A pilot study of heated and humidified low flow oxygen therapy: An assessment in infants with mild and moderate bronchiolitis (HHOT AIR study).

BACKGROUND: Heated and humidified high flow nasal cannula oxygen therapy has been used in children with severe bronchiolitis. No data exists in children with mild to moderate bronchiolitis requiring lower flows of heated and humidified oxygen therapy. METHODS: We conducted a prospective, randomized pilot study of standard dry oxygen (control) versus heated and humidified low flow nasal cannula (HHLFNC), <4 liters per minute (LPM) oxygen, (treatment) in healthy children ≤24 months old with bronchiolitis. Clinical assessments were made using Respiratory Distress Assessment Instrument (RDAI), respiratory rate (RR), and oxygen saturation. RESULTS: Thirty-two children were enrolled (16 participants in each group). There was no significant difference in mean RDAI over time between groups. There was a significant difference in mean RDAI over time within control group, at hour 12, and treatment group, at hour 1, compared to baseline. RDAI in the treatment group was overall lower over time compared to control group. There was no significant difference in mean RR over time between or within groups, between mean length of stay and duration of oxygen requirement. Subgroup analyses showed lower RDAI in subjects that had RSV infection, male gender, and non-black race. CONCLUSIONS: The use of HHLFNC oxygen therapy may provide more comfort and may result in more rapid improvements in RDAI compared to standard dry oxygen therapy over time. HHFLNC is safe and well tolerated compared to standard dry oxygen. Larger studies are needed to assess the clinical efficacy of HHLFNC oxygen therapy.

Hypoxia upregulates lung microvascular neurokinin-1 receptor expression.

Subacute exposure to moderate hypoxia can promote pulmonary edema formation. The tachykinins, a family of proinflammatory neuropeptides, have been implicated in the pathogenesis of pulmonary edema in some settings, including the pulmonary vascular leak associated with exposure to hypoxia. The effects of hypoxia on tachykinin receptor and peptide expression in the lung, however, remain poorly understood. We hypothesized that subacute exposure to moderate hypoxia increases lung neurokinin-1 (NK-1) receptor expression as well as lung substance P levels. We tested this hypothesis by exposing weanling Sprague-Dawley rats to hypobaric hypoxia (barometric pressure 0.5 atm) for 0, 24, 48, or 72 h. Hypoxia led to time-dependent increases in lung NK-1 receptor mRNA expression and lung NK-1 receptor protein levels at 48 and 72 h of exposure (P < 0.05). Immunohistochemistry and in situ NK-1 receptor labeling with substance P-conjugated fluorescent nanocrystals demonstrated that hypoxia increased NK-1 expression primarily in the pulmonary microvasculature and in alveolar macrophages. Hypoxia also led to increases in lung substance P levels by 48 and 72 h (P < 0.05) but led to a decrease in preprotachykinin mRNA levels (P < 0.05). We conclude that subacute exposure to moderate hypoxia upregulates lung NK-1 receptor expression and lung substance P peptide levels primarily in the lung microvasculature. We speculate that this effect may contribute to the formation of pulmonary edema in the setting of regional or environmental hypoxia.