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At least 433 records · Page 24Linked to original sources
PubMed1985

Chest percussion and postural drainage in patients with bronchiectasis.

Patients with chronic obstructive pulmonary disease have been treated routinely with chest physical therapy for many years in spite of a lack of scientific validation of this procedure. Only recently have the indications for chest physical therapy been clarified. It is currently believed that such therapy is especially beneficial in patients with copious secretions, and that it is less effective in patients with scanty secretions. No study has specifically evaluated the efficacy of chest physical therapy in patients with bronchiectasis. We accordingly evaluated 13 patients with stable bronchiectasis to determine the effects of chest physical therapy on pulmonary function, arterial oxygenation, and sputum production and to assess whether this therapy was associated with any significant side-effects. We found that chest physical therapy was safe and well tolerated and assisted the patients in mobilization of their sputum. However, such therapy had no immediate delayed effects on pulmonary function or oxygen saturation.

Adult↗
PubMed1993

Effect of neonatal capsaicin treatment on neurogenic pulmonary edema from fluid-percussion brain injury in the adult rat.

The frequent occurrence of acute death from pulmonary failure in experimental head injury studies on Sprague-Dawley rats prompted an investigation into the manner in which acute neurogenic pulmonary edema develops in these animals as a result of an applied fluid pressure pulse to the cerebral hemispheres. Studies were performed in adult animals using histamine H1 and H2 blocking agents, or in adult animals treated as neonates with capsaicin to destroy unmyelinated C-fibers. Recordings were made of either the pulmonary arterial or the right ventricular pressure, and the left atrial and femoral arterial pressures before, during, and after injury to provide a record of the hemodynamic response throughout the development of neurogenic pulmonary edema. Head injury triggered the almost immediate development of pressure transients with and without neurogenic pulmonary edema. All rats, regardless of treatment, reacted with nearly identical systemic arterial pressure responses; however, the pulmonary responses followed a time course that was independent of systemic arterial pressure changes. Acute neurogenic pulmonary edema was always associated with a substantial increase in pulmonary arterial and left atrial pressures; conversely, pressure increases of similar magnitude were not always associated with edema. Histamine H1 and H2 blockers significantly reduced the pulmonary pressure surges only in rats free of neurogenic pulmonary edema. All capsaicin-treated rats showed suppressed pulmonary pressure responses, normal lung water content, elevated lung surface tension, and significantly reduced levels of immunoreactive substance P in the spinal cord and vagus nerve. While the pressures cannot clarify how edema influences the observed hemodynamics, they do not support the view that edema is the direct consequence of pulmonary hypertension. It is proposed that neurogenic pulmonary edema is a functional disturbance provoked by adverse stimuli from outside the lungs and that in the rat the primary afferent fiber is essential to the production of this entity.

Animals↗