Bronkodilataation

Bronkodilatatsioon, or bronchodilatation, is the widening of the airways caused by relaxation of the smooth muscle in the walls of the bronchi and bronchioles. This leads to decreased airway resistance and easier air flow during breathing. Bronchodilatation can occur naturally in response to physiological stimuli such as exercise or autonomic nervous system activity, or be induced by medications.

The process is governed mainly by the autonomic nervous system. Activation of β2-adrenergic receptors on airway smooth muscle increases intracellular cyclic adenosine monophosphate (cAMP), promoting muscle relaxation and bronchodilatation. Conversely, stimulation of muscarinic receptors by acetylcholine promotes bronchoconstriction. Other mediators, such as leukotrienes and certain inflammatory cytokines, can influence tone and responsiveness of the airways, contributing to variability in bronchodilatation.

Clinically, bronchodilatation is a central goal in the treatment of obstructive airway diseases such as asthma and chronic obstructive pulmonary disease (COPD). Medications that induce bronchodilatation include inhaled β2-adrenergic agonists (short-acting like albuterol and long-acting like salmeterol or formoterol), anticholinergic agents (ipratropium, tiotropium), and, less commonly, methylxanthines (theophylline). Inhaled corticosteroids and other anti-inflammatory therapies are often used alongside bronchodilators to reduce airway inflammation and hyperresponsiveness.

Assessment of bronchodilatation commonly involves spirometry, measuring the bronchodilator response as an improvement in lung function (for example, an increase in FEV1 after inhalation of a bronchodilator). Side effects and risks vary by drug class and route of administration, but proper inhalation technique and individualized therapy help maximize benefit and minimize adverse effects.