Asthma, allergen challenge and gas exchange.

Until the late 1960's there was a remarkable lack of information on the consequences of asthma on arterial oxygenation [1, 2). Since then, it has been known that arterial blood gas abnormalities can range from overt hypoxaemia, usually associated with hypocapnia and respiratory alkalosis, as shown in acute severe asthma, to mild increases in the alveolar-arterial 0 2 tension difference (AaPo,) alone, as seen in asymptomatic patients with mild-asthma [3). The identification of the features of gas exchange impairment and their impact on the guidelines for clinical management of the disease were progressively established during the 1970's [4, 5) . However, a full understanding of the underlying physiological mechanisms accounting for the abnormalities of arterial blood gases in asthma was only achieved after 1978 with the advent of early studies assessing the ventilation-perfusion (VA/0) ratio distributions in patients with asthma [6).