Monday, June 11, 2018

To open or close the lungs – that is the question!

Although often necessary, mechanical ventilation of small animals during pulmonary measurements can lead to both acute and chronic damage to their lungs, also known as ventilator-induced lung injury (VILI). The injury happens as a result of the frequent opening and closing of alveolar air sacs. Nevertheless, the two most common, and greatly contrasting methods, to study respiratory diseases include open lung- and closed lung-approaches. This has led to many pulmonary researchers conducting experiments with the goal of determining which approach is the least harmful and the best possible way to minimize VILI.


Open-chest models are often used to study ARDS and acute myocardial ischemia and reperfusion. These models allow for investigating cardiac physiology, morphological changes of the lungs, as well as the evaluation of therapeutic interventions. This procedure allows for invasive lung function measurements and tissue harvesting for further experimentation, but must be performed under deep anesthesia. Since opening the chest causes the lungs to collapse, the animals must be mechanically ventilated throughout the process.

The flexiVent has often been used in open-chest experiments, as the system allows for ventilation of the subject with a user-defined positive end-expiratory pressure (PEEP), which can be set to prevent airway collapse. Further, it can facilitate the complete recruitment of the lungs, using the Deep Inflation perturbation, before measurements can be taken.


Recent experimental evidence suggests that high PEEP does not necessarily reduce lung injury but instead, may lead to the contrary. Higher PEEP results in overstretching the alveolar sacs and potential development of edema, among other cardiopulmonary impairment. Moreover, a recent article by Dr. Patricia Rocco and team1, points out that most publications comparing high PEEP with no PEEP, do so with a combination of low tidal volume and high tidal volume, respectively. Thus, there is no clear indication as to what exactly led to the observed outcomes – high PEEP or low tidal volume.

Dr. Rocco goes on to recommend “in order to minimize VILI, we should consider moving away from the classical concept of ‘open up the lungs and keep them open’ towards ‘close down the lungs and keep them closed’”. Fortunately, the flexiVent can be adapted to different experimental conditions, and can provide detailed pulmonary measurements even as research trends change.

1Pelosi, P. et al. 2018. Close down the lungs and keep them resting to minimize ventilator-induced lung injury. Critical Care 22 (1):72.

Monday, May 14, 2018

Must see posters at ATS!

ATS is just around the corner and we hope to see you in San Diego!

We are looking forward to learning more about respiratory research, especially these interesting flexiVent poster sessions:

During our annual breakfast event at ATS on Monday, May 21st, Dr. Otmar Schmid (Helmholtz Zentrum, Germany) will discuss his “off-label” use of the flexiVent for the delivery of inhaled compounds. By optimizing the ventilation profiles and nebulizer settings, Dr. Schmid and Dr. Annette Robichaud obtained significant improvements in aerosol deposition rates, as well as homogenous deposition profiles.

The technique developed by Dr.Schmid could be useful in studies for optimized inhaled drug delivery using the flexiVent. If you are interested, please feel free to join us by registering here.

We would love to learn more about your research and discuss some tailored solutions. Find us at Booth #1535 in Exhibit Hall D.

Exhibit Hours

Sunday, May 20       10:30 am – 3:30 pm
Monday, May 21      10:30 am – 3:30 pm
Tuesday, May 22      10:30 am – 3:30 pm

Monday, April 16, 2018

Cardiopulmonary Solutions by emka & SCIREQ

emka & SCIREQ offer a unique perspective into the preclinical study of heart and lung diseases, allowing for novel insights into cardiopulmonary diseases such as heart failure, arrhythmia, COPD, pulmonary hypertension and more.

Will you be attending the Experimental Biology meeting in San Diego next week? If so, visit booth #1624 to learn more about our range of cardiopulmonary solutions, including:

Model Development with the inExpose:
  • In vivo disease models that mimic complex pathophysiological mechanisms of cardiopulmonary diseases using the inExpose, an automated platform for reproducible inhalation exposure (1,2)
  • Smoke-induced alterations in cardiac and respiratory function through cigarette or e-cigarette exposure (3,4)
  • Effective drug intervention for both preclinical subjects and cell culture exposures through aerosols (5,6).
 Respiratory Mechanics Measurements with the flexiVent:
  • Studying the underlying pathophysiology of cardiopulmonary diseases by measuring the structure and function of the lung, along with quantifying the effects of pulmonary hypertension and decreased vascularization with the flexiVent (7,8,9).
  • Pressure-volume manoeuvres, forced expired volume and other endpoints of clinical translational value performed by the flexiVent (10,11).

High-throughput Screening Using Whole Body Plethysmography
  • Whole Body Plethysmography can be an easy tool for screening subjects quickly for preliminary respiratory data with the option of delivering inhaled therapeutics (12,13,14).
  • Easy integration with simultaneous cardio and neuro recordings: electroencephalogram (EEG), electrocardiogram (ECG) & electromyogram (EMG).

Wireless Biopotential Monitoring using Implantable Telemetry
  • Monitoring physiological data from conscious freely moving rodents and large animals using easyTEL implantable telemetry systems. Different models are available to meet your study needs and provide monitoring of ECG, EEG, blood pressure, breathing rate, temperature and acceleration from 3-axis accelerometer (activity).

Exhibit Hours - Booth 1624
Sunday, April 22nd 9:00am – 4pm
Monday, April 23rd 9:00am – 4pm
Tuesday, April 24th 9:00am – 4pm

Click here to set-up a meeting to learn more about our solutions for cardiopulmonary studies.


1) Weist, E.F., et al. (2017). Omega-3 Polyunsaturated Fatty Acids Protect Against Cigarette Smoke-Induced Oxidative Stress and vascular Dysfunction. Toxicological Sciences, 156(1): 300-310
2) Tewari et al. (2011). Identification of differentially expressed proteins in blood plasma of control and cigarette smoke-exposed mice by 2-D DIGE/MS. Proteomics, 11: 2051, 2011.
3) Olfert, M. et al. (2018). Chronic exposure to electronic cigarette results in impaired cardiovascular function in mice. J of Applied Physiology, 124(3): 573-582
4) Alasmari F, Crotty Alexander LE, Nelson JA, et al. (2017). Effects of Chronic Inhalation of Electronic Cigarettes Containing Nicotine on Glial Glutamate Transporters and α-7 Nicotinic Acetylcholine Receptor in Female CD-1 Mice. Vol 77. Elsevier Inc
5) Patolla et al. (2010). Formulation, characterization and pulmonary deposition of nebulized celecoxib encapsulated nanostructured lipid carriers. J Control Release. 144: 233-241
6) De Santis, et al. (2014). Pharmaceutical composition of oxidised avidin suitable for inhalation - De Santis. U.S. patent application 14/236,445
7) Alsaid, H., et al. (2011). Serial MRI characterization of the functional and morphological changes in mouse lung in response to cardiac remodeling following myocardial infarction. Magnetic Resonance in Medicine, 67(1): 191-200
8) Dayeh, N.R et al. (2017). Echocardiographic validation of pulmonary hypertension due to heart failure with reduced ejection fraction in mice. Scientific Reports, 1363
9) Karmouty-Quintana, H., et al. 2012. The A2B Adenosine Receptor Modulates Pulmonary Hypertension Associated With Interstitial Lung Disease. The FASEB Journal, 26(6): 2546-2557
10) Devos, F.C et al. (2017). Forced expiration measurements in mouse models of obstructive and restrictive lung diseases. Respiratory Research, 18(123)
11) Vanoirbeek, J. (2016). Forced Expiratory Volume (FEV) Measurements in Mouse Models of Lung Disease. American Journal of Respiratory and Critical Care Medicine, 193, A5957
12) Olea et al. (2011). Effects of cigarette smoke and chronic hypoxia on airways remodelling and resistance. Clinical Significance, 15; 179(2-3): 305-313
13) Ramnath et al. (2014). Extracellular matrix defects in aneurysmal fibulin-4 mice predispose to lung emphysema. PLOS One, 9(9): 106054
14) Zhuang, P., et al. (2016). cAMP-PKA-CaMKII signalling pathway is involved in aggravated cardiotoxicity during Fuzi and Beimu Combination Treatment of Experimental Pulmonary Hypertension. Scientific Reports, 6, 34903

Friday, April 13, 2018

Hypoxia studies using EMKA whole-body plethysmography

Oxygen deficiency or hypoxia can contribute to the development or exacerbation of many disorders including strokes or chronic lung diseases. The first defense against hypoxia is the hypoxic ventilatory response (HVR). These cardiorespiratory reflexes, like hyperventilation or sympathetic activation, increase gas exchange in the lungs and oxygen delivery to vital organs. Genetically modified mice help researchers identify the processes involved in a hypoxic response, however in order to properly study these responses, reliable methodologies are necessary to understand changes in breathing patterns. Whole-body plethysmography is one important technique for in vivo assessment. 

The most important chemoreceptor in mammals is the carotid body (CB), and this organ contains O2-sensing neuron-like glomus cells among others. Dr. Ortega-Sáenz’ group studied the hypoxic response in the CB by using whole-body plethysmography combined with gas mixing. They generated normoxic, hypoxic, or hypercapnic conditions to compare ventilatory responses. The Ndufs2 gene was deleted in a genetically modified mouse (TH-NDUFS2 mouse) which removed the responsiveness to hypoxia while leaving the response to hypercapnia. In their studies, the wild-type mouse responded to hypoxia and hypercapnia with an increase in breathing frequency, while the TH-NDUFS2 mouse only mediated its response in hypercapnic conditions. Although many respiratory variables can be recorded, this group chose breathing frequency as the most reliable and informative parameter and concluded that normal O2-sensing in CB glomus cells is necessary for a normal HVR. 

Plethysmography is a standard method for studying pulmonary function in conscious, spontaneously breathing laboratory subjects. The barometric plethysmography technique measures flow and pressure changes that occur while the subject is breathing, before and after exposure to a drug or other challenges. It is easily adapted to various subject sizes and species, and is often used for longitudinal studies where the subjects are studied for multiple hours on successive experiment days. 

To learn more about, visit our website at or contact [email protected].

Ortega-Sáenz, Patricia, et al. "Testing Acute Oxygen Sensing in Genetically Modified Mice: Plethysmography and Amperometry." Hypoxia. Humana Press, New York, NY, 2018. 139-153.

Phone 1.514.286.1429 | Toll Free 1.877.572.4737
Email [email protected]

Monday, April 2, 2018

FlexiVent – Used in Recent Pulmonary Fibrosis Research

Pulmonary fibrosis describes a condition in which the normal lung anatomy is replaced by a process of active remodeling, deposition of extracellular matrix and dramatic changes in the phenotype of both fibroblasts and alveolar epithelial cells. This condition can be idiopathic, as in idiopathic pulmonary fibrosis (IPF), or secondary to genetic disorders, autoimmune disorders or exposure to environmental toxins, chemical warfare, drugs, foreign antigens or radiation1.

Recent publication in Nature Medicine
A research group from Yale School of Medicine (Yu, Guoying, et al.)2 hypothesized that the Thyroid hormone (TH) would inhibit pulmonary fibrosis by improving mitochondrial function. Thyroid hormone (TH) is known for being critical to maintaining cellular homeostasis during stress responses. In this study, fibrotic murine models were developed by injecting their mice with bleomycin and then the flexiVent was used to evaluate in vivo respiratory mechanics to assess therapeutic efficacy of TH in their murine models. Results showed that TH has antifibrotic properties and may present a potential therapy for pulmonary fibrosis. These great findings were recently published in Nature Medicine.

flexiVent – used across many pulmonary applications 
Pulmonary fibrosis in humans is typically diagnosed using computed tomography (CT) scans and pulmonary function tests, both of which can be performed in small laboratory animals using the flexiVent. The system can synchronize with micro-CT scanners to reduce motion artifacts, and be used separately to provide static and dynamic measurements of respiratory mechanics, as well as to capture information on specific lung volumes or flows. All these features make the flexiVent a valuable and comprehensive tool to investigate pulmonary fibrosis at the preclinical level. 

To learn more about this system, please visit our website at

1Travis, W.D. et al. An official American Thoracic Society/European Respiratory Society statement: update of the international multidisciplinary classification of the idiopathic interstitial pneumonias. Am. J. Respir. Crit. Care Med. 188, 733–748 (2013).
2Yu, Guoying, et al. "Thyroid hormone inhibits lung fibrosis in mice by improving epithelial mitochondrial function." Nature medicine (2017).

Wednesday, March 28, 2018

Why should you and your team join us for the flexiVent User Group Meeting in San Diego on 26th April 2018:

         » This is a free User Group Meeting.
         » It is open to everyone interested in respiratory research with the flexiVent.
         » It is beneficial for current flexiVent users and newcomers to 
            SCIREQ’s research equipment.
         » It will refresh your knowledge of key aspects of flexiVent experimentation 
            and learn how others use the flexiVent.
         » You will have the chance to ask flexiVent experts your questions.
         » It is a networking opportunity for respiratory researchers.
         » You will connect with potential future collaborators.

Please complete your REGISTRATION HERE and be part of this event.

WHEN:          Thursday April 26, 2018
WHERE:       San Diego, California (Hilton San Diego Bayfront)

AGENDA: 9:00    Registration
        9:30    Welcome & Introduction
        9:45    Presentations:
                                   » SCIREQ flexiVent to Measure Respiratory Mechanics
                                   » Troubleshooting flexiVent Data
                                   » Aspects of Preclinical Lung Function Measurement
                                   » Product-Related Considerations
                                   » Full-Range PV curves and Lung Volumes
                                   » Current flexiVent User Presentations
        16:00  Closing Remarks

If you are interested in presenting your pulmonary research with the flexiVent during this user group, do not hesitate to contact us as soon as possible, to include your presentation in the agenda.

If you have any questions, do not hesitate to contact us at [email protected] or toll-free at 1-877-572-4737.

We look forward to seeing you in San Diego!

Your SCIREQ Team

Monday, March 19, 2018

A step in moving towards the low frequency range

In clinical medicine, spirometry continues to dominate as the pulmonary function test of choice. This is despite the issues which limit its utility, largely patient compliance and the limited inferences which can be made regarding the mechanical properties of the respiratory system. Alternatively, the forced oscillation technique (FOT), utilized by the flexiVent preclinically, is well-known for its rich description of the mechanical properties of the respiratory system. However, despite becoming the gold-standard in preclinical research, the approach has yet to make significant in-roads into the clinical domain, especially in the low frequency range (0-2 Hz) that gives access to the peripheral lung, the area most sensitive to pathological changes.

In ventilated patients FOT solutions do exist, however free-breathing patients present obstacles as accurate measurements of the respiratory system rely on precise measurements of pressure and flow. Potential solutions to this problem have been trialed, for instance training patients to perform voluntary apnea1 or by triggering an apneic event in infants using the Hering-Breuer reflex2.

A recent doctoral thesis by Dr. Hannes Maes, under the supervision of Prof. Gerd Vandersteen at Vrije Universiteit Brussel (Free University of Brussels), titled, Low Frequency Forced Oscillation Technique in Clinical Practice, proposes an innovative solution to overcome confounding breathing frequencies, as well as a comprehensive review of the field3.

Dr. Maes presents a novel fan-based setup specifically designed for FOT measurements between 0-5 Hz in free-breathing subjects1 Pressure signals (multi-sine wave) are superimposed on the patients normal tidal breathing by controlling two fans (one pushing and one pulling air). Compensatory signals are also applied to the fans to ensure a predefined power spectrum and to suppress the nonlinear influences of the equipment or the subject’s breathing, along with post-measurement modeling techniques.

Schematic of fan-based FOT measurement device for free-breathing subjects

Results from a clinical trial on 60 subjects, that included healthy individuals as well as asthmatic and COPD patients, are also presented and, in the end, Dr. Maes offers a new framework for the time-varying behavior of the respiratory system during spontaneous breathing.

We congratulate Dr. Maes on this achievement and very interesting approach. This elegant work contributes towards the advances required to ultimately enable routine provision of the low-frequency FOT in patient populations and for clinicians to benefit from its diagnostic capacity.

For more information on the work of Dr. Maes and access to the full manuscript, please click here.

1. Hantos, Z., Daróczy, B., Suki, B., Galgóczy, G. & Csendes, T. Forced oscillatory impedance of the respiratory system at low frequencies. J. Appl. Physiol. 60, 123–32 (1986).
2. Hall, G. L., Hantos, Z., Wildhaber, J. H. & Sly, P. D. Contribution of nasal pathways to low frequency respiratory impedance in infants. Thorax 57, 396–9 (2002).
3. Maes, H. Low Frequency Forced Oscillation Technique in Clinical Practice. (Vrije Universiteit Brussel, Belgium, 2017).