Ten patients with status asthmaticus and respiratory or combined respiratory and metabolic acidosis were treated with a mixture of helium-oxygen (He-O2) in addition to the usual bronchodilator therapy and corticosteroids. A significant reversal of the acidosis was noted within the first 20 minutes, and no patient required subsequent intubation. The He-O2 mixture was started after the aerosolized and subcutaneous bronchodilators, but before intravenous corticosteroids and aminophylline had reached their peak effects. There were no untoward reactions and most of the patients sensed an immediate reduction in their dyspnea with the onset of He-O2 therapy. We conclude that He-O2 may be a useful adjunct to the usual medications employed in the treatment of status asthmaticus and may allow some patients to avoid intubation and mechanical ventilation.

In the rat model of lung injury induced by oleic acid (OA), we studied the effect of corticosteroid therapy on pulmonary inflammation and compliance at acute (1 day post OA) and recovery (3 and 7 days post OA) stages. Methylprednisolone (MP) and dexamethasone (DM) were examined for therapeutic benefit in this model. Histologic examination, lung compliance, and analysis of bronchoalveolar lavage (BAL) fluid were used to assess lung injury. Our results demonstrated that, at 1 day post OA, both steroids effectively reduced pulmonary inflammation and restored lung compliance when compared to animals that received only OA. In comparison to DM, MP was more effective in inhibiting the pulmonary inflammation induced by OA, but was less effective in restoring lung compliance. However, at 3 and 7 days post OA, cell and/or protein levels in BAL fluid from both MP- and DM-treated OA animals were significantly higher than levels observed in animals that received only OA. Lung compliance returned to normal by 3 days in animals that received only OA. This effect, however, was blocked in OA animals that were treated with either steroid, MP, or DM. Our data suggest that steroid therapy can be beneficial in the acute stage of OA-induced lung injury, but appears to be detrimental during the early recovery stage, perhaps by inhibiting the repair process.

No abstract