Respiratory physiology & neurobiology
-
Respir Physiol Neurobiol · Aug 2014
Does expiratory muscle activity influence dynamic hyperinflation and exertional dyspnea in COPD?
Increased expiratory muscle activity is common during exercise in patients with COPD but its role in modulating operating lung volumes and dyspnea during incremental cycle ergometry is currently unknown. We compared gastric (Pga) and esophageal (Pes) pressures, operating lung volumes and qualitative descriptors of dyspnea during exercise in 12 COPD patients and 12 age- and sex-matched healthy controls. Pes- and Pga-derived measures of expiratory muscle activity were significantly (p<0.05) greater in COPD than in health during exercise. ⋯ Dynamic function of the diaphragm was not different in health and COPD throughout exercise. In both groups, dyspnea descriptors alluding to increased work and inspiratory difficulty predominated whereas expiratory difficulty was rarely reported, even at the limits of tolerance. In conclusion, increased expiratory muscle activity did not mitigate the rise in EELV, the relatively early respiratory mechanical constraints or the attendant perceived inspiratory difficulty during exercise in COPD.
-
Respir Physiol Neurobiol · Aug 2014
Protective role of peroxisome proliferator-activated receptor β/δ in acute lung injury induced by prolonged hyperbaric hyperoxia in rats.
Peroxisome proliferator-activated receptor (PPAR)-β/δ is a transcription factor that belongs to the PPAR family, but the role of PPAR-β/δ in acute lung injury (ALI) induced by hyperbaric oxygen is unknown. In this study we investigated if PPAR-β/δ activation protects from hyperoxia-induced ALI in a rat model. ⋯ However, administration of the PPAR-β/δ antagonist GSK0660 abolished these protective effects. These findings indicate that activation of PPAR-β/δ ameliorates hyperoxia-induced ALI in rats by up-regulating antioxidant enzyme activity as well as suppressing inflammation and apoptosis.
-
Respir Physiol Neurobiol · Jul 2014
Breathing hot humid air induces airway irritation and cough in patients with allergic rhinitis.
We studied the respiratory responses to an increase in airway temperature in patients with allergic rhinitis (AR). Responses to isocapnic hyperventilation (40% of maximal voluntary ventilation) for 4min of humidified hot air (HA; 49°C) and room air (RA; 21°C) were compared between AR patients (n=7) and healthy subjects (n=6). In AR patients, cough frequency increased pronouncedly from 0.10±0.07 before to 2.37±0.73 during, and 1.80±0.79coughs/min for the first 8min after the HA challenge, but not during the RA challenge. ⋯ The HA challenge also caused respiratory discomfort (mainly throat irritation) measured by the handgrip dynamometry in AR patients, but not in healthy subjects. Bronchoconstriction was not detected after the HA challenge in either group of subjects. In conclusion, hyperventilation of HA triggered vigorous cough response and throat irritation in AR patients, indicating the involvement of sensory nerves innervating upper airways.
-
Respir Physiol Neurobiol · Jun 2014
Excess ventilation and ventilatory constraints during exercise in patients with chronic obstructive pulmonary disease.
We assessed the relationship between minute ventilation/carbon dioxide output (VE/VCO2) and ventilatory constraints during an incremental cardiopulmonary exercise testing (CPET) in patients with chronic obstructive pulmonary disease (COPD). Slope and intercept of the VE/VCO2 linear relationship, the ratios of inspiratory capacity/total lung capacity (IC/TLC) and of tidal volume (VT) over vital capacity (VTpeak/VC) and IC (VTpeak/IC) and over forced expiratory volume at 1st second (VTpeak/FEV1) at peak of exercise were measured in 52 COPD patients during a CPET. ⋯ VE/VCO2 slope was negatively related to VTpeak/VC, VTpeak/IC and VTpeak/FEV1 (all correlations p<0.05) and to PETCO2 peak-rest (p<0.01). In COPD, VE/VCO2 slope and intercept provide complementary information on the ventilatory limitation to exercise, as assessed by changes in the end-expiratory lung volume and in tidal volume excursion.
-
Respir Physiol Neurobiol · Jun 2014
β-hydroxy-β-methylbutyrate (HMB) prevents sepsis-induced diaphragm dysfunction in mice.
Infections induce severe respiratory muscle weakness. Currently there are no treatments for this important clinical problem. We tested the hypothesis that β-hydroxy-β-methylbutyrate (HMB) would prevent sepsis-induced diaphragm weakness. ⋯ HMB blocked sepsis-induced caspase 3, 20S proteasomal and PKR activation, but did not prevent calpain activation. Most importantly, HMB administration significantly attenuated sepsis-induced diaphragm weakness, preserving muscle force generation at all stimulation frequencies (p<0.01). We speculate that HMB may prove to be an important therapy in infected patients, with the potential to increase diaphragm strength, to reduce the duration of mechanical ventilation and to decrease mortality in this patient population.