为学

Induction and Testing of Hypoxia in Cell Culture

Hypoxia is defined as the reduction or lack of oxygen in organs, tissues, or cells. This decrease of oxygen tension can be due to a reduced supply in oxygen (causes include insufficient blood vessel network, defective blood vessel, and anemia) or to an increased consumption of oxygen relative to the supply (caused by a sudden higher cell proliferation rate). Hypoxia can be physiologic or pathologic such as in solid cancers 1-3, rheumatoid arthritis, atherosclerosis etc&#x2026; Each tissues and cells have a different ability to adapt to this new condition. During hypoxia, hypoxia inducible factor alpha (HIF) is stabilized and regulates various genes such as those involved in angiogenesis or transport of oxygen 4. The stabilization of this protein is a hallmark of hypoxia, therefore detecting HIF is routinely used to screen for hypoxia 5-7. 
In this article, we propose two simple methods to induce hypoxia in mammalian cell cultures and simple tests to evaluate the hypoxic status of these cells.

Here we propose simple methods to induce hypoxia in cell cultures and simple tests to evaluate the hypoxic status of the cultures.

在细胞培养中缺氧诱导和测试

Hypoxia is defined as the reduction or lack of oxygen in organs, tissues, or cells.  This decrease of oxygen tension can be due to a reduced supply in ...

生物学

Translational 3D-Cell Culture Model to Assess Hyperoxia Effects on Human Neonatal Airway Epithelial Cells

The preterm neonatal airway epithelium is constantly exposed to environmental stressors. One of these stressors in neonates with lung disease includes oxygen (O2) tension higher than the ambient atmosphere - termed hyperoxia (&gt;21% O2). The effect of hyperoxia on the airway depends on various factors, including the developmental stage of the airway, the degree of hyperoxia, and the duration of exposure, with variable exposures potentially leading to unique phenotypes. While there has been extensive research on the effect of hyperoxia on neonatal lung alveolarization and airway hyperreactivity, little is known about the short and long-term underlying effect of hyperoxia on human neonatal airway epithelial cells. A major reason for this is the scarcity of an effective in vitro model to study human neonatal airway epithelial development and function. Here, we describe a method for isolating and expanding human neonatal tracheal airway epithelial cells (nTAECs) utilizing human neonatal tracheal aspirates and culturing these cells in air-liquid interface (ALI) culture. We demonstrate that nTAECs form a mature polarized cell-monolayer in ALI culture and undergo mucociliary differentiation. We also present a method for moderate hyperoxia exposure of the cell monolayer in ALI culture using a specialized incubator. Additionally, we describe an assay to measure cellular oxidative stress following hyperoxia exposure in ALI culture using fluorescent quantification, which confirms that moderate hyperoxia exposure induces cellular oxidative stress but does not cause significant cell membrane damage or apoptosis. This model can potentially be used to simulate clinically relevant hyperoxia exposure encountered by neonatal airways in the Neonatal Intensive Care Unit (NICU) and used to study the short and long-lasting effects of O2 on neonatal airway epithelial programming. Studies using this model could be utilized to explore ways to mitigate early-life oxidative injury to developing airways, which is implicated in the development of long-term airway diseases in former premature infants.

We describe a protocol to establish an air-liquid interface (ALI) culture model utilizing neonatal tracheal airway epithelial cells (nTAEC) and perform physiologically relevant hyperoxia exposure to study the effect of atmospheric-induced oxidative stress on cells derived from the developing neonatal airway surface epithelium.

评估高氧对人新生儿气道上皮细胞影响的转化 3D 细胞培养模型

The preterm neonatal airway epithelium is constantly exposed to environmental stressors. One of these stressors in neonates with lung disease includes ...

Induction and Characterization of Pulmonary Hypertension in Mice using the Hypoxia/SU5416 Model

Pulmonary Hypertension (PH) is a pathophysiological condition, defined by a mean pulmonary arterial pressure exceeding 25 mm Hg at rest, as assessed by right heart&#160;catheterization. A broad spectrum of diseases can lead to PH, differing in their etiology, histopathology, clinical presentation, prognosis, and response to&#160;treatment. Despite significant progress in the last years, PH remains an uncured disease. Understanding the underlying mechanisms can pave the way for the development of new therapies. Animal models are important research tools to achieve this goal. Currently, there are several models available for recapitulating PH. This protocol describes a two-hit mouse PH model. The stimuli for PH development are hypoxia and the injection of SU5416, a vascular endothelial growth factor (VEGF) receptor antagonist. Three weeks after initiation of Hypoxia/SU5416, animals develop pulmonary vascular remodeling imitating the histopathological changes observed in human PH (predominantly Group 1). Vascular remodeling in the pulmonary circulation results in the remodeling of the right&#160;ventricle (RV). The procedures for measuring RV pressures (using the open chest method), the morphometrical analyses of the RV (by dissecting and weighing both cardiac ventricles) and the histological assessments of the remodeling (both pulmonary by assessing vascular remodeling and cardiac by assessing RV cardiomyocyte hypertrophy and fibrosis) are described in detail. The advantages of this protocol are the possibility of the application both in wild type and in genetically modified mice, the relatively easy and low-cost implementation, and the quick development of the disease of interest (3 weeks). Limitations of this method are that mice do not develop a severe phenotype and PH is reversible upon return to normoxia. Prevention, as well as therapy studies, can easily be implemented in this model, without the necessity of advanced skills (as opposed to surgical rodent models).

This protocol describes the induction of pulmonary hypertension (PH) in mice based on the exposure to hypoxia and the injection of a VEGF receptor antagonist. The animals develop PH and right ventricular (RV) hypertrophy 3 weeks after the initiation of the protocol. The functional and morphometrical characterization of the model is also presented.

使用缺氧/SU5416模型对小鼠的肺高血压进行诱导和特征

Pulmonary Hypertension (PH) is a pathophysiological condition, defined by a mean pulmonary arterial pressure exceeding 25 mm Hg at rest, as assessed by ...

Multiple Intravenous Bolus Dosing and Invasive Hemodynamic Assessment in a Hypoxia-Induced Mouse Pulmonary Artery Hypertension Model

Pulmonary arterial hypertension (PAH) is a progressive life-threatening disease, primarily affecting small pulmonary arterioles of the lung. Currently, there is no cure for PAH. It is important to discover new compounds that can be used to treat PAH. The mouse hypoxia-induced PAH model is a widely used model for PAH research. This model recapitulates human clinical manifestations of PAH Group 3 disease and is an important research tool to evaluate the effectiveness of new experimental therapies for PAH. Research using this model often requires the administration of compounds in mice. For a compound that needs to be given directly into the bloodstream, optimizing intravenous (IV) administration is a key part of the experimental procedures. Ideally, the IV injection system should permit multiple injections over a set time course. Although the mouse hypoxia-induced PAH model is very popular in many laboratories, it is technically challenging to perform multiple IV bolus dosing and invasive hemodynamic assessment in this model. In this protocol, we present step-by-step instructions on how to carry out multiple IV bolus dosing via mouse jugular vein and perform arterial and right ventricle catheterization for hemodynamic assessment in mouse hypoxia-induced PAH model.

This protocol provides a step-by-step procedure for executing multiple intravenous bolus dose administration and invasive hemodynamic monitoring in mice. Investigators can use this protocol for future therapeutic compound screening for pulmonary artery hypertension.

缺氧诱导小鼠肺动脉高压模型中的多次静脉推注给药和侵入性血流动力学评估

Pulmonary arterial hypertension (PAH) is a progressive life-threatening disease, primarily affecting small pulmonary arterioles of the lung. Currently, ...

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

An adipocyte-produced hormone leptin is a potent respiratory stimulant, which may play an important role in defending respiratory function in obesity. The carotid bodies (CB), a key organ of peripheral hypoxic sensitivity, express the long functional isoform of leptin receptor (LepRb) but the role of leptin signaling in control of breathing has not been fully elucidated. We examined the hypoxic ventilatory response (HVR) (1) in C57BL/6J mice before and after leptin infusion at baseline and after CB denervation; (2) in LepRb-deficient obese db/db mice at baseline and after LepRb overexpression in CBs. In C57BL/6J mice, leptin increased HVR and effects of leptin on HVR were abolished by CB denervation. In db/db mice, LepRb expression in CB augmented the HVR. Therefore, we conclude that leptin acts in CB to augment responses to hypoxia.

Our study focuses on the effects of leptin signaling in carotid body (CB) on the hypoxic ventilatory response (HVR). We performed &#39;loss of function&#39; experiments measuring the effect of leptin on HVR after CB denervation and &#39;gain of function&#39; experiments measuring HVR after overexpression of the leptin receptor in CB.

检查胡萝卜体瘦素信号的实验方法及其对呼吸控制的影响

An adipocyte-produced hormone leptin is a potent respiratory stimulant, which may play an important role in defending respiratory function in obesity. The ...