Pulmonary pharmacology & therapeutics
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Pulm Pharmacol Ther · Jan 2003
The use of surfactant in children with acute respiratory distress syndrome: efficacy in terms of oxygenation, ventilation and mortality.
The aim of this prospectively designed study was to investigate the efficacy of surfactant (S) for acute respiratory distress syndrome (ARDS) in children. ⋯ Modified natural surfactant is an effective treatment option in children with ARDS for improving gas exchange, decreasing the use of ventilatory support and increasing survival time.
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Pulm Pharmacol Ther · Jan 2003
Mechanisms of bronchopulmonary C-fiber hypersensitivity induced by cationic proteins.
Cationic proteins secreted by inflammatory cells infiltrating into the airways are known to cause mucosal injury and bronchial hyperresponsiveness. Although an involvement of bronchopulmonary C-fiber afferents in the cationic protein-induced airway hyperresponsiveness has been suggested, direct electrophysiological evidence has not been established. Accordingly, a series of studies was recently carried out using the single-fiber recording technique to determine the responses of pulmonary C fibers to cationic proteins and to investigate the mechanisms possibly underlying these effects. ⋯ Furthermore, the stimulatory and sensitizing effects of these proteins were completely nullified when their cationic charges were neutralized with negatively charged heparin before delivery. However, heparin administered 5-10 min after the delivery of cationic proteins was ineffective in reversing the effects. In conclusion, intratracheal instillation of cationic proteins consistently induces intense stimulation and sensitization of pulmonary C fibers, and an interaction between the cationic charges carried by these proteins and the airway mucosa is probably responsible.
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Pulm Pharmacol Ther · Jan 2002
Randomized Controlled Trial Clinical TrialEffects of inhaled furosemide on CO(2) ventilatory responsiveness in humans.
We previously showed that inhaled furosemide improves experimentally induced dyspnea. In order to test the possibility that inhaled furosemide may alter the CO(2) chemosensitivity and thereby reduce the dyspneic sensation, the effect of inhaled furosemide on CO(2) chemosensitivity was evaluated with a double-blinded, randomized crossover design in 10 healthy subjects. ⋯ Our results showed that (1) inhaled furosemide does not affect the breathing patterns of resting breathing, (2) inhaled furosemide does not affect the slope and intercept of the CO(2) response curve, regardless of whether the CO(2) chemosensitivity is measured by the steady-state technique or rebreathing technique and (3) inhaled furosemide improves the dyspneic sensation produced during hypercapnic hyperpnea. These results suggest that the mechanism of the improvement of dyspnea by inhaling furosemide is not associated with the decrease in the ventilatory drive to CO(2).
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The mucus lining of the respiratory tract originates from products of secretory cells interspersed among mucosal cells or within submucosal glands and protects the underlying mucosa from dehydration. Current understanding is that the lining is a two-fluid model in which the upper layer is a viscoelastic gel (mucus, cross-linked glycoproteins) that overlies a sol layer (serous). Thus mucus propelled by ciliary beating, flows above the sol layer and contains sloughed cells and xenobiotic materials that come into contact with it. ⋯ If high velocity of expiratory airflow is preserved then even with chronic exposure to respiratory irritants and cigarette smoke, mucus clearance remains effective due to cough and two-phase, gas-liquid interactions. However, in patients with advanced airway obstruction and incapable of generating forceful expiratory flows, cough and shearing are ineffective and mucociliary clearance is disparate with markedly slowed mucus layer transport within central airways. Mucolytic therapy for patients with advanced airway obstruction improves ventilation and reduces the frequency of exacerbation.
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Pulm Pharmacol Ther · Jan 2002
ReviewDelta-opioid receptor antagonists as a new concept for central acting antitussive drugs.
Our recent findings indicated that mu- and kappa-opioid receptors enhance each other's antitussive processes. However, delta-opioid receptors played an inhibitory role in antitussive processes mediated by the mu- and kappa-opioid receptors. ⋯ These delta-opioid receptor-mediated antitussive effects may be mediated by the antagonism of delta(1)-, but not delta(2)-opioid receptors. In this review, we study the possibility of the delta-opioid receptor antagonist as a new concept for central acting antitussive drugs.