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The accessory muscles of inspiration are the sternocleidomastoid and scalene muscles. These muscles are not associated with the other options.
The respiratory center is made up of several groups of neurons located bilaterally in the brainstem: the DRG, the VRG, the pneumotaxic center, and the apneustic center. Of the options available, only the DRG group in the medulla oblongata receives afferent impulses in the situation described.
Surfactant, a lipoprotein produced by type II alveolar cells, has a detergent-like effect that separates the liquid molecules, thereby decreasing alveolar surface tension. This selection is the only option that accurately describes the mechanism that allows surfactant to facilitate alveolar distention and ventilation.
The right mainstem bronchus extends from the trachea more vertically than the left mainstem bronchus; therefore aspirated fluids or foreign particles tend to enter the right lung rather than the left. The size of both mainstems is equal. The trachea comes into contact with food and drink first, and the carina is the site where the bronchi bifurcate.
Two major types of epithelial cells appear in the alveolus. Type I alveolar cells provide structure, and type II alveolar cells secrete surfactant, a lipoprotein that coats the inner surface of the alveolus and facilitates its expansion during inspiration, lowers alveolar surface tension at end-expiration, and thereby prevents lung collapse. Neither alveolar macrophages nor stretch receptors secrete surfactant.
Tiny passages called pores of Kohn permit some air to pass through the septa from alveolus to alveolus, promoting collateral ventilation and even distribution of air among the alveoli. This selection is the only option that accurately describes the function that allows air passage among alveoli.
Pressure in the pleural space is usually negative or subatmospheric (−4 to −10 mm Hg). This selection is the only option that accurately describes pleural space pressure.
Muscarinic receptors play a double role in airway disorders, mediating an increase in mucus secretion, as well as constriction of smooth muscle. Cholinergic activity of the lung is more pronounced in large than in peripheral airways; in the nose parasympathetic stimulation leads to hypersecretion and vasodilation. This article reviews the differences in muscarinic subreceptors in the upper and lower airways and discusses the effectiveness of anticholinergic agents in blocking parasympathetic stimulation at these sites. (J ALLERGY C LIN I MMUNOL 1995;95:1065-8.)
19, 20, 21 The nasal mucosa is capable of a limited repertoire of responses: congestion (induced by vasodilation, vascular permeability, and sinusoidal pooling), sneezing and itching (induced by sensory nerve stimulation), and secretion of mucus derived both from glandular cells and vascular permeability. Both nasal secretion and vasomotor tone are under parasympathetic regulation. The ability of atropine to block both hypersecretion and vasodilation induced by parasympathetic stimulation suggests that these actions are mediated through cholinergic muscarinic receptors. 22, 23, 24, 25, 26, 27, 28
Muscarinic antagonists have proved useful in the treatment of obstructive respiratory disorders and various forms of rhinitis. In this review the role of muscarinic receptors and their antagonists in human airway disease will be discussed.
Airway smooth muscle (ASM) is the primary effector cell responsible for controlling airway caliber and thus the resistance to airflow of the entire tracheobronchial tree. The autonomic nervous system is the principal regulator of the ASM tone and consists of three separate neural pathways. First, parasympathetic (vagal) innervation ...
Thus in these airways, airway circumference and stiffness is regulated primarily by the smooth muscle tissue. The constriction of the airway smooth muscle in the smaller bronchi and bronchioles can result in airway closure and obstruction of the airway lumen, completely blocking airflow, as occurs in asthma (7).
The majority of mitogens identified fall into two broad categories: polypeptide growth factors that activate receptors with intrinsic protein tyrosine kinase activity and those that act through receptors coupled to heterotrimeric G-proteins, which includes the thromboxanes, acetylcholine, endothelin-1, leukotriene D 4, and inflammatory cell-derived proteases. Many of these are co-mitogens that synergize with polypeptide growth factors to promote accelerated growth in vitro. Major effector signaling pathways include activation of phosphoinositide 3-kinase and extracellular signal-regulated kinase as well as NADPH oxidase pathways ( Figure 4 ). Phosphoinositide 3′-kinase activation may also be important in airway smooth muscle hypertrophic changes. Initial reports suggest that airway smooth muscle cells cultured from asthmatics have an increased ability to proliferate, and that the altered composition of the airway wall extracellular matrix environment that predominates in asthma amplifies growth while impairing the antiproliferative effect of glucocorticoids. These observations may provide a mechanism for steroid-resistant asthma and may inform the design of future therapies that target airway smooth muscle accumulation in lung disease.
In the canine trachea, the ASM cell is elongated and spindle shaped, and measures about 250 μm long and 3–5 μm wide on average at the level of the nucleus ( Stephens, 2002 ).
In addition to these calcium-dependent pathways, other partially independent-Ca 2+ pathways are differentially regulated in asthma-derived ASM that requires activation of Rho kinase (ROCK). A target of ROCK, MLC phosphatase target subunit 1 (MYPT1), is phosphorylated following contractile agonist stimulation and/or after exposure to inflammatory mediators. Activation of MYPT1 prevents dephosphorylation of MLC and thus promotes persistent actin-myosin crossbridge engagement and ASM shortening. In severe asthma-derived ASM, ROCK activity was higher than that found in non-asthma-derived ASM from age- and gender-matched controls. Collectively, these studies suggest that intrinsically asthma-derived ASM manifest a phenotype of differential E-C coupling that ultimately manifest as a hyper contractile state at baseline and after agonist stimulation.
Bronchoconstriction is an important component of the airway defense reflexes elicited by inhaled irritants. Three subtypes of vagal bronchopulmonary afferents function as the primary sensors of inhaled irritants: C-fiber afferents (tachykinin-containing afferents), rapidly adapting pulmonary receptors, and laryngeal afferents.
The contraction of the smooth muscle in the alveolar ducts and small airways can markedly influence the distensibility of the lungs; thus changes in bronchomotor tone might influence ventilation distribution by locally modulating lung compliance, thus improving the homogeneity of lung expansion. An additional mechanism by which airway smooth muscle ...