Abstract
The purpose of this investigation was to ascertain whether nitric oxide (NO) released into the circulation by a noninvasive technology called whole body periodic acceleration (WBPA) could increase mucociliary clearance (MCC). It was based on observations by others that nitric oxide donor drugs increase ciliary beat frequency of nasal epithelium without increasing mucociliary clearance. Tracheal mucous velocity (TMV), a reflection of MCC, was measured in sheep after 1-hour treatment of WBPA and repeated after pretreatment with the NO synthase inhibitor, L-NAME to demonstrated action of NO. Aerosolized human neutrophil elastase (HNE) was administered to sheep to suppress TMV as might occur in cystic fibrosis and other inflammatory lung diseases. WBPA increased TMV to a peak of 136% of baseline 1h after intervention, an effect blocked by L-NAME. HNE reduced TMV to 55% of baseline but slowing was reversed by WBPA, protection lost in the presence of L-NAME. NO released into the circulation from eNOS by WBPA can acutely access airway epithelium for improving MCC slowed in cystic fibrosis and other inflammatory lung diseases as a means of enhancing host defense against pathogens.
Highlights
Airway inflammation occurs in asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF)
Evidence supporting this comes from clinical observations impaired mucociliary clearance (MCC) during exacerbations of asthma [1, 2], COPD [3] and CF [4] as well as experimental data that inhaled inflammatory mediators, such as neutrophil elastase slows whole lung MCC and tracheal mucus velocity (TMV). [5, 6] TMV reflects changes in whole lung clearance measured with radiolabeled human serum albumin [7, 8] Effective mucus transport depends on the coordinated relationship among ciliated surface epithelium, the mucous layer, and the periciliary fluid
Within 0.5h after stopping whole body periodic acceleration (WBPA), TMV increased to 114 ± 4% above baseline and TMV continued to increase to a maximum of 136 ± 9% 1h after treatment
Summary
Airway inflammation occurs in asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF). Inflammation is most commonly linked to bronchoconstriction and airway hyper-responsiveness, mucociliary clearance (MCC) may be diminished. Evidence supporting this comes from clinical observations impaired MCC during exacerbations of asthma [1, 2], COPD [3] and CF [4] as well as experimental data that inhaled inflammatory mediators, such as neutrophil elastase slows whole lung MCC and tracheal mucus velocity (TMV). [5, 6] TMV reflects changes in whole lung clearance measured with radiolabeled human serum albumin [7, 8] Effective mucus transport depends on the coordinated relationship among ciliated surface epithelium, the mucous (gel) layer, and the periciliary fluid (sol). Evidence supporting this comes from clinical observations impaired MCC during exacerbations of asthma [1, 2], COPD [3] and CF [4] as well as experimental data that inhaled inflammatory mediators, such as neutrophil elastase slows whole lung MCC and tracheal mucus velocity (TMV). [5, 6] TMV reflects changes in whole lung clearance measured with radiolabeled human serum albumin [7, 8] Effective mucus transport depends on the coordinated relationship among ciliated surface epithelium, the mucous (gel) layer, and the periciliary fluid (sol)
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