Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Aug 2011
Sex differences in exertional dyspnea in patients with mild COPD: physiological mechanisms.
The purpose of this study was to evaluate the physiological basis for sex-differences in exercise-induced dyspnea in patients with mild COPD. We compared operating lung volumes, breathing pattern and dyspnea during incremental cycling in 32 men (FEV(1)=86±10% predicted) and women (FEV(1)=86±12% predicted) with mild COPD and 32 age-matched controls. There were no sex differences in dyspnea in the control group at any work-rate or ventilation (V(E)). ⋯ At 80 W, dyspnea ratings were 5.7±2.3 and 3.3±2.5 Borg units (P<0.05) and the V(E) to maximal ventilatory capacity ratio was 72% and 55% in women and men, respectively (P<0.05). Comparable increases in dynamic hyperinflation were seen in both male and female COPD groups at symptom limitation but women reached tidal volume constraints at a lower work rate and V(E) than men. Superimposing mild COPD on the normal aging effects had greater sensory consequences in women because of their naturally reduced ventilatory reserve.
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Respir Physiol Neurobiol · Aug 2011
Effects of different forms of dyspnoea on pain perception induced by cold-pressor test.
Although dyspnoea has been shown to attenuate pain, whether different forms of dyspnoea exert a similar inhibitory effect on pain has never been tested. We examined the effects of two different forms of dyspnoea, i.e., "air hunger" sensation (AIR HUNGER) and "work/effort" sensation (WORK/EFFORT), on pain induced by a cold-pressor test. ⋯ Both AIR HUNGER and WORK/EFFORT caused an increase in PTT and an increase in PET or a decrease in maximal pain VAS. Our findings suggest that AIR HUNGER and WORK/EFFORT exert a similar analgesic effect although the WORK/EFFORT-induced analgesia was slightly more effective.
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Respir Physiol Neurobiol · Aug 2011
Compartmental chest wall volume changes during volitional normocapnic hyperpnoea.
During increased ventilation, inspiratory rib cage muscles have been suggested to take over part of diaphragmatic work after the diaphragm fatigues. We investigated the extent to which this proposed change in muscle recruitment is associated with changes in the relative contribution of chest wall compartments to tidal volume (V(T)). ⋯ While breathing frequency increased (43±3 to 56±5 breaths min(-1), p=0.006) and V(T) decreased during normocapnic hyperpnoea (2.6±0.2 to 1.9±0.1l, p<0.001), the relative contribution of chest wall compartments to V(T) remained unchanged (pulmonary rib cage: 48±9 versus 51±14%; abdominal rib cage: 24±4 versus 23±9%; abdomen: 28±8 versus 26±9%; all p>0.05). In conclusion, fatiguing respiratory work is not associated with a change in compartmental contribution to V(T), even in the presence of a change in breathing pattern.
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Respir Physiol Neurobiol · Aug 2011
Alteration of carotid body chemoreflexes after neonatal intermittent hypoxia and caffeine treatment in rat pups.
In human neonates, caffeine therapy for apnoea of prematurity, especially when associated with hypoxemia, is maintained for several weeks after birth. In the present study, we used newborn rats and whole-body plethysmography to test whether chronic exposure to neonatal caffeine treatment (NCT), alone or combined with neonatal intermittent hypoxia (n-IH) alters: (1) baseline ventilation and response to hypoxia (12% O(2), 20 min); and (2) response to acute i.p. injection of caffeine citrate (20 mg/kg) or domperidone, a peripheral dopamine D2 receptor antagonist (1 mg/kg). Four groups of rats were studied as follows: raised under normal conditions with daily gavage with water (NWT) or NCT, or exposed to n-IH (n-IH+NWT and n-IH+NCT) from postnatal days 3 to 12. ⋯ During the late response phase to hypoxia (20 min), ventilation was lower in n-IH+NWT and n-IH+NCT rats compared to NWT or NCT, and were not affected by caffeine or domperidone injection. NCT or caffeine injection decreased baseline apnoea frequency in all groups. These data suggest that chronic exposure to NCT alters both carotid body dopaminergic and adenosinergic systems and central regulation of breathing under baseline conditions and in response to hypoxia.