Samuel J Evans | PubMed Health

PubMed2003

Passive smoke effects on cough and airways in young guinea pigs: role of brainstem substance P.

Children raised with extended exposure to environmental tobacco smoke (ETS) experience increased cough and wheeze. This study was designed to determine whether extended ETS exposure enhances citric acid-induced cough and bronchoconstriction in young guinea pigs via a neurokinin-1 (NK-1) receptor mechanism at the first central synapse of lung afferent neurons, the nucleus tractus solitarius. Guinea pigs were exposed to ETS from 1 to 6 weeks of age. At 5 weeks of age, guide cannulae were implanted bilaterally in the medial nucleus tractus solitarius at a site that produced apnea in response to the glutamate agonist D,L-homocysteic acid. At 6 weeks of age, either vehicle or a NK-1 receptor antagonist, SR 140333, was injected into the nucleus tractus solitarius of the conscious guinea pigs who were then exposed to citric acid aerosol. ETS exposure significantly enhanced citric acid-induced cough by 56% and maximal Penh (a measure of airway obstruction) by 43%, effects that were attenuated by the NK-1 receptor antagonist in the nucleus tractus solitarius. We conclude that in young guinea pigs extended exposure to ETS increases citric acid-induced cough and bronchoconstriction in part by an NK-1 receptor mechanism in the nucleus tractus solitarius.

Aerosols↗

PubMed2003

Severe bronchiectasis.

Bronchiectasis is primarily the result of airway injury and remodeling attributable to recurrent or chronic inflammation and infection. The underlying etiologies include autoimmune diseases, severe infections, genetic abnormalities, and acquired disorders. Recurrent airway inflammation and infection may also be the result of allergic or immunodeficiency states such as allergic bronchopulmonary mycoses or HIV/AIDS. Bronchiectasis should be included in the differentiation diagnosis of any patient with chronic respiratory complaints such as cough and sputum production. Early clinical manifestations may be subtle. Hallmarks of severe bronchiectasis include fetid breath, chronic cough, and sputum production. The associated chronic respiratory infections and airway sepsis are punctuated by episodes of acute exacerbation. Prompt recognition and treatment of bronchiectasis may allow for prevention of disease progression and irreversible loss of lung function. This review of severe non-cystic fibrosis bronchiectasis describes the current pathophysiology, clinical presentations, and management of bronchiectasis. We review how impaired airway clearance and the inability to resolve infection and inflammation creates a vicious cycle of recurrent injury. The common clinical features of bronchiectasis and findings are presented and illustrated by radiographic images. The common species and significance of various organisms often recovered from the distal airways including: tuberculous and environmental mycobacteria, aspergillus, and bacteria such as Pseudomonas aeruginosa will be covered. Management strategies including sputum surveillance, sputum clearance, antimicrobial therapy including antifungal and antimyobacterial agents as well as the evidence for the use of inhalational and anti-inflammatory therapies such as corticosteroids are also discussed. Recommendations for the work-up and therapy of complications including hemoptysis and respiratory failure are presented.

Bronchiectasis↗