Lung
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Sneezing, cough, mucus secretion, and bronchoconstriction represent the main components of a coordinated and efficient reaction direct to expel or neutralize irritant agents from the respiratory system. A dense network of sensory nerves localized from the nose to the lower airways beneath the epithelium subserves this function. A variety of receptors and channels present in sensory nerve terminals by sensing irritant stimuli activate the system in emergence and initiate protective reflex responses, including cough. Previous and recent literature highlights the prominent role of some transient receptor potential (TRP) ion channels, and specifically the vanilloid 1 (TRPV1) and the ankyrin 1 (TRPA1) as sensors of airway irritation and initiators of the cough reflex.
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In healthy nonsmokers, inhalation of one single puff of cigarette smoke immediately evoked airway irritation and cough, which were either prevented or markedly diminished after premedication with hexamethonium. Single-fiber recording experiments performed in anesthetized animals showed that both C fibers and rapidly adapting receptors in the lungs and airways were stimulated by inhalation of one breath of cigarette smoke. Application of nicotine evoked an inward current and triggered depolarization and action potentials in a concentration-dependent manner in a subset of isolated vagal pulmonary sensory neurons. ⋯ In contrast to the observations in animal studies, both enhanced and diminished cough sensitivities to tussive agents have been reported in chronic smokers. This discrepancy is probably related to the history of chronic smoking of the individual smokers and the severity of existing airway inflammation and dysfunction. Furthermore, several other factors possibly contributing to the regulation of cough receptor sensitivity in chronic smokers should also be considered.
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Heart disease (HD) can stress the alveolar blood-gas barrier, resulting in parenchymal inflammation and remodeling. Patients with HD may therefore display any of the symptoms commonly attributed to primary pulmonary disease, although tissue documentation of corresponding changes through surgical lung biopsy (SLB) is rarely done. Intent on exploring the basis of HD-related alveolar-capillary barrier dysfunction, a retrospective analysis of SLB histopathology was conducted in patients with clinically diagnosed HD, diffuse pulmonary infiltrates, and no evidence of primary pulmonary disease. ⋯ Based on observed alveolar-capillary barrier (ACB) alterations, three main morphologic groups emerged: one group (6 patients) with alveolar edema; a second group (11 patients) characterized by pulmonary congestion; and a final group (6 patients) showing microscopic foci of acute ACB lung injury. Alveolar-capillary stress due to acute high-pressure or volume overload often manifests as diffuse pulmonary infiltrates with variable but generally predictable histopathology. In patients with biopsy-proven alveolar edema, pulmonary congestion, or acute microscopic lung injury, the clinician must be alert for the possibility of primary heart disease, particularly if the patient is elderly or when a history of myocardial, valvular, or coronary vascular disease exists.
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Comparative Study
Transthoracic sonography in comparison to multislice computed tomography in detection of peripheral pulmonary embolism.
The aim of the study was to compare transthoracic sonography (TS) with multislice computed tomography (MSCT) in the detection of peripheral pulmonary embolism (PE). In addition, the study verified peripheral parenchymal findings visualized by TS and MSCT. A total of 33 patients (16 females, 17 males; mean age = 65.4 years) with symptoms of suspected PE were enrolled in the study. ⋯ Furthermore, the study revealed that PE is often associated with peripheral parenchymal changes, both of which are detectable by TS and MSCT. In case of contraindication with MSCT, TS is a potential technique for diagnosing PE-related parenchymal findings and can serve as an alternative method in the diagnosis of PE. However, a negative result with TS does not rule out a PE.
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Cough is a defense mechanism for promoting airway hygiene when mucociliary clearance is ineffective due to increased mucus secretion, inflammation, infection, or ciliary dysfunction. Secretions can contribute to airflow limitation and chronic hypersecretion can worsen airway inflammation with retained inflammatory cells and mediators. The focus of the Second Annual Cough Conference has been on cough as a troublesome symptom; but to understand the importance and effectiveness of cough clearance, it is critical to understand airway secretions. The biophysical properties of mucus and phlegm determine how readily these secretions can be cleared by coughing.