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Histamine receptors and pulmonary epithelial permeability
British Journal of Diseases of the Chest
|July 1, 1987
Summary
Histamine and betahistine, but not impromidine, increased lung permeability and narrowed airways in normal and asthmatic subjects. These effects were blocked by an H1-receptor antagonist, confirming H1-receptor mediation.
Area of Science:
- Pulmonary Physiology
- Pharmacology
- Respiratory Medicine
Background:
- Histamine plays a role in respiratory responses.
- Understanding histamine receptor involvement in asthma is crucial.
Purpose of the Study:
- To compare the effects of histamine, betahistine (H1 agonist), and impromidine (H2 agonist) on lung permeability and airflow.
- To determine the histamine receptor subtype mediating these effects in normal and asthmatic subjects.
Main Methods:
- Inhaled histamine, betahistine, and impromidine were administered to normal and asthmatic subjects.
- Pulmonary epithelial permeability was assessed using 99mTc-DTPA lung-to-blood clearance (t1/2LB).
- Peak expiratory flow rate (PEFR) was measured. Terfenadine (H1 antagonist) and cimetidine (H2 antagonist) were used for pretreatment.
Main Results:
- Histamine and betahistine significantly reduced t1/2LB and PEFR in both groups.
- Impromidine had no significant effect on t1/2LB or PEFR.
- Terfenadine, but not cimetidine, blocked histamine-induced changes.
Conclusions:
- Histamine-induced increases in lung permeability and bronchoconstriction are mediated by H1-receptors.
- These findings apply to both normal and asthmatic individuals.