Bronchoconstriction/bronchospasm

Adverse reactions may include stomatitis nausea vomiting fever rhinorrhea drowsiness clamminess chest tightness bronchoconstriction bronchospasm irritation to the tracheal and bronchial tracts. 

Ipratropium (Atrovent) Muscarinic antagonist. Reverses acetyichoiine -induced bronchoconstriction. Bronchospasm associated with COPD in aduits. Few systemic anticholinergic side effects because it is a quaternery ammonium compound which crosses into systemic circulation poorly. 

Asthma is a reversible obstructive disease of the lower airway. With asthma there is increasing airway obstruction caused by bronchospasm and bronchoconstriction, inflammation and edema of the lining of the bronchioles, and the production of thick mucus that can plug the airway (see Pig. 37-1). There are three types of asthma ... 

Adrenaline (epinephrine) is a sympathomimetic agent that causes bronchodilatation. It is used to relieve bronchospasm in anaphylactic shock reactions. Histamine, kinins and prostaglandins, such as prostaglandin E2, are inflammatory mediators. In response to allergic stimuli, inflammatory mediators may cause bronchoconstrictions. Guaifenesin is an expectorant preparation that increases bronchial secretions to promote the expulsion of the mucus coughed up. 

Cromones such as cromolyn sodium (Intal, Nasal-crom) and nedocromil sodium (Tilade) can help prevent bronchospasm in people with asthma. These drugs are not bronchodilators and will not reverse bronchoconstriction during an asthmatic attack. Hence, these agents must be taken prior to the onset of bronchoconstriction, and they must typically be administered prophylactically to prevent asthma attacks that are initiated by specific, well-defined activities (e.g., exercise, exposure to a friend s pet, pollen).107 Likewise, the regular use of these drugs several times each day for several months may decrease airway hyperresponsiveness so that the incidence of asthmatic attacks decreases.102,113... 

Aspirin, cyclooxygenase, and the provocation of asthma A few people with asthma suffer from a unique syndrome in which the ingestion of 40 to 300 mg of aspirin produces rhinorrhea and acute bronchoconstriction. All cyclooxygenase inhibitors will precipitate bronchospasm in patients with aspirin-evoked asthma. 

Whatever the mechanisms responsible for bronchial hyperreactivity, bronchoconstriction itself seems to result not simply from the direct effect of the released mediators but also from their activation of neural or humoral pathways. Evidence for the importance of neural pathways stems largely from studies of laboratory animals. Thus, the bronchospasm provoked in dogs by histamine can be greatly reduced by pretreatment with an inhaled topical anesthetic agent, by transection of the vagus nerves, and by pretreatment with atropine. Studies of asthmatic humans, however, have shown that treatment with atropine causes only a reduction in—not abolition of—the... 

Cough, dyspnea, wheezing, edema, bronchospasms, bronchoconstrictions, tightness, excessive bronchial secretions... 

In children, capsaicin spray was demonstrated to cause a severe bronchospasm and pulmonary edema (Winograd, 1977 Bdlmire et al, 1996). In the Billmire study, a 4-week-old infant was exposed to 5% pepper spray after discharge from a self-defense device. The infant suffered respiratory failure and hypoxemia, requiring immediate extracorporeal membrane oxygenation. Inhaled capsaicin causes an immediate increase in airway resistance (Fuller, 1991). This dose-dependent bronchoconstriction after capsaicin inhalation in humans is the same as that demonstrated in asthmatics and smokers (Fuller et al, 1985). The capsaicin-induced bronchoconstriction and release of substance P is due to stimulation of nonmyelinated afferent C-fibers. 

The parasympathetic division is the dominant portion of the pulmonary autonomic nervous system in all mammals. Airway smooth muscle is richly supplied with muscarinic receptors and stimulation of M3 receptors results in smooth muscle contraction and bronchoconstriction. Cholinergic stimulation is the primary mechanism of bronchospasm in horses with recurrent airway obstruction (Robinson et al 1996). Parasympathetic innervation can be demonstrated throughout the tracheobronchial tree of the horse but smooth muscle contraction evoked by stimulation of cholinergic nerves is more pronounced in the trachea than in the smaller bronchi. It is expected that parasympathetic blockade with a muscarinic antagonist will have the greatest effect in large, central airways. 

Asthma is defined clinically by recurrent episodes of airway obstruction that reverse either spontaneously or with bronchodilator therapy. The airway obstruction is accompanied by increase in airway resistance due to bronchospasm, inflammation, and excessive mucus production. Bronchoconstriction, airway closure, and gas trapping may eventually lead to respiratory failure. Hyperresponsiveness is considered a hallmark of asthma, making these individuals uniquely sensitive to exposure to airborne chemicals such as isocyanates. 

Acute asthma is a reactive airway disease (RAD) occurring when extrinsic (environmental) or intrinsic (internal) allergens stimulate bronchoconstriction, causing bronchospasms that result in wheezing and difficulty breathing. 

Inflammatory disease associated with bronchial hyperactivity (BHR), bronchospasm, T mucus secretion, edema, and cellular infiltration. Early asthmatic responses (EAR) lasting from 30 to 60 min are associated with bronchospasm from the actions of released histamine and leukotrienes late asthmatic responses (LAR) involve infiltration of eosinophils and lymphocytes into airways - > bronchoconstriction and inflammation with mucus plugging. 

Respiratory Bronchorrhea, rhinitis, pulmonary edema, chest tightness, wheezing, bronchoconstriction, cough, dyspnea, bronchospasms Cardiovascular Same if chronically exposed... 

EXTRAVASCULAR SMOOTH MUSCLE Histamine stimulates or, more rarely, relaxes various extravascular smooth muscles. Contraction is due to activation of H j receptors (linked to and Ca + mobilization) relaxation (for the most part) is due to activation of Hj receptors. Minute doses of histamine will evoke intense bronchoconstriction in patients with bronchial asthma and certain other pulmonary diseases. Although the spasmogenic influence of Hj receptors is dominant in bronchial muscle, receptors with dilator function also are present. Thus, histamine-induced bronchospasm is potentiated slightly by blockade. 

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