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Sympathomimetic enantiomers and asthma
D A Handley1, J R McCullough, S D Crowther
1Sepracor Inc., Marlborough, Massachusetts, USA.
Chirality
|March 21, 1998
Summary
Regular use of certain asthma medications can lead to airway hyperreactivity. This effect may be caused by drug distomers, not the active drug, potentially worsening asthma outcomes.
Area of Science:
- Pharmacology
- Respiratory Medicine
- Asthma Research
Background:
- Regular use of isoprenaline or beta 2-selective sympathomimetics can cause airway hyperresponsiveness in asthma patients.
- This hyperreactivity is not linked to vagal nerve activity or beta 2-adrenoceptor function.
- Existing research suggests drug distomers, not the active eutomer, may induce airway hyperreactivity.
Purpose of the Study:
- To investigate the role of sympathomimetic distomers in inducing airway hyperreactivity.
- To explore the mechanisms underlying drug-induced airway hyperresponsiveness in asthma.
Main Methods:
- Studies involved acute and regular exposure of animal models (guinea-pigs) and asthmatic patients to sympathomimetics.
- Evaluated airway reactivity to spasmogens after drug exposure.
- Assessed the influence of vagal section and beta 2-adrenoceptor antagonism on hyperreactivity.
Main Results:
- Exposure to S-isoprenaline, S-salbutamol, or S-terbutaline increased airway reactivity in guinea-pigs.
- S-isoprenaline or S-salbutamol exposure intensified asthma symptoms in patients.
- Regular exposure to racemic mixtures predisposed to hyperreactivity, which was acutely reversed by the eutomer.
Conclusions:
- Sympathomimetic distomers, not the active eutomers, may induce airway hyperreactivity.
- These distomer effects could contribute to increased morbidity and mortality in asthma patients.
- Further research into distomer pharmacology is crucial for asthma management.