Information om | Engelska ordet BRONCHOCONSTRICTION

Exempel på hur man kan använda BRONCHOCONSTRICTION i en mening

• It is used to treat asthma, including asthma attacks and exercise-induced bronchoconstriction, as well as chronic obstructive pulmonary disease (COPD).
• Activation of H1 receptors mediates various responses, including smooth muscle contraction (leading to bronchoconstriction, intestinal cramping), increased vascular permeability (resulting in edema), and stimulation of sensory nerve endings (causing itching and pain).
• Chemoreceptors are responsible for signaling vasoconstriction, vasodilation, bronchoconstriction, and bronchodilation.
• Montelukast functions as a leukotriene receptor antagonist (cysteinyl leukotriene receptors) and consequently opposes the function of these inflammatory mediators; leukotrienes are produced by the immune system and serve to promote bronchoconstriction, inflammation, microvascular permeability, and mucus secretion in asthma and COPD.
• With emphysema the shortness of breath due to effective bronchoconstriction from excessive very thick mucus blockage (it is so thick that great difficulty is encountered in expelling it resulting in near exhaustion at times) can bring on panic attacks unless the individual expects this and has effectively learned pursed lip breathing to more quickly transfer oxygen to the blood via the damaged alveoli resulting from the disease.
• Damage to lower airways, air sacs, and lung tissue is due to an inflammatory cascade in response to the noxious chemicals which causes a variety of downstream effects such as increased secretions and exudative material thus clogging the airways and/or air sacs, collapse of air sacs (atelectasis), vascular permeability leading to pulmonary edema (fluid in the lungs), bronchoconstriction, activation of the coagulation cascade, and impaired function of the mucociliary escalator.
• EIB seems to be caused by the loss of water caused by increased ventilation, which may lead to the release of mediators such as histamine, prostaglandins, and leukotrienes, all of which cause bronchoconstriction.
• An antileukotriene, also known as leukotriene modifier and leukotriene receptor antagonist, is a medication which functions as a leukotriene-related enzyme inhibitor (arachidonate 5-lipoxygenase) or leukotriene receptor antagonist (cysteinyl leukotriene receptors) and consequently opposes the function of these inflammatory mediators; leukotrienes are produced by the immune system and serve to promote bronchoconstriction, inflammation, microvascular permeability, and mucus secretion in asthma and COPD.
• All three leukotrienes then bind at different affinities to two G-protein coupled receptors: CYSLTR1 and CYSLTR2, triggering pulmonary vasoconstriction and bronchoconstriction.
• When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur.
• Other symptoms include hyperemia of the conjunctiva, dimness of vision, rhinorrhea, bronchoconstriction, cough, fasciculation, anorexia, incontinence, eye changes, weakness, dyspnea, bronchospasm, hypotension or hypertension due to asphyxia, restlessness, anxiety, dizziness, drowsiness, tremor, ataxia, depression, confusion, neuropathy (rare), coma and death from depression of respiratory or cardiovascular systems.
• CysLTR1 activation by LTC4 and/or LTD4 in animal models and humans causes: airway bronchoconstriction and hyper-responsiveness to bronchoconstriction agents such as histamine; increased vascular permeability, edema, influx of eosinophils and neutrophils, smooth muscle proliferation, collagen deposition, and fibrosis in various tissue sites; and mucin secretion by goblet cells, goblet cell metaplasia, and epithelial cell hypertrophy in the membranes of the respiratory system.
• Cilomilast is a second-generation PDE4 inhibitor with anti-inflammatory effects that target bronchoconstriction, mucus hypersecretion, and airway remodeling associated with COPD.
• Actions on the parasympathetic nervous system, (the parasympathetic branch of the autonomic nervous system) may cause bradycardia, hypotension, hypersecretion, bronchoconstriction, GI tract hypermotility, and decrease intraocular pressure, increase lower esophageal sphincter (LES) tone.
• The post bronchodilator test (Post BD), also commonly referred to as a reversibility test, is a test that utilizes spirometry to assess possible reversibility of bronchoconstriction in diseases such as asthma.
• NSAIDs-exacerbated respiratory disease (NERD) is an acute (immediate to several hours) exacerbation of bronchoconstriction and other symptoms of asthma in individuals with a history of asthma and/or nasal congestion, rhinorrhea or other symptoms of rhinitis and sinusitis in individuals with a history of rhinosinusitis after ingestion of various NSAIDs, particularly those that act by inhibiting the COX-1 enzyme.
• β-2 adrenergic receptor agonists act as bronchodilators, having an effect of inducing bronchodilation to relieve bronchoconstriction; Inhaled corticosteroids act as anti-inflammatory drugs to decrease the inflammatory response.
• The accumulation of proinflammatory leukotrienes would overstimulate the cysteinyl leukotriene receptors in the respiratory system, leading to bronchoconstriction and the over-secretion of mucus, thus blocking the airway.
• PCLS derived from healthy and asthmatic lungs exhibit altered responses to various stimuli, including bronchoconstriction and hyperresponsiveness, which closely resemble those observed in patients and various animal models.
• This type of targeted therapy reduces the concentration of IgEs, which normally bind to allergens and cause the release of mast cell mediators and alarmins, promoting type 2 airway inflammation and bronchoconstriction.

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