Bronkodilaation

Bronkodilaation, more commonly referred to as bronchodilation, is the widening of the airways in the lungs, including the bronchi and bronchioles. This widening reduces airway resistance and allows increased airflow to the alveoli.

Mechanism and physiology: Bronchodilation results from relaxation of airway smooth muscle. The autonomic nervous system regulates this process: sympathetic stimulation of β2-adrenergic receptors activates signaling pathways that relax smooth muscle, increasing airway diameter. Parasympathetic activity releases acetylcholine, which tends to constrict airways via muscarinic receptors. Local mediators can either promote relaxation (for example, nitric oxide) or constriction (such as histamine and leukotrienes). Inflammation can alter responsiveness, making airways more prone to constriction in diseases like asthma.

Pharmacology: Pharmacologic bronchodilators include inhaled β2-agonists (short-acting like albuterol/salbutamol for quick relief; long-acting such as salmeterol and formoterol for maintenance), anticholinergic agents (ipratropium, tiotropium), methylxanthines (theophylline), and phosphodiesterase inhibitors. Inhaled corticosteroids reduce airway inflammation and can improve overall bronchodilatory responsiveness. Combination inhalers pair corticosteroids with long-acting β2-agonists. Non-drug approaches to promote bronchodilation include physical conditioning and avoidance of triggers.

Clinical relevance: Bronchodilation is central to the management of obstructive airway diseases such as asthma and chronic obstructive pulmonary disease (COPD). Clinically, the bronchodilator response is assessed with spirometry by measuring changes in metrics like FEV1 after administration of a bronchodilator. Rescue inhalers provide immediate relief, while maintenance therapies aim to reduce symptoms and exacerbations.

See also: bronchodilators, bronchoconstriction, spirometry.