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).