Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Jan 2014
A fibre optic oxygen sensor that detects rapid PO2 changes under simulated conditions of cyclical atelectasis in vitro.
Two challenges in the management of Acute Respiratory Distress Syndrome are the difficulty in diagnosing cyclical atelectasis, and in individualising mechanical ventilation therapy in real-time. Commercial optical oxygen sensors can detect [Formula: see text] oscillations associated with cyclical atelectasis, but are not accurate at saturation levels below 90%, and contain a toxic fluorophore. ⋯ Our sensor was able to detect the whole amplitude of the imposed [Formula: see text] oscillations, even at the highest respiratory rate. We also examined our sensor's resistance to clot formation by continuous in vivo deployment in non-heparinised flowing animal blood for 24h, after which no adsorption of organic material on the sensor's surface was detectable by scanning electron microscopy.
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Respir Physiol Neurobiol · Jan 2014
Homothety ratio of airway diameters and site of airway resistance in healthy and COPD subjects.
Our objective was to evaluate whether a decrease in the homothety ratio (h: diameter of child/parent bronchus, constant over generations) explains the shift in airway resistance toward periphery in chronic obstructive pulmonary disease (COPD). Using a validated computational model of fluid motion, we determined that reduced values of h (<0.76) were associated with a shift in resistance toward periphery. The calculated luminal diameters of terminal bronchioles using normal h (0.80-0.85) or reduced h (0.70-0.75) fitted well with measured micro-CT values obtained by McDonough et al. (N. ⋯ Physiol. Neurobiol., 2010; 173:1-10]), we verified the agreement between measured and calculated resistance (r=0.42). In conclusion, the remodeling process of COPD may reduce h and explain the shift in resistance toward lung periphery.
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Respir Physiol Neurobiol · Jan 2014
Quantifying oscillatory ventilation during exercise in patients with heart failure.
This study examined the validity of a novel software application to quantify measures of periodic breathing rest (PB) and oscillatory ventilation during exercise (EOV) in heart failure patients (HF). ⋯ These data suggest PK consistently captures amplitudes while underestimating period. In contrast, SINE and FOUR consistently capture period although SINE underestimates amplitude. Thus, an optimal algorithm for the quantification of PB and/or EOV in patients with HF might combine multiple analysis methods.
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Respir Physiol Neurobiol · Jan 2014
Interactive effects of mechanical ventilation, inhaled nitric oxide and oxidative stress in acute lung injury.
To compare conventional mechanical ventilation (CMV) and high-frequency oscillatory ventilation (HFOV), with/without inhaled nitric oxide (iNO), for oxygenation, inflammation, antioxidant/oxidative stress status, and DNA damage in a model of acute lung injury (ALI). Lung injury was induced by tracheal infusion of warm saline. Rabbits were ventilated at [Formula: see text] 1.0 and randomly assigned to one of five groups. ⋯ HFOV with and without iNO, and CMV with iNO showed significantly increased antioxidant defense and reduced DNA damage than CMV without iNO. Inhaled nitric oxide did not beneficially affect HFOV in relation to antioxidant defense/oxidative stress and pulmonary DNA damage. Overall, lung injury was reduced using HFOV or CMV with iNO.
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Respir Physiol Neurobiol · Jan 2014
Analgesic effects of dyspnoea: "Air hunger" does not inhibit the spinal nociception reflex in humans.
Dyspnoea has distinct sensory modalities, including air hunger and the sensation of excessive breathing "work/effort". Both have analgesic properties. In the case of work/effort, spinal mechanisms have been documented (inhibitory effect on the spinal nociceptive flexor reflex, RIII). ⋯ Electromyography of the biceps femoris was used to record the amplitude of RIII in response to painful electrical sural nerve stimulation. Air hunger failed to inhibit the RIII reflex. We conclude that the mechanisms of air hunger induced analgesia do not include a spinal contribution and are therefore mostly central.