Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Mar 2013
Differences in gas exchange between severities of chronic obstructive pulmonary disease.
Impaired ventilation on cardiopulmonary exercise test (CPET) is seen in patients with chronic obstructive pulmonary disease (COPD). However, evaluation of the differences of abnormal gas exchange in COPD according to GOLD severity criteria is limited. A retrospective review was performed on all COPD patients referred for CPET at our center between 1998 and 2010. ⋯ Ratio of minute ventilation to carbon dioxide production ( [Formula: see text] ) and exercise capacity as measured by and [Formula: see text] % and work rate in watts% was inversely proportional to GOLD severity. Breathing reserve, minute ventilation, and tidal volume at peak exercise were significantly decreased with increasing disease severity between GOLD groups. We concluded that gas exchange is distinctive among different GOLD severity groups; specifically, GOLD 3 and 4 have a significantly higher [Formula: see text] and a significantly lower [Formula: see text] than GOLD 2.
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Respir Physiol Neurobiol · Mar 2013
ReviewMechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading.
Patients with chronic heart failure (CHF) suffer increased alveolar VD/VT (dead-space-to-tidal-volume ratio), yet they demonstrate augmented pulmonary ventilation such that arterial [Formula: see text] ( [Formula: see text] ) remains remarkably normal from rest to moderate exercise. This paradoxical effect suggests that the control law governing exercise hyperpnea is not merely determined by metabolic CO2 production ( [Formula: see text] ) per se but is responsive to an apparent (real-feel) metabolic CO2 load ( [Formula: see text] ) that also incorporates the adverse effect of physiological VD/VT on pulmonary CO2 elimination. By contrast, healthy individuals subjected to dead space loading also experience augmented ventilation at rest and during exercise as with increased alveolar VD/VT in CHF, but the resultant response is hypercapnic instead of eucapnic, as with CO2 breathing. ⋯ These observations are consistent with the hypothesis that the increased series VD/VT in dead space loading adds to [Formula: see text] as with increased alveolar VD/VT in CHF, but this is through rebreathing of CO2 in dead space gas thus creating a virtual (illusory) airway CO2 load within each inspiration, as opposed to a true airway CO2 load during CO2 breathing that clogs the mechanism for CO2 elimination through pulmonary ventilation. Thus, the chemosensing mechanism at the respiratory controller may be responsive to putative drive signals mediated by within-breath [Formula: see text] oscillations independent of breath-to-breath fluctuations of the mean [Formula: see text] level. Skeletal muscle afferents feedback, while important for early-phase exercise cardioventilatory dynamics, appears inconsequential for late-phase exercise hyperpnea.
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Respir Physiol Neurobiol · Mar 2013
Uncoupling mitochondrial activity maintains body [Formula: see text] during hemorrhage-induced O2 deficit in the anesthetized rat.
During a hemorrhagic shock (HS), O2 uptake ( [Formula: see text] ) decreases as soon as the rate of O2 delivery ( [Formula: see text] ) drops below a "critical level", a response accounted for by the reduction in mitochondrial O2supply. In urethane-anesthetized rats, [Formula: see text] was decreased within 20min from 21.5 to 2.8mlmin(-1) by slowly withdrawing 18mlkg(-1) of blood. ⋯ This was associated with higher levels of O2 extraction, cardiac output and ventilation than in control HS. [Formula: see text] relationship was shifted upward and to the left following DNP. In conclusion, cellular and systemic mechanisms, decreasing O2demand, account for a large part of HS induced [Formula: see text] decline resulting in an additional reduction in [Formula: see text] .