Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Jan 2015
Case ReportsPhysiological mechanisms of dyspnea relief following ivacaftor in cystic fibrosis: a case report.
Ivacaftor is a novel oral pharmacologic agent that specifically targets the genetic defect of cystic fibrosis (CF) by augmenting chloride conductance through the CF transmembrane regulator (CFTR) protein. For individuals with CF and at least one copy of the G551D gating mutation, improvements in sweat chloride, nutritional parameters, lung function, respiratory symptoms, and exercise tolerance (i.e., 6-min walk distance) are attained within 2 weeks of initiating ivacaftor. ⋯ An improvement of FEV1 (by 16%) following ivacaftor was accompanied by clinically significant improvements in exercise capacity (by 14%) and exertional dyspnea (by up to 5 Borg scale units). These improvements were attributable, at least in part, to favorable alterations in the ventilatory response to exercise, including improvements in breathing patterns (e.g., increased tidal volume and reduced breathing frequency) and dynamic operating lung volumes (e.g., increased inspiratory reserve volume and inspiratory capacity) and decreases in dynamic mechanical ventilatory constraints.
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Respir Physiol Neurobiol · Jan 2015
Electrical activity of the diaphragm during progressive cycling exercise in endurance-trained men.
The study aimed to investigate diaphragm respiratory drive modulation through electrical activity of the diaphragm (EADi) during progressive cycling in endurance-trained men (N=7) and to test day-to-day measurement reliability. Normalized EADi increased at exercise intensities from 40% workload (WL) to 70% and 85%WL but plateaued from 70% to 85% (p<0.05). ⋯ Within-day variability appeared constant indicating that measurements within a trial are reliable. Results suggest that diaphragm respiratory drive increases at moderate exercise intensities, but plateaus at high intensities where other respiratory muscles might contribute significantly to the breathing effort, perhaps to "protect" against diaphragm fatigue.
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Respir Physiol Neurobiol · Jan 2015
Orexin-B antagonized respiratory depression induced by sevoflurane, propofol, and remifentanil in isolated brainstem-spinal cords of neonatal rats.
Orexins (hypocretins) play a crucial role in arousal, feeding, and endocrine function. We previously reported that orexin-B activated respiratory neurons in the isolated brainstem-spinal cords of neonatal rats. We herein determined whether orexin-B antagonized respiratory depression induced by sevoflurane, propofol, or remifentanil. ⋯ The decrease induced in the C4 burst rate by 10 μM propofol or 0.01 μM remifentanil was significantly antagonized by 0.1 μM orexin-B. Respiratory depression induced by a higher concentration (0.1 μM) of remifentanil was not restored by 0.1 μM orexin-B. These results demonstrated that orexin-B antagonized respiratory depression induced by sevoflurane, propofol, or remifentanil.
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During submaximal exercise, some otherwise healthy obese women experience breathlessness, or dyspnea on exertion (+DOE), while others have mild or no DOE (-DOE). We investigated whether weight loss could reduce DOE. Twenty nine obese women were grouped based on their Ratings of Perceived Breathlessness (RPB) during constant load 60 W cycling: +DOE (n = 14, RPB ≥ 4, 34 ± 8 years, and 36 ± 3 kg/m(2)) and -DOE ( n= 15, RPB ≤ 2, 32 ± 8 years, and 36 ± 4 kg/m(2)) and then completed a 12-week weight loss program. ⋯ RPB decreased significantly in the +DOE group (from 4.7 ± 1.1 to 3.1 ± 1.6) and remained low in the -DOE (from 1.5 ± 0.7 to 1.6 ± 1.1) (interaction p < 0.002). Most physiological variables measured (i.e. body composition, fat distribution, pulmonary function, oxygen cost of breathing, and cardiorespiratory measures) improved with weight loss; however, the decrease in RPB was not correlated with any of these variables (p > 0.05). In conclusion, moderate weight loss was effective in reducing breathlessness on exertion in obese women who experienced DOE at baseline.
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Respir Physiol Neurobiol · Dec 2014
Respiratory responses following blast-induced traumatic brain injury in rats.
Blast overpressure (OB) injury in rodents has been employed for modeling the traumatic brain injury (TBI) induced by an improvised explosive device (IED) in military service personnel. IED's can cause respiratory arrest if directed at the thorax due to the fluid-tissue interface of the lungs but it is unclear what respiratory changes occur in a head-directed OB injury. ⋯ The breathing pattern of the rodents will be recorded during the OB injury. Our results indicate that a dorsal directed closed-head OB injury results in a neurally mediated apnea followed by respiratory timing changes.