Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Jan 2015
Effects of acute hypercapnia with and without acidosis on lung inflammation and apoptosis in experimental acute lung injury.
We investigated the effects of acute hypercapnic acidosis and buffered hypercapnia on lung inflammation and apoptosis in experimental acute lung injury (ALI). Twenty-four hours after paraquat injection, 28 Wistar rats were randomized into four groups (n=7/group): (1) normocapnia (NC, PaCO2=35-45 mmHg), ventilated with 0.03%CO2+21%O2+balancedN2; (2) hypercapnic acidosis (HC, PaCO2=60-70 mmHg), ventilated with 5%CO2+21%O2+balancedN2; and (3) buffered hypercapnic acidosis (BHC), ventilated with 5%CO2+21%O2+balancedN2 and treated with sodium bicarbonate (8.4%). ⋯ Lung and kidney cell apoptosis was reduced in HC and BHC in comparison with NC and NV. In conclusion, in this experimental ALI model, hypercapnia, regardless of acidosis, reduced lung inflammation and lung and kidney cell apoptosis.
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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
Derivation of recruitment function from the pressure-volume curve in an acute lung injury model.
Lung volume changes involve the recruitment of collapsed alveoli and the expansion of already opened alveoli. This study aimed to determine the alveolar recruitment function by using a mathematical model from a pressure-volume curve (P-V curve). ⋯ We obtained the P-R curve from the P-V curve, and two curves were differently shaped after lung injury. We concluded that the recruitment function was obtained from the P-V curve and that the P-R curve estimated the recruitment and derecruitment status.
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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.
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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.