Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • 1995-1999  (4)
  • 1975-1979
  • 1997  (4)
Material
Years
  • 1995-1999  (4)
  • 1975-1979
Year
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 27 (1997), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background In the small airway, surfactant reduces surface tension, prevents liquid filling of bronchioles, thereby maintaining patency in the small airways. Recent reports demonstrated that surfactant dysfunction develops in experimental asthma in immunized guinea pigs. However, there are few reports concerning surfactant and lung function in an experimental asthma model.Objective To examine whether inhaled surfactant improves lung mechanics in antigen-induced bronchoconstriction in guinea pigs.Method We developed a passively immunized guinea pig model for allergic bronchoconstriction induced by antigen inhalation. Using this model, we investigated the effect of inhaled exogenous surfactant, surfactant TA. on the airway opening pressure (Pao) after antigen challenge.Results Aerosol antigen challenge produced a gradual and long-lasting increase in Pao. Twenty minutes after antigen challenge, aerosolized surfactant TA, 20 mg/ml. was inhaled for 90 s, and it significantly reduced the Pao by 32.8% in 12 min, while a 10.2% reduction was observed in a control group in the same period. When surfactant TA was administered by 90-s inhalation before antigen challenge, it inhibited the Pao increase in a dose-dependent manner: mean inhibitory rates of Pao were 33.6% in surfactant TA 10 mg/ml and 61.9% in surfactant TA 20 mg/mI, respectively.Conclusion Inhaled surfactant showed preventive and recovery effects on antigeninduced bronchoconstriction in an immunized guinea pig model.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 27 (1997), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Administration of propranolol can provoke bronchoconstriction only in asthmatic patients. Recently we developed an animal model for propranolol-induced bronchoconstriction (PIB). Our working hypothesis is that such bronchoconstriction may result from the inflammatory mediators released by an allergic reaction.Objectives Our goal in this study was to determine which products of arachidonate 5-lipoxygenase pathway are involved in the PIB.Methods Propranolol at a concentration of 10mg/mL was inhaled 20min after antigen challenge in passively sensitized, anaesthetized and artificially ventilated guinea-pigs. Two different sulfidopeptide leukotriene (s-LT) antagonists, ICI198 615 in the doses of 0.03 and 0.3 mg/kg and vehicle and KCA757 in the doses of 1 and 5 mg/kg and vehicle, and a LTB4 antagonist ONO4057 in the doses of 1 and 10 mg/kg and vehicle were injected intravenously 15min after antigen challenge. Effects of an anticholinergic agent atropine sulphate (5 mg/kg) and an α-adrenergic biocker pbentolamine (0.3 and 3 mg/kg) were exatnined in the same way.Results Bronchoconstriction occurred when 10 mg/mL of propranolol was inhaled 20 min after antigen challenge. Both ICI198 615 and KCA757 administered intravenously 15 min after antigen challenge reduced the PIB in a dose-dependent manner while ONO4057 did not alter the PIB. Atropine or phentolamine did not change the PIB.Conclusions These results suggest that mediator mechanism, but not cholinergic or α-adrenergic nerve, is important in the PIB which developed after the allergic bronchoconstriction in our guinea-pig model and that s-LTs but not LTB4 have an important role in the pathophysiology of the PIB.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 27 (1997), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background We previously reported that inhaled acetaldehyde, a metabolite of ethanol atid a maiti factor in alcohol-induced asthma, causes bronchial hyper-responsiveness (BHR) in asthmatics. However, the mechanisms are unclear.Objective The purpose of this study was to investigate a role of a peptide leukotriene (LT) in acetaldehyde-induced BHR.Methods Effects of LT antagonists, ONO-1078 (O.l-l.Omg/kg) and ICI-198, 615 (0.03–0.3 mg/kg), on acetaldehyde-induced bronchoconstriction and BHR to inhaled methacho-line were examined using a modified Konzett-Rössler method in guinea pigs.Results Aeetaldehyde at 0.8mg/ml, which failed to induce significant changes in Pao (pressure at the airway opening), enhanced an increase in Pao induced by subsequent inhalations of ascending doses (50–200 μg/ml) of methacholine. suggesting a potentiating effect of acetaldehyde oti bronchial responsiveness. Although ONO-1078 had no inhibitory effect on bronchoconstriction caused by ascending doses (5.0–20 mg/ml) of acetaldehyde, ONO-1078 and ICI-198, 615 reduced the acetaldehyde-induced BHR.Conclusion Acetaldehyde causes BHR via LT release in guinea-pigs.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 52 (1997), S. 0 
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We describe a patient who presented with hypoxemia and diffuse bilateral pulmonary infiltrates. The diagnosis of eosinophilic pneumonia was confirmed by bronchoalveolar lavage and transbronchial lung biopsy. The remarkable characteristic was reappearance of the symptoms on the patient's return home, suggesting the existence of etiologic agents in his house. An environmental survey of the patient's house yielded Alternaria alternata. A high liter of anti-A alternata antibody (IgG) was detected in his serum, and the inhalation bronchoprovocation test with A. alternata antigen was positive. This case indicates that A. alternata is a probable cause of eosinophilic pneumonia.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...