Beta agonists and ventilation.

This is the authors' abstract. We don't add key points for this paper.

Acute treatment with a high dose of f, agonist can cause an increase in oxygen uptake (Vo2), carbon dioxide out- put (Vco2), and ventilation of the order of 20-50%.1 In this issue of Thorax Amoroso et al5 describe a dose dependent increase in oxygen uptake and CO2 output with smaller doses of inhaled salbutamol (up to 1200 pg in 10 normal subjects). The changes were maximal at the time of the initial measurement five minutes after inhalation of salbutamol and the increase in CO2 output of about 30% was then greater than the increase in oxygen uptake. This caused an increase in the ratio of Vco2 toVo2 (the respiratory exchange ratio (R)) from 0-85 to 0 93. Output of CO2 subsequently fell more rapidly than oxygen uptake so that by 30 minutes the respiratory exchange ratio was marginally lower after salbutamol than after placebo. In a companion paper6 the group compared the change in Vo2 and Vco2 after 800 ,ug of salbutamol eight to 10 hours after completing 10 days of treatment with placebo or salbutamol (200 jug four times a day) in a crossover study. An acute increase inVo2 and Vco2 was seen after 800 ,ig salbutamol after 10 days of placebo but not after 10 days of regular salbutamol. These papers raise questions about the mechanisms underlying the change in oxygen uptake and CO2 output with the acute administration of a ,B agonist, the clinical relevance of the findings, and, once again, the question of tolerance or tachyphylaxis.