Clinics in chest medicine
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Clinics in chest medicine · Jun 1986
ReviewAbnormal respiratory epithelial ion transport in cystic fibrosis.
The respiratory epithelium of cystic fibrosis patients exhibits excessive sodium (and volume) absorption and an absence of chloride (and volume) secretion in response to usual stimuli. These abnormalities likely contribute to the pathophysiology of cystic fibrosis lung disease, and provide a rationale for a novel therapeutic approach to this problem.
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The afferent activity originating from the larynx shows a considerable respiratory modulation. Receptors responding to pressure changes, inspiratory airflow (cold), and laryngeal movements have been identified. In addition, other receptors without a respiratory modulation are also described. Possible reflex effects of these receptors on breathing pattern, upper airway patency, and defense mechanisms in both adults and newborns are discussed.
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Neurogenic pulmonary edema is an anomaly because it cannot be categorized into either of the two major types of pulmonary edema. Both high-pressure and increased-permeability abnormalities may be involved in the pathogenesis of neurogenic pulmonary edema. Furthermore, the mechanisms responsible for these abnormalities appear quite complex. ⋯ Although the high-pressure and increased-permeability abnormalities seem to develop through separate mechanisms, their combined effect is probably synergistic on the accumulation of extravascular lung water. The neurologic pathways responsible for initiating neurogenic pulmonary edema remains a mystery. Despite the questions and uncertainties still surrounding neurogenic pulmonary edema, the substantial progress made in understanding the clinical expression, incidence, and pathogenesis of this syndrome does provide a framework for a reasonable approach to its clinical management.
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Pleural effusions are a common clinical problem, yet the mechanisms of pleural fluid formation have only recently been investigated. In this article, the anatomy and physiology of the normal pleural space is discussed, as well as the pathophysiology of pleural effusion formation.
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Clinics in chest medicine · Sep 1985
ReviewUltrastructural abnormalities in increased-permeability pulmonary edema.
A general clinical impression is that increased microvascular permeability following acute lung injury always leads to pulmonary edema. The ARDS is a final pathway of acute lung injury. A number of agents may initiate acute lung injury, either directly or indirectly, via cellular and humoral mediators. ⋯ Thus pathologic examination often reveals little about the exact underlying etiology of the lung injury. This situation has minimized the diagnostic value of lung biopsies in clinical cases of increased-permeability pulmonary edema. Nonetheless, the pathologic information has been, and will continue to be, invaluable to understanding the structural and functional relationships present in experimental models of increased-permeability pulmonary edema.