Editorial
Revisiting interactions between hypoxaemia and 
2
agonists in asthma
| The first 150 words of the full text of this article appear below. |
The excessive use of 
2 agonists has been
associated with increased asthma mortality, although this seems to be
due to confounding by disease severity rather than direct drug
toxicity.1 2 Dose-response studies in stable asthmatics
have shown the potential for high doses of salbutamol to produce direct
or indirect cardiovascular sequelae mediated by extrapulmonary
2 adrenoceptor stimulation including chronotropic and
inotropic activity, peripheral vasodilatation, electrocardiographic
changes, as well as hypokalaemia and hypomagnesaemia.3 4
The potential for cardiovascular toxicity with high doses of inhaled
2 agonists may be considered in the context of "the seed and the soil". In terms of the "seed", there are conflicting reports as to whether a full agonist such as fenoterol produces greater
dose related systemic 2 mediated systemic effects than a
partial agonist such as salbutamol in asthmatic patients when comparing
microgram equivalent doses with the same bronchodilator potency.4-6 In terms of the "soil" for salbutamol
mediated adverse effects, concomitant diuretic
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This article has been cited by other articles:
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Salpeter, S. R., Ormiston, T. M., Salpeter, E. E.
(2004). Cardiovascular Effects of {beta}-Agonists in Patients With Asthma and COPD: A Meta-Analysis. Chest
125: 2309-2321
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