1,721,043 research outputs found
Lung tissue behavior in the mouse during constriction induced by methacholine and endothelin-1
No full text Nagase, Takahide, Hirotoshi Matsui, Tomoko Aoki, Yasuyoshi Ouchi, and Yoshinosuke Fukuchi. Lung tissue behavior in the mouse during constriction induced by methacholine and endothelin-1. J. Appl. Physiol. 81(6): 2373–2378, 1996.—Recently, mice have been extensively used to investigate the pathogenesis of pulmonary disease because appropriate murine models, including transgenic mice, are being increasingly developed. However, little information about the lung mechanics of mice is currently available. We questioned whether lung tissue behavior and the coupling between dissipative and elastic processes, hysteresivity (η), in mice would be different from those in the other species. To address this question, we investigated whether tissue resistance (Rti) and η in mice would be affected by varying lung volume, constriction induced by methacholine (MCh) and endothelin-1 (ET-1), and high-lung-volume challenge during induced constriction. From measured tracheal flow and tracheal and alveolar pressures in open-chest ICR mice during mechanical ventilation [tidal volume = 8 ml/kg, frequency (f) = 2.5 Hz], we calculated lung resistance (Rl), Rti, airway resistance (Raw), lung elastance (El), and η (= 2πfRti/El). Under baseline conditions, increasing levels of end-expiratory transpulmonary pressure decreased Raw and increased Rti. The administration of aerosolized MCh and intravenous ET-1 increased Rl, Rti, Raw, and El in a dose-dependent manner. Rti increased from 0.207 ± 0.010 to 0.570 ± 0.058 cmH2O ⋅ ml−1 ⋅ s after 10−7 mol/kg ET-1 ( P < 0.01). After induced constriction, increasing end-expiratory transpulmonary pressure decreased Raw. However, η was not affected by changing lung volume, constriction induced by MCh and ET-1, or high-lung-volume challenge during induced constriction. These observations suggest that 1) η is stable in mice regardless of various conditions, 2) Rti is an important fraction of Rl and increases after induced constriction, and 3) mechanical interdependence may affect airway smooth muscle shortening in this species. In mammalian species, including mice, analysis of η may indicate that both Rti and El essentially respond to a similar degree. </jats:p
ET-1-induced bronchoconstriction is mediated via ET<sub>B</sub> receptor in mice
No full text Nagase, Takahide, Tomoko Aoki, Teruaki Oka, Yoshinosuke Fukuchi, and Yasuyoshi Ouchi. ET-1-induced bronchoconstriction is mediated via ETB receptor in mice. J. Appl. Physiol. 83(1): 46–51, 1997.—Endothelin (ET)-1 is one of the most potent agonists of airway smooth muscle and can act via two different ET receptor subtypes, i.e., ETA and ETB. To determine the effects of ET-1 on in vivo pulmonary function and which ET receptors are involved in murine lungs, we investigated 1) the effects of ET and sarafotoxin S6c (S6c), a selective ETB agonist, on pulmonary function and 2) the effects of BQ-123 and BQ-788, specific ETA- and ETB-receptor antagonists, on ET-1-induced bronchoconstriction. ICR mice were anesthetized and mechanically ventilated (frequency = 2.5 Hz, tidal volume = 8 ml/kg, positive end-expiratory pressure = 3 cmH2O). Intravenous ET-1, ET-2, and ET-3 increased lung resistance similarly and equipotently, whereas S6c elicited a greater degree of bronchoconstriction. Mice were then pretreated with saline (Sal), BQ-123 (0.2, 1, and 5 mg/kg), or BQ-788 (0.2, 1, and 5 mg/kg) before administration of ET-1 (10−7 mol/kg iv). No dose of BQ-123 blocked ET-1-induced constriction, whereas pretreatment with each dose of BQ-788 significantly inhibited ET-1-induced responses. There were significant differences in morphometrically assessed airway constriction between Sal and BQ-788 and between BQ-123 and BQ-788, whereas no significant difference was observed between Sal and BQ-123. There were no significant morphometric differences in the airway wall area among the three groups. These observations suggest that the ETB- but not ETA-receptor subtype may mediate the changes in murine pulmonary function in response to ET-1. In addition, the ETB-receptor antagonist reduces ET-1-induced airway narrowing by affecting airway smooth muscle contraction in mice. </jats:p
Message from president of the 11th APSR Congress in Kyoto on the occasion of the educational seminar of the APSR (ESAP), Tokyo, 2006
No full text2. RISK FACTORS IN ACUTE EXACERBATION AND THEIR INFLUENCE ON THE PROGNOSIS OF CHRONIC RESPIRATORY FAILURE
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2. Risk Factors in Acute Exacerbation and their Influence on the Prognosis of Chronic Respiratory Failure
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