PubMed Health⌕ Search

PubMed · 12577607

[Tachypnea--when breathing induces panic].

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B Schwizer. 2003-01-08. [Tachypnea--when breathing induces panic].. https://doi.org/10.1024/0369-8394.92.1.29

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Pressure-volume curve does not predict steady-state lung volume in canine lavage lung injury.

To better understand strategies for recruiting and maintaining lung volume in acute lung injury, we examined relationships between steady-state lung volume and cumulative cyclic recruitment/derecruitment volume history and the quasi-static pressure-volume curve, in an animal saline lavage lung injury model. Small-volume tidal pressure-volume loops performed after inflation from functional residual capacity demonstrated incremental, cyclic recruitment only if the peak pressure achieved exceeded the pressure at which the compliance increased (Pflex) on the pressure-volume curve, whereas loops performed after deflation from total lung capacity remained close to the envelope deflation curve. Recruitment continued to occur up to and beyond a peak inspiratory airway pressure of 40 cm H(2)O, as demonstrated by both the tidal loops and by computed tomography-derived lung volume data. Tidal-specific compliance was relatively constant across positive end-expiratory pressure levels after inflation from functional residual capacity, but peaked at moderate positive end-expiratory pressure after deflation from total lung capacity, further demonstrating the effects of volume history and providing experimental validation of the recruitment models of Hickling (AJRCCM 2001;163:69-78). These results support the interpretation of Pflex as pressure threshold for recruitment, but otherwise do not suggest a role for the pressure-volume curve in predicting steady-state lung volume.

Airway Resistance↗

Regional effects of selective pharyngeal muscle activation on airway shape.

Pharyngeal airway fiberoptic imaging was performed in 10 decerebrate cats to determine the effect of selective pharyngeal muscle activation on airway shape. At intraluminal pressures from 6 to -6 cm H2O, maximum anteroposterior and lateral diameters were measured in the rostral oropharynx, caudal oropharynx, and velopharynx with and without bilateral stimulation of the medial hypoglossus (HG), lateral HG, whole HG, glossopharyngeus, and pharyngeal branch of vagus nerves. At all three airway levels without nerve stimulation, the increase in diameter with increasing pressure was greater in the lateral than anteroposterior dimension. Stimulation of the hypoglossal and glossopharyngeus nerves caused greater increases in lateral than anteroposterior diameter in all three regions with different effects across nerves and regions. Stimulation of these four nerves frequently caused greater increases in both diameters, as the airway cross-sectional area was decreased by lowering airway pressure. Stimulation of the pharyngeal branch of vagus resulted in greater decreases in lateral than anteroposterior dimension in the caudal oropharynx and velopharynx, especially as airway cross-sectional area was increased by increasing intraluminal pressure. The results indicate that selective activation of pharyngeal muscles in cats frequently results in greater changes in lateral than anteroposterior airway diameter and that these effects are dependent on airway region and cross-sectional area.

Airway Resistance↗

Mannose-binding lectin deficiency alters the development of fungal asthma: effects on airway response, inflammation, and cytokine profile.

Aspergillus fumigatus is a major fungal pathogen that may be fatal to immunocompromised individuals and causes airway hyperreactivity and remodeling in sensitized individuals. Herein, we examined the role of mannose-binding lectin (MBL), a complement-activating plasma protein, during pulmonary innate and allergic immune responses directed against A. fumigatus spores or conidia. Neither group of nonsensitized MBL-A-sufficient (MBL-A+/+) nor -deficient (MBL-A-/-) mice challenged with an intravenous or intratracheal (i.t.) bolus of A. fumigatus spores experienced fungus-induced mortality, but marked airway remodeling was observed in MBL-A-/- mice challenged i.t. with conidia. In a model of chronic fungal asthma, MBL-A+/+ and MBL-A-/- A. fumigatus-sensitized mice were examined at days 4 and 28 after an i.t. challenge with A. fumigatus conidia. Airway hyperresponsiveness in sensitized MBL-A-/- mice was significantly decreased at both times after conidia challenge compared with the sensitized MBL-A+/+ group. In the sensitized MBL-A-/- mice, whole lung T helper cell type 2 cytokine levels were significantly decreased at day 4 after conidia, and whole lung interferon-gamma levels were significantly increased at day 28 after conidia when compared with controls. However, histological evidence showed similar airway remodeling at day 28 after conidia (i.e., subepithelial fibrosis and goblet cell metaplasia) in the two groups of mice. Thus, these findings show that MBL-A is not required for mouse survival following exposure to A. fumigatus conidia, and this murine collectin isoform contributes to the development and maintenance of airway hyperresponsiveness but not chronic airway remodeling during chronic fungal asthma.

Airway Resistance↗