Publications by authors named "Nicolle J Domnik"

16 Publications

  • Page 1 of 1

Compensatory responses to increased mechanical abnormalities in COPD during sleep.

Eur J Appl Physiol 2022 Jan 16. Epub 2022 Jan 16.

Department of Medicine, Queen's University, Kingston, Canada.

Purpose: To assess whether night-time increases in mechanical loading negatively impact respiratory muscle function in COPD and whether compensatory increases in inspiratory neural drive (IND) are adequate to stabilize ventilatory output and arterial oxygen saturation, especially during sleep when wakefulness drive is withdrawn.

Methods: 21 patients with moderate-to-severe COPD and 20 age-/sex-matched healthy controls (CTRL) participated in a prospective, cross-sectional, one-night study to assess the impact of COPD on serial awake, supine inspiratory capacity (IC) measurements and continuous dynamic respiratory muscle function (esophageal manometry) and IND (diaphragm electromyography, EMGdi) in supine sleep.

Results: Supine inspiratory effort and EMGdi were consistently twice as high in COPD versus CTRL (p < 0.05). Despite overnight increases in awake total airways resistance and dynamic lung hyperinflation in COPD (p < 0.05; not in CTRL), elevated awake EMGdi and respiratory effort were unaltered in COPD overnight. At sleep onset (non-rapid eye movement sleep, N2), EMGdi was decreased versus wakefulness in COPD (- 43 ± 36%; p < 0.05) while unaffected in CTRL (p = 0.11); however, respiratory effort and arterial oxygen saturation (SpO) were unchanged. Similarly, in rapid eye movement (stage R), sleep EMGdi was decreased (- 38 ± 32%, p < 0.05) versus wakefulness in COPD, with preserved respiratory effort and minor (2%) reduction in SpO.

Conclusions: Despite progressive mechanical loading overnight and marked decreases in wakefulness drive, inspiratory effort and SpO were well maintained during sleep in COPD. Preserved high inspiratory effort during sleep, despite reduced EMGdi, suggests continued (or increased) efferent activation of extra-diaphragmatic muscles, even in stage R sleep.

Clinical Trial Information: The COPD data reported herein were secondary data (Placebo arm only) obtained through the following Clinical Trial: "Effect of Aclidinium/Formoterol on Nighttime Lung Function and Morning Symptoms in Chronic Obstructive Pulmonary Disease" ( https://clinicaltrials.gov/ct2/show/NCT02429765 ; NCT02429765).
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http://dx.doi.org/10.1007/s00421-021-04869-0DOI Listing
January 2022

Mechanisms of Exertional Dyspnea in Patients with Mild COPD and a Low Resting DL.

COPD 2021 10 8;18(5):501-510. Epub 2021 Sep 8.

Respiratory Investigation Unit, Department of Medicine, Queen's University, and Kingston Health Sciences Centre, Kingston, Ontario, Canada.

Patients with mild chronic obstructive pulmonary disease (COPD) and lower resting diffusing capacity for carbon monoxide (DL) often report troublesome dyspnea during exercise although the mechanisms are not clear. We postulated that in such individuals, exertional dyspnea is linked to relatively high inspiratory neural drive (IND) due, in part, to the effects of reduced ventilatory efficiency. This cross-sectional study included 28 patients with GOLD I COPD stratified into two groups with ( = 15) and without ( = 13) DL less than the lower limit of normal (
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http://dx.doi.org/10.1080/15412555.2021.1932782DOI Listing
October 2021

Moving average and standard deviation thresholding (MAST): a novel algorithm for accurate R-wave detection in the murine electrocardiogram.

J Comp Physiol B 2021 11 25;191(6):1071-1083. Epub 2021 Jul 25.

School of Computing, Queen's University, Kingston, ON, Canada.

Advances in implantable radio-telemetry or diverse biologging devices capable of acquiring high-resolution ambulatory electrocardiogram (ECG) or heart rate recordings facilitate comparative physiological investigations by enabling detailed analysis of cardiopulmonary phenotypes and responses in vivo. Two priorities guiding the meaningful adoption of such technologies are: (1) automation, to streamline and standardize large dataset analysis, and (2) flexibility in quality-control. The latter is especially relevant when considering the tendency of some fully automated software solutions to significantly underestimate heart rate when raw signals contain high-amplitude noise. We present herein moving average and standard deviation thresholding (MAST), a novel, open-access algorithm developed to perform automated, accurate, and noise-robust single-channel R-wave detection from ECG obtained in chronically instrumented mice. MAST additionally and automatically excludes and annotates segments where R-wave detection is not possible due to artefact levels exceeding signal levels. Customizable settings (e.g. window width of moving average) allow for MAST to be scaled for use in non-murine species. Two expert reviewers compared MAST's performance (true/false positive and false negative detections) with that of a commercial ECG analysis program. Both approaches were applied blindly to the same random selection of 270 3-min ECG recordings from a dataset containing varying amounts of signal artefact. MAST exhibited roughly one quarter the error rate of the commercial software and accurately detected R-waves with greater consistency and virtually no false positives (sensitivity, Se: 98.48% ± 4.32% vs. 94.59% ± 17.52%, positive predictivity, +P: 99.99% ± 0.06% vs. 99.57% ± 3.91%, P < 0.001 and P = 0.0274 respectively, Wilcoxon signed rank; values are mean ± SD). Our novel, open-access approach for automated single-channel R-wave detection enables investigators to study murine heart rate indices with greater accuracy and less effort. It also provides a foundational code for translation to other mammals, ectothermic vertebrates, and birds.
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http://dx.doi.org/10.1007/s00360-021-01389-3DOI Listing
November 2021

Sleep quality and architecture in COPD: the relationship with lung function abnormalities.

J Bras Pneumol 2021 19;47(3):e20200612. Epub 2021 Jul 19.

. Division of Respiratory & Sleep Medicine, Department of Medicine, Queen's University, Kingston (ON) Canada.

Objective: Impaired respiratory mechanics and gas exchange may contribute to sleep disturbance in patients with COPD. We aimed to assess putative associations of different domains of lung function (airflow limitation, lung volumes, and gas exchange efficiency) with polysomnography (PSG)-derived parameters of sleep quality and architecture in COPD.

Methods: We retrospectively assessed data from COPD 181 patients ≥ 40 years of age who underwent spirometry, plethysmography, and overnight PSG. Univariate and multivariate linear regression models predicted sleep efficiency (total sleep time/total recording time) and other PSG-derived parameters that reflect sleep quality.

Results: The severity of COPD was widely distributed in the sample (post-bronchodilator FEV1 ranging from 25% to 128% of predicted): mild COPD (40.3%), moderate COPD (43.1%), and severe-very severe COPD (16.6%). PSG unveiled a high proportion of obstructive sleep apnea (64.1%) and significant nocturnal desaturation (mean pulse oximetry nadir = 82.2% ± 6.9%). After controlling for age, sex, BMI, apnea-hypopnea index, nocturnal desaturation, comorbidities, and psychotropic drug prescription, FEV1/FVC was associated with sleep efficiency (β = 25.366; R2 = 14%; p < 0.001), whereas DLCO predicted sleep onset latency (β = -0.314; R2 = 13%; p < 0.001) and rapid eye movement sleep time/total sleep time in % (β = 0.085; R2 = 15%; p = 0.001).

Conclusions: Pulmonary function variables reflecting severity of airflow and gas exchange impairment, adjusted for some potential confounders, were weakly related to PSG outcomes in COPD patients. The direct contribution of the pathophysiological hallmarks of COPD to objectively measured parameters of sleep quality seems to be less important than it was previously assumed.
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http://dx.doi.org/10.36416/1806-3756/e20200612DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8332731PMC
August 2021

Reduced exercise tolerance in mild chronic obstructive pulmonary disease: The contribution of combined abnormalities of diffusing capacity for carbon monoxide and ventilatory efficiency.

Respirology 2021 08 7;26(8):786-795. Epub 2021 Apr 7.

Respiratory Investigation Unit, Department of Medicine, Queen's University and Kingston Health Sciences Centre, Kingston General Hospital Campus, Kingston, Ontario, Canada.

Background And Objective: The combination of both reduced resting diffusing capacity of the lung for carbon monoxide (DL ) and ventilatory efficiency (increased ventilatory requirement for CO clearance [V˙ /V˙CO ]) has been linked to exertional dyspnoea and exercise intolerance in chronic obstructive pulmonary disease (COPD) but the underlying mechanisms are poorly understood. The current study examined if low resting DL and higher exercise ventilatory requirements were associated with earlier critical dynamic mechanical constraints, dyspnoea and exercise limitation in patients with mild COPD.

Methods: In this retrospective analysis, we compared V˙ /V˙CO , dynamic inspiratory reserve volume (IRV), dyspnoea and exercise capacity in groups of patients with Global Initiative for Chronic Obstructive Lung Disease stage 1 COPD with (1) a resting DL at or greater than the lower limit of normal (≥LLN; Global Lung Function Initiative reference equations [n = 44]) or (2) below the
Results: Spirometry and resting lung volumes were similar in the two COPD groups. During exercise, V˙ /V˙CO (nadir and slope) was consistently higher in the DL  < LLN compared with the other groups (all p < 0.05). The DL  < LLN group had lower IRV and greater dyspnoea intensity at standardized submaximal work rates and lower peak work rate and oxygen uptake than the other two groups (all p < 0.05).

Conclusion: Reduced exercise capacity in patients with DL  < LLN was related to higher ventilatory requirements, a faster rate of decline in dynamic IRV and greater dyspnoea during exercise. These simple measurements should be considered for the clinical evaluation of unexplained exercise intolerance in individuals with ostensibly mild COPD.
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http://dx.doi.org/10.1111/resp.14045DOI Listing
August 2021

Elevated exercise ventilation in mild COPD is not linked to enhanced central chemosensitivity.

Respir Physiol Neurobiol 2021 02 5;284:103571. Epub 2020 Nov 5.

Respiratory Investigation Unit, Department of Medicine, Queen's University and Kingston Health Sciences Centre Kingston General Hospital Campus, Kingston, Ontario, Canada. Electronic address:

Background: The purpose of this study was to determine if altered central chemoreceptor characteristics contributed to the elevated ventilation relative to carbon dioxide production (V̇/V̇CO) response during exercise in mild chronic obstructive pulmonary disease (COPD).

Methods: Twenty-nine mild COPD and 19 healthy age-matched control participants undertook lung function testing followed by symptom-limited incremental cardiopulmonary exercise testing . On a separate day, basal (non-chemoreflex) ventilation (V̇), the central chemoreflex ventilatory recruitment threshold for CO (VRTCO), and central chemoreflex sensitivity (V̇) were assessed using the modified Duffin's CO rebreathing method. Resting arterialized blood gas data were also obtained.

Results: At standardized exercise intensities, absolute V̇ and V̇/V̇CO were consistently elevated and the end-tidal partial pressure of CO was relatively decreased in mild COPD versus controls (all p < 0.05). There were no between-group differences in resting arterialized blood gas parameters, basal V̇, VRTCO, or V̇ (all p > 0.05).

Conclusion: These data have established that excessive exercise ventilation in mild COPD is not explained by altered central chemosensitivity.
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http://dx.doi.org/10.1016/j.resp.2020.103571DOI Listing
February 2021

Evaluation of Dynamic Respiratory Mechanical Abnormalities During Conventional CPET.

Front Med (Lausanne) 2020 10;7:548. Epub 2020 Sep 10.

Respiratory Investigation Unit, Division of Respirology, Department of Medicine, Kingston Health Sciences Centre & Queen's University, Kingston, ON, Canada.

Assessment of the ventilatory response to exercise is important in evaluating mechanisms of dyspnea and exercise intolerance in chronic cardiopulmonary diseases. The characteristic mechanical derangements that occur during exercise in chronic respiratory conditions have previously been determined in seminal studies using esophageal catheter pressure-derived measurements. In this brief review, we examine the emerging role and clinical utility of conventional assessment of dynamic respiratory mechanics during exercise testing. Thus, we provide a physiologic rationale for measuring operating lung volumes, breathing pattern, and flow-volume loops during exercise. We consider standardization of inspiratory capacity-derived measurements and their practical implementation in clinical laboratories. We examine the evidence that this iterative approach allows greater refinement in evaluation of ventilatory limitation during exercise than traditional assessments of breathing reserve. We appraise the available data on the reproducibility and responsiveness of this methodology. In particular, we review inspiratory capacity measurement and derived operating lung volumes during exercise. We demonstrate, using recent published data, how systematic evaluation of dynamic mechanical constraints, together with breathing pattern analysis, can provide valuable insights into the nature and extent of physiological impairment contributing to exercise intolerance in individuals with common chronic obstructive and restrictive respiratory disorders.
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http://dx.doi.org/10.3389/fmed.2020.00548DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7533639PMC
September 2020

Clinical Utility of Measuring Inspiratory Neural Drive During Cardiopulmonary Exercise Testing (CPET).

Front Med (Lausanne) 2020 18;7:483. Epub 2020 Sep 18.

Research Group for Rehabilitation in Internal Disorders, Respiratory Rehabilitation and Respiratory Division, Department of Rehabilitation Sciences, University Hospital Leuven, KU Leuven, Leuven, Belgium.

Cardiopulmonary exercise testing (CPET) has traditionally included ventilatory and metabolic measurements alongside electrocardiographic characterization; however, research increasingly acknowledges the utility of also measuring inspiratory neural drive (IND) through its surrogate measure of diaphragmatic electromyography (EMGdi). While true IND also encompasses the activation of non-diaphragmatic respiratory muscles, the current review focuses on diaphragmatic measurements, providing information about additional inspiratory muscle groups for context where appropriate. Evaluation of IND provides mechanistic insight into the origins of dyspnea and exercise limitation across pathologies; yields valuable information reflecting the integration of diverse mechanical, chemical, locomotor, and metabolic afferent signals; and can help assess the efficacy of therapeutic interventions. Further, IND measurement during the physiologic stress of exercise is uniquely poised to reveal the underpinnings of physiologic limitations masked during resting and unloaded breathing, with important information provided not only at peak exercise, but throughout exercise protocols. As our understanding of IND presentation across varying conditions continues to grow and methods for its measurement become more accessible, the translation of these principles into clinical settings is a logical next step in facilitating appropriate and nuanced management tailored to each individual's unique physiology. This review provides an overview of the current state of understanding of IND measurement during CPET: its origins, known patterns of behavior and links with dyspnea in health and major respiratory diseases, and the possibility of expanding this approach to applications beyond exercise.
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http://dx.doi.org/10.3389/fmed.2020.00483DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7530180PMC
September 2020

Mechanisms of orthopnoea in patients with advanced COPD.

Eur Respir J 2021 03 11;57(3). Epub 2021 Mar 11.

Division of Respiratory Medicine, Dept of Medicine, Queen's University and Kingston Health Sciences Centre, Kingston, ON, Canada

Many patients with severe chronic obstructive pulmonary disease (COPD) report an unpleasant respiratory sensation at rest, which is further amplified by adoption of a supine position (orthopnoea). The mechanisms of this acute symptomatic deterioration are poorly understood.Sixteen patients with advanced COPD and a history of orthopnoea and 16 age- and sex-matched healthy controls underwent pulmonary function tests (PFTs) and detailed sensory-mechanical measurements including inspiratory neural drive (IND) assessed by diaphragm electromyography (EMG), oesophageal pressure ( ) and gastric pressure ( ), in both sitting and supine positions.Patients had severe airflow obstruction (forced expiratory volume in 1 s (FEV): 40±18% pred) and lung hyperinflation. Regardless of the position, patients had lower inspiratory capacity (IC) and higher IND for a given tidal volume ( ) ( greater neuromechanical dissociation (NMD)), higher intensity of breathing discomfort, higher minute ventilation (') and higher breathing frequency ( ) compared with controls (all p<0.05). For controls in a supine position, IC increased by 0.48 L sitting erect, with a small drop in ', mainly due to reduced (all p<0.05). By contrast, IC remained unaltered in patients with COPD, but dynamic lung compliance ( ) decreased (p<0.05) in the supine position. Breathing discomfort, inspiratory work of breathing (WOB), inspiratory effort, IND, NMD and neuroventilatory uncoupling all increased in COPD patients in the supine position (p<0.05), but not in the healthy controls. Orthopnoea was associated with acute changes in IND (r=0.65, p=0.01), neuroventilatory uncoupling (r=0.76, p=0.001) and NMD (r=0.73, p=0.002).In COPD, onset of orthopnoea coincided with an abrupt increase in elastic loading of the inspiratory muscles in recumbency, in association with increased IND and greater NMD of the respiratory system.
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http://dx.doi.org/10.1183/13993003.00754-2020DOI Listing
March 2021

Deterioration of Nighttime Respiratory Mechanics in COPD: Impact of Bronchodilator Therapy.

Chest 2021 01 27;159(1):116-127. Epub 2020 Jun 27.

Department of Medicine, Queen's University, Kingston, Canada; Division of Respiratory Medicine, Queen's University, Kingston, Canada. Electronic address:

Background: COPD is associated with nighttime respiratory symptoms, poor sleep quality, and increased risk of nocturnal death. Overnight deterioration of inspiratory capacity (IC) and FEV have been documented previously. However, the precise nature of this deterioration and mechanisms by which evening bronchodilation may mitigate this occurrence have not been studied.

Research Question: What is the effect of evening dosing of dual, long-acting bronchodilation on detailed nocturnal respiratory mechanics and inspiratory neural drive (IND)?

Study Design And Methods: A double-blind, randomized, placebo-controlled crossover study assessed the effects of evening long-acting bronchodilation (aclidinium bromide/formoterol fumarate dihydrate: 400/12 μg) or placebo on morning trough IC (12 h after the dose; primary outcome) and serial overnight measurements of spirometry, dynamic respiratory mechanics, and IND (secondary outcomes). Twenty participants with COPD (moderate/severe airway obstruction and lung hyperinflation) underwent serial measurements of IC, spirometry, breathing pattern, esophageal and transdiaphragmatic pressures, and diaphragm electromyography (diaphragmatic electromyography as a percentage of maximum; IND) at 6 time points from 0 to 12 h after the dose and compared with sleeping IND.

Results: Compared with placebo, evening bronchodilation was not associated with increased morning trough IC 12 h after the dose (P = .48); however, nadir IC (lowest IC, independent of time), peak IC, area under the curve for 12 h after the dose, and IC for 10 h after the dose were improved (P < .05). During placebo, total airways resistance, lung hyperinflation, IND, and tidal esophageal and transdiaphragmatic pressure swings all increased significantly overnight compared with baseline evening values; however, each of these parameters improved with bronchodilator treatment (P < .05) with no change in ventilation or breathing pattern.

Interpretation: Respiratory mechanics significantly deteriorated at night during placebo. Although the morning trough IC was unchanged, evening bronchodilator treatment was associated consistently with sustained overnight improvements in dynamic respiratory mechanics and inspiratory neural drive compared with placebo CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov identifier NCT02429765.
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http://dx.doi.org/10.1016/j.chest.2020.06.033DOI Listing
January 2021

Acute bronchodilator therapy does not reduce wasted ventilation during exercise in COPD.

Respir Physiol Neurobiol 2018 06 22;252-253:64-71. Epub 2018 Mar 22.

Department of Medicine, Queen's University and Kingston Health Sciences Centre, Kingston, ON, Canada. Electronic address:

This randomized, double-blind, crossover study aimed to determine if acute treatment with inhaled bronchodilators, by improving regional lung hyperinflation and ventilation distribution, would reduce dead space-to-tidal volume ratio (V/V); thus contributing to improved exertional dyspnea in COPD. Twenty COPD patients (FEV = 50 ± 15% predicted; mean ± SD) performed pulmonary function tests and symptom-limited constant-work rate exercise at 75% peak-work rate (with arterialized capillary blood gases) after nebulized bronchodilator (BD; ipratropium 0.5mg + salbutamol 2.5 mg) or placebo (PL; normal saline). After BD versus PL: Functional residual capacity decreased by 0.4L (p = .0001). Isotime during exercise after BD versus PL (p < .05): dyspnea decreased: 1.2 ± 1.9 Borg-units; minute ventilation increased: 3.8 ± 5.5 L/min; IC increased: 0.24 ± 0.28 L and V increased 0.19 ± 0.16 L. There was no significant difference in arterial CO tension or V/V, but alveolar ventilation increased by 3.8 ± 5.5 L/min (p = .02). Post-BD improvements in respiratory mechanics explained 51% of dyspnea reduction at a standardized exercise time. Bronchodilator-induced improvements in respiratory mechanics were not associated with reduced wasted ventilation - a residual contributory factor to exertional dyspnea during exercise in COPD.
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http://dx.doi.org/10.1016/j.resp.2018.03.012DOI Listing
June 2018

Advances in the Evaluation of Respiratory Pathophysiology during Exercise in Chronic Lung Diseases.

Front Physiol 2017 22;8:82. Epub 2017 Feb 22.

Division of Respiratory Medicine, Department of Medicine, Queen's University and Kingston General Hospital Kingston, ON, Canada.

Dyspnea and exercise limitation are among the most common symptoms experienced by patients with various chronic lung diseases and are linked to poor quality of life. Our understanding of the source and nature of perceived respiratory discomfort and exercise intolerance in chronic lung diseases has increased substantially in recent years. These new mechanistic insights are the primary focus of the current review. Cardiopulmonary exercise testing (CPET) provides a unique opportunity to objectively evaluate the ability of the respiratory system to respond to imposed incremental physiological stress. In addition to measuring aerobic capacity and quantifying an individual's cardiac and ventilatory reserves, we have expanded the role of CPET to include evaluation of symptom intensity, together with a simple "non-invasive" assessment of relevant ventilatory control parameters and dynamic respiratory mechanics during standardized incremental tests to tolerance. This review explores the application of the new advances in the clinical evaluation of the pathophysiology of exercise intolerance in chronic obstructive pulmonary disease (COPD), chronic asthma, interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH). We hope to demonstrate how this novel approach to CPET interpretation, which includes a quantification of activity-related dyspnea and evaluation of its underlying mechanisms, enhances our ability to meaningfully intervene to improve quality of life in these pathologically-distinct conditions.
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http://dx.doi.org/10.3389/fphys.2017.00082DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5319975PMC
February 2017

Automated Non-invasive Video-Microscopy of Oyster Spat Heart Rate during Acute Temperature Change: Impact of Acclimation Temperature.

Front Physiol 2016 22;7:236. Epub 2016 Jun 22.

Biomedical and Molecular Sciences, Queen's UniversityKingston, ON, Canada; Medicine, Division of Respirology, Queen's UniversityKingston, ON, Canada.

We developed an automated, non-invasive method to detect real-time cardiac contraction in post-larval (1.1-1.7 mm length), juvenile oysters (i.e., oyster spat) via a fiber-optic trans-illumination system. The system is housed within a temperature-controlled chamber and video microscopy imaging of the heart was coupled with video edge-detection to measure cardiac contraction, inter-beat interval, and heart rate (HR). We used the method to address the hypothesis that cool acclimation (10°C vs. 22°C-Ta10 or Ta22, respectively; each n = 8) would preserve cardiac phenotype (assessed via HR variability, HRV analysis and maintained cardiac activity) during acute temperature changes. The temperature ramp (TR) protocol comprised 2°C steps (10 min/experimental temperature, Texp) from 22°C to 10°C to 22°C. HR was related to Texp in both acclimation groups. Spat became asystolic at low temperatures, particularly Ta22 spat (Ta22: 8/8 vs. Ta10: 3/8 asystolic at Texp = 10°C). The rate of HR decrease during cooling was less in Ta10 vs. Ta22 spat when asystole was included in analysis (P = 0.026). Time-domain HRV was inversely related to temperature and elevated in Ta10 vs. Ta22 spat (P < 0.001), whereas a lack of defined peaks in spectral density precluded frequency-domain analysis. Application of the method during an acute cooling challenge revealed that cool temperature acclimation preserved active cardiac contraction in oyster spat and increased time-domain HRV responses, whereas warm acclimation enhanced asystole. These physiologic changes highlight the need for studies of mechanisms, and have translational potential for oyster aquaculture practices.
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http://dx.doi.org/10.3389/fphys.2016.00236DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916204PMC
July 2016

Recent advances and contraversies on the role of pulmonary neuroepithelial bodies as airway sensors.

Semin Cell Dev Biol 2013 Jan 26;24(1):40-50. Epub 2012 Sep 26.

Division of Pathology, Department of Paediatric Laboratory Medicine, The Research Institute, The Hospital for Sick Children, Toronto, Ontario, Canada.

Pulmonary neuroepithelial bodies are polymodal sensors widely distributed within the airway mucosa of mammals and other species. Neuroepithelial body cells store and most likely release serotonin and peptides as transmitters. Neuroepithelial bodies have a complex innervation that includes vagal sensory afferent fibers and dorsal root ganglion fibers. Neuroepithelial body cells respond to a number of intraluminal airway stimuli, including hypoxia, hypercarbia, and mechanical stretch. This article reviews recent findings in the cellular and molecular biology of neuroepithelial body cells and their potential role as airway sensors involved in the control of respiration, particularly during the perinatal period. Alternate hypotheses and areas of controversy regarding potential function as mechanosensory receptors involved in pulmonary reflexes are discussed.
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http://dx.doi.org/10.1016/j.semcdb.2012.09.003DOI Listing
January 2013

Pulmonary neuroepithelial bodies as airway sensors: putative role in the generation of dyspnea.

Curr Opin Pharmacol 2011 Jun 27;11(3):211-7. Epub 2011 Apr 27.

Department of Physiology, Queen's University, 3rd Floor Botterell Hall, 18 Stuart Street, Kingston, ON, K7L 2V5, Canada.

The neuroepithelial bodies (NEB) of the intrapulmonary airways (AW) are multimodal AW sensors responding to a variety of stimuli including hypoxia, hypercarbia, and mechanical stretch. NEBs are richly innervated by a diverse population of mostly vagal afferent nerve fibers and owing to their early developmental maturation may be especially important during the perinatal period. This article reviews recent findings of NEB functional morphology and innervation, and postulates a role in the generation of dyspnea. This is based on their potential for transduction of dyspneic stimuli and findings of NEB cell abnormalities in a number of pulmonary disorders presenting with this symptom.
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http://dx.doi.org/10.1016/j.coph.2011.04.003DOI Listing
June 2011
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