Breath-by-breath measurement of the volume displaced by diaphragm motion

Singh, Bhajan; Panizza, Janine A.; Finucane, Kevin E.

doi:10.1152/japplphysiol.00256.2002

Cited by 12 publications

(15 citation statements)

References 13 publications

(51 reference statements)

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“…Because diaphragmatic muscle is the only effective respiratory muscle pump and its action contributes to more than 66% of the TV (Mead et al, 1995; Singh et al, 2003), our efforts were focused on analyzing diaphragm muscle fibers and NMJs. Several of the alterations observed in DMSXL diaphragm muscle lead us to believe that they might cause, at least partially, the respiratory failure in these mice.…”

Section: Discussionmentioning

confidence: 99%

Functional and histopathological identification of the respiratory failure in a DMSXL transgenic mouse model of Myotonic Dystrophy

Panaite¹,

Küntzer²,

Gourdon

et al. 2012

Disease Models &Amp; Mechanisms

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SUMMARYAcute and chronic respiratory failure is one of the major and potentially life-threatening features in individuals with myotonic dystrophy type 1 (DM1). Despite several clinical demonstrations showing respiratory problems in DM1 patients, the mechanisms are still not completely understood. This study was designed to investigate whether the DMSXL transgenic mouse model for DM1 exhibits respiratory disorders and, if so, to identify the pathological changes underlying these respiratory problems. Using pressure plethysmography, we assessed the breathing function in control mice and DMSXL mice generated after large expansions of the CTG repeat in successive generations of DM1 transgenic mice. Statistical analysis of breathing function measurements revealed a significant decrease in the most relevant respiratory parameters in DMSXL mice, indicating impaired respiratory function. Histological and morphometric analysis showed pathological changes in diaphragmatic muscle of DMSXL mice, characterized by an increase in the percentage of type I muscle fibers, the presence of central nuclei, partial denervation of end-plates (EPs) and a significant reduction in their size, shape complexity and density of acetylcholine receptors, all of which reflect a possible breakdown in communication between the diaphragmatic muscles fibers and the nerve terminals. Diaphragm muscle abnormalities were accompanied by an accumulation of mutant DMPK RNA foci in muscle fiber nuclei. Moreover, in DMSXL mice, the unmyelinated phrenic afferents are significantly lower. Also in these mice, significant neuronopathy was not detected in either cervical phrenic motor neurons or brainstem respiratory neurons. Because EPs are involved in the transmission of action potentials and the unmyelinated phrenic afferents exert a modulating influence on the respiratory drive, the pathological alterations affecting these structures might underlie the respiratory impairment detected in DMSXL mice. Understanding mechanisms of respiratory deficiency should guide pharmaceutical and clinical research towards better therapy for the respiratory deficits associated with DM1.

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Section: Discussionmentioning

confidence: 99%

Functional and histopathological identification of the respiratory failure in a DMSXL transgenic mouse model of Myotonic Dystrophy

Panaite¹,

Küntzer²,

Gourdon

et al. 2012

Disease Models &Amp; Mechanisms

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show abstract

“…The mean internal anterior-posterior (APrc) and lateral (LArc) ribcage diameters at the level of the third, fifth, seventh and ninth thoracic vertebrae and ribs, respectively, were measured and their product used to estimate ribcage cross-sectional area (Arc), assuming a cross-sectional shape one-third of the way between an ellipse and a rectangle [16,17]. The rib cage was also divided into an upper (U) and a lower (L) segment defined by the mean diameters and cross-sectional areas at the levels of the 3rd and 5th thoracic vertebrae and ribs (APrc_U, LArc_U, Arc_U) and at the level of the 7th and 9th thoracic vertebrae and ribs, respectively (APrc_L, LArc_L, Arc_L).…”

Section: Chest Wall Configurationmentioning

confidence: 99%

Sex differences in thoracic adaptation to pulmonary hyperinflation in cystic fibrosis

Bellemare¹,

Jeanneret²

2006

European Respiratory Journal

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Sex differences in thoracic adaptation have been reported in patients with cystic fibrosis (CF). The interplay between the pattern of thoracic adaptation and the function of the respiratory muscles in male and female CF patients with pulmonary hyperinflation was investigated.Thoracic dimensions and diaphragm length were measured at residual volume, functional residual capacity and total lung capacity using chest radiography in 23 CF (12 males) and 18 normal (11 males) subjects. Respiratory muscle recruitment during resting breathing was assessed by recording intrathoracic and intra-abdominal pressures.In female CF patients, ribcage expansion was predominant, tending to preserve diaphragm length. In male CF patients, thoracic configuration was normal and diaphragm shortening consequently greater. Ribcage cross-sectional area for a given rib inclination was greater in CF patients, indicating a structural expansion of the ribcage 2.5 times greater in females than males. The contribution of inspiratory ribcage muscles to inspiratory pressure was also greater relative to the diaphragm in the CF group.In conclusion, a structural expansion of the ribcage occurs in cystic fibrosis patients with lung hyperinflation that is greater in females than males. This is associated with an apparent greater contribution of inspiratory ribcage muscles to inspiratory pressure.

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“…Lateral fluoroscopic images of the diaphragm and adjacent chest wall were recorded digitally at a frame rate of 7.5 per second. Magnification and distortion of images in each subject were defined using fluoroscopic images of a radiopaque grid of precise squares (16,44). Signals from a Geiger-Muller (GM) radiation counter were used to define onset and offset of fluoroscopy.…”

Section: Methodsmentioning

confidence: 99%

Diaphragm efficiency estimated as power output relative to activation in chronic obstructive pulmonary disease

Finucane

Singh

2012

Journal of Applied Physiology

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Muscle efficiency increases with fiber length and decreases with load. Diaphragm efficiency (Eff(di)) in healthy humans, measured as power output (Wdi) relative to the root mean square of diaphragm electromyogram (RMS(di)), increases with hyperpnea due to phasic activity of abdominal muscles acting to increase diaphragm length at end expiration (L(di ee)) and decrease inspiratory load. In chronic obstructive pulmonary disease (COPD), hyperpnea may decrease Eff(di) if L(di ee) decreases and load increases due to airflow obstruction and dynamic hyperinflation. To examine this hypothesis, we measured Eff(di) in six COPD subjects (mean forced expiratory volume in 1 s: 54% predicted) when breathing air and at intervals during progressive hypercapnic hyperpnea. Wdi was measured as the product of mean inspiratory transdiaphragmatic pressure (ΔPdi(mean)), diaphragm tidal volume measured fluoroscopically, and 1/inspiratory duration. Results were compared with those of six healthy subjects reported previously. In COPD, L(di ee) was normal when breathing air. ΔPdi(mean) and Wdi increased normally, and RMS(di) increased disproportionately (P = 0.01) with hyperpnea, and, unlike health, inspiratory capacity (IC), L(di ee), and Eff(di) did not increase. IC and L(di ee) were constant with hyperpnea because mean expiratory flow increased as expiratory duration decreased (r(2) = 0.65), and because expiratory flow was terminated actively by the balance between expiratory and inspiratory muscle forces near end expiration, and these forces increased proportionately with hyperpnea (r(2) = 0.49). At maximum ventilation, diaphragm radius of curvature at end inspiration increased in COPD (P = 0.04) but not controls; diaphragm radius of curvature at end inspiration and ln(Eff(di)) were negatively correlated (P = 0.01). Thus in COPD with modest airflow obstruction, Eff(di) did not increase normally with hyperpnea due to a constant L(di ee) and inspiratory flattening of the diaphragm.

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Breath-by-breath measurement of the volume displaced by diaphragm motion

Cited by 12 publications

References 13 publications

Functional and histopathological identification of the respiratory failure in a DMSXL transgenic mouse model of Myotonic Dystrophy

Functional and histopathological identification of the respiratory failure in a DMSXL transgenic mouse model of Myotonic Dystrophy

Sex differences in thoracic adaptation to pulmonary hyperinflation in cystic fibrosis

Diaphragm efficiency estimated as power output relative to activation in chronic obstructive pulmonary disease

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