Constriction of airways

Q2 COPD can be defined as a chronic, slowly progressive disorder characterized by airflow obstruction, which is not fully reversible and does not change significantly over several months. The major forms of COPD are chronic bronchitis and emphysema both conditions may be present in a patient. Although asthma is also an obstructive disorder, it is usually considered separately. The main difference between asthma and conditions now classified as COPD is the reversibility of bronchoconstriction in the former. In chronic bronchitis and emphysema, the constriction of airways cannot be fully reversed and obstruction progressively increases. 

The work-to-rest transition results in a decrease of the O2 consumption in cells, a rise in the blood O2 concentration, and consequent lowering of O2 diffusion from the lungs to the blood. As a result, [O2] outside the neuroepithelial cells rises, NADPH oxidase is activated, [H2O2] increases, channel opens, and serotonin is not released. The final event will be a decrease in the O2 supply to the body due to a constriction of airways [8]. 

Carbon dioxide is a rapid, potent stimulus to ventilation. Inhalation of 10% CO can produce minute volumes of 75 L/min in normal individuals. Carbon dioxide acts at multiple sites to stimulate ventilation. Elevated Pco causes bronchodilation, whereas hypocarbia causes constriction of airway smooth muscle these responses may play a role in matching pulmonary ventilation and perfusion. Circulatory effects of CO result from the combination of direct local effects and centrally mediated effects on the autonomic nervous system. The direct effects are diminished contractility of the heart and vascular smooth muscle (vasodilation). The indirect effects result from the capacity of CO to activate the sympathetic nervous system these indirect effects generally oppose the local effects ofCO. Thus, the balance of opposing local and sympathetic effects determines the total circulatory response to CO. The net effect of CO inhalation is an increase in cardiac output, heart rate, and blood pressure. In blood vessels, however, the direct vasodilating actions of carbon dioxide appear more important, and total peripheral resistance decreases when the Pco is increased CO also is a potent coronary vasodilator. Cardiac arrhythmias associated with increased Pco are due to the release of catecholamines. 

ASTHMA Periodic attacks of wheezing, chest tightness and breatlilessness resulting from constriction of the airways. 

Edema Edema is an abnormal accumulation of body fluid in tissues. An edema can be as trivial as a blister on your thumb, as life-threatening as a constriction of your airway. As in real estate, the three factors that determine the dangers associated with an edema are location, location, location. Exposure to toxic chemicals can cause a variety of edemas. Pulmonary edema (fluid in the lungs) is particularly dangerous, if not treated. Be sure to avoid inhalation of chemicals whenever possible and to use proper protective measures, as suggested on the MSDS (fume hoods, respirators, etc.). 

The placebo effect in asthma is one of the most well-studied and robust placebo effects on physiological function. The wheezing that sufferers of asthma experience is accompanied by a constriction of the bronchial airways that makes it difficult for them to breathe. Asthma medications dilate the bronchial tubes, making it easier to breathe, but a large number of studies have shown that placebos can also affect bronchial dilation. In fact, about two-thirds of the response to real asthma medication is also produced by placebo treatment, leaving about one-third of the effect as a true drug effect.40... 

At the cellular level, eosinophils, mast cells, alveolar macrophages, lymphocytes and neutrophils recruited to the airways of asthmatics produce a variety of inflammatory mediators, such as histamine, kinins, neuropeptides, and leukotrienes, which lead to airway smooth muscle constriction and obstruction of airflow, and the perpetuation of airway inflammation [20, 21]. An understanding of the inflammatory processes and the molecular pathways of these mediators has led to the development and widespread use of several pharmacologic agents that mitigate airway inflammation and bronchoconstriction. 

Ventilate the patient. There may be an increase in airway resistance due to constriction of the airway and the presence of secretions. If breathing is difficult, administer oxygen. As soon as possible administer of atropine alone or in combination with pralidoxime chloride (2-PAMC1) or other appropriate oxime. Diazepam may be required to prevent or control severe convulsions. If diazepam is not administered within 40-minutes postexposure, then its effectiveness at controlling seizures is minimal. 

Within 30 minutes of their administration, 6 -adrenergic drugs often reverse most of the functional deficit in Monday morning byssinotics. As there is no mucous secretion, airway smooth muscle contraction is considered the primary response. Exposure of man to histamine aerosols produces pulmonary function changes similar to those seen after exposure to dust extract. However, exposure to histamine aerosol invariably initiates constriction of smooth muscle more rapidly than exposure to cotton dust ( <15 minutes), and dissipates within minutes, while the acute effects of inhalation of cotton dust and dust extracts lasts for hours. The slowly developing and prolonged effects of dust and extracts suggest that mediators other than histamine are involved. 

Because the respiratory tract is an initial target of any air pollutant challenge, it usually receives primary attention in tests to determine irritant effects of exposure. Other aspects of interest include hematology, blood enzyme biochemistry, eye irritation, and p chomotor performance. Constriction of the large airways, maldistribution of ventilation due to narrowing in some small airways, constriction of peripheral lung units, and mechanical or gas diffusion impairment due to edema are possible effects of insult by pollutants. A variety of pulmonary tests is required to examine the possibilities. 

Short-term relief is thus most effectively achieved by agents that relax airway smooth muscle, of which B-adrenoceptor stimulants (see Chapter 9) are the most effective and most widely used. Theophylline, a methylxanthine drug, and antimuscarinic agents (see Chapter 8) are also used for reversal of airway constriction. 

Volatile irritants such as ammonia and chlorine initially cause constriction of the bronchioles. These two gases are water soluble, are absorbed in the aqueous secretions of the upper airways of the respiratory system, and may not cause permanent damage. Irritant damage may however lead to changes in permeability and edema, the accumulation of fluid. Some irritants such as arsenic compounds cause bronchitis. 

Bronchoconstriction Constriction of the smooth muscle in airways in the lungs due to exposure to irritant chemicals or to an immunological reaction involving release of inflammatory mediators. 

Asthma a respiratory condition associated with constriction of the airways. Atelectasis a condition when the lungs are collapsed with no air in the alveoli. Atheroma a fatty material deposited inside an artery. 

Biguanide a drug used in diabetes that reduces the level of glucose in the blood. Bronchoconstrictor a drug that causes constriction of the airways. Bronchodilator a drug that causes dilation of the airways. 

Bronchodilator A drug that relaxes the smooth muscles of the airways and relieves constriction of the bronchi... 

Wheezing Breathing with a rasp or whistling sound a sign of airway constriction or obstruction... 

Asthma is an obstructive lung disease that affects millions of Americans. Because it involves episodic constriction of small airways, bronchodilators such as albuterol (Figure 9.10) are used to treat symptoms by widening airways. Because asthma is also characterized by chronic inflammation, inhaled steroids that reduce inflammation are also commonly used. 

There are some indications that mammals possess at least two H2O2 sensors. One is located in cells of the lung neuroepithelial bodies, being responsible for constriction of the lung airways when the H2O2 level rises [6,7]. The other performs the same function in the blood vessels, being found in cells of the carotid body [8-10]. 

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