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POINT-COUNTERPOINT
e-mail: jerendot{at}adelphia.net
POINT: AIRWAY SMOOTH MUSCLE IS USEFUL
Some ideas just sit and stare at you. Here is one that has bothered me for a year or so. It is hard for me to regard smooth muscles as vestigial (3, 4) and they can not be solely mean-spirited, so they probably have useful function. With no library and no computer, I just fell back on Intelligent Design UnGoogled. And off I went job hunting on behalf of airway smooth muscles.
Do they manage the distribution of inspired gas? Apparently not. In normal breathing, the time constants of the pathways are so low that elasticity of the parenchyma does the job.
Do they influence mucus clearance? The airways are unique conduits. They transport gases and quasi-liquids side by side, the first by the distant pumping of the respiratory muscles; the second, by mucosa-based cilia forming a linear pump, not at a distance but right there along the way. The mucus layer is essentially two phases (1): a periciliary liquid layer (PCL) and a gellike phase, the two forming the airway surface layer (ASL). The PCL, where the cilia beat, lies against the airway wall and is confined by it. Its other side is covered by the gellike phase and it, in turn, by gas. So this luminal side is not physically confined at all. As a result, its volume within a single branch can occupy little space or fill it entirely. And here lies a hitch: the bronchial tree narrows in the direction of transport. If the density of ciliary forcing were the same at all points, the amount of the ASL leaving a given generation would be greater than the next generation can handle, and the ASL would pile up. This does not happen in healthy lungs so it must be that forcing increases progressively down the bronchial tree. (It should be discernible histologically in terms of ciliary density.) This would be an innate answer to the problem. But there is no place for airway smooth muscle action here, so I moved on.
Next I considered factors that influence ASL thickness; not the ones that produce it or modify its constituents, but short-term mechanical influences, which are more my line. During inspiration, the airways are expanded and lengthened, and the surface area of the mucus layer lining the airways is increased. As it is incompressible it must become thinner. Airway smooth muscle contraction would have an opposite effect: since the muscles wrap the airways geodesically (2), their contraction would have little effect on airway length, and this would be advantageous; smooth muscle would have no effect on lung volume per se. And smooth muscle action would be suited for stabilizing ASL thickness in the face of lung volume change. The fractional changes in ASL thickness are the same as the sum of the fractional changes of airway diameter and length. The PCL is a free-flowing portion of the ASL. It will change thickness along with the rest if it is not displaced in the process. Short-term displacements in health are unlikely.
I wondered how ASL thickness might be controlled. Isotropic volume change could be monitored by a few stretch receptors even down to lobular levels, but how to inform the smooth muscle? Why involve the nervous system at all? Let the airways themselves do the job. The goal is the PCL thickness, which yields maximal ciliary forcing, and there is a local solution to consider. Ciliary forcing must result in equal and opposite forcing of the parent mucosa, and there must be local distortion associated with the forcing. Let this be sensed and activate smooth muscle. The goal is the level of contraction that provides the optimal thickness for maximum ciliary forcing.
Where is the physiology in this? When are there maintained shifts in lung volume that need attention? I see them mainly as a matter of gravity. We humans unwittingly allow it to produce and maintain higher mean lung volume upright than recumbent. Side-to-side shifts while recumbent shift volume from the upper to the lower lung. The weight of the abdominal contents and the flexibility of the diaphragm are the agents in both instances. Astronauts and small animals are excluded.
A striking aspect of all of this, for me, is the notion that airway smooth muscle action in defense of ciliary effectiveness would be complete at the branch level. This bucket brigade would involve myriad buckets, each self-governed. If we are born that way, it is innateness crying for a fall. And one instance of this may be asthma, the mean-spirited action of airway smooth muscle revealed! Inspired allergens hit us not in gaseous form but as discrete items that land within airway branches indiscreetly—hit or miss—and, to shift the metaphor more, throw wrenches into the works. And here is what I have in mind. Airway smooth muscle contraction thickens the PCL and narrows the airway. The first effect optimizes ciliary function and is physiological. The second is potentially pathological. So it is good news and bad news, respectively, or negative feedback and positive feedback, or innateness and inanity, if you will. In health, the bad news is kept out of the way; the flow resistance of the airways peripheral to, say, the third generation of dichotomous bronchial branching is so low that a doubling of it would hardly be sensed. In an asthmatic attack, however, positive feedback is on display. Scattered obstruction of small airways hit by the allergen bullets necessitates tidal volume increases in the unobstructed regions if total ventilation is to be maintained. The attendant regional increase in average volume would get smooth muscle contraction underway, and there is no reason to expect that the process would be homogeneous. Regional increases in flow resistance would result in mean volume increases in other unobstructed regions if overall ventilation is maintained, and the process would be self-potentiating. It would slow down only as the tidal volumes of the unobstructed region approach elastic limits. Patient responses fit this story. Bronchodilators bring substantial but transient relief. The severe symptoms reflect abnormal functioning of normal lung. The slower and more lasting improvement with steroids allows the bullet-riddled regions that upset the innate apple cart to heal.
But back to physiology. After all, lungs do have nerves to account for, and in my job hunt, I have not needed them. Now, in a roundabout way, I have found a spot for them. Bronchial mucus clearance has two regimens: a ciliary realm in the periphery and a gas shearing realm centrally. The periphery realm is calm; the gentle breezes are too low to move much of anything. But ciliated surfaces are extensive, and the cilia can do the entire job. Mouthward, the ciliated surface area decreases as does the total cross-section. The first decreases ciliary effectiveness and the second increases the breeze and brings the gas shearing realm into action. During breathing, there are dynamic swings in airway transmural pressures that are maximal at the thoracic outlet and decrease up the tree. Airways are dynamically expanded during inspiration and dynamically compressed during expiration. Accordingly there are swings in flow velocities and attendant fluctuations in gas shearing: greater mouthward during expiration than in the opposite direction during inspiration, and the net movement would be mouthward. This effect would be greatest near the thoracic outlet and diminish up the tracheobronchial tree. Overall mucus clearance would combine a diminuendo of ciliary action overlapping a gas shearing crescendo, the latter providing percussive sforzandos during coughing. And with coughing, I can put airway smooth muscle back to work. Nerve-activated generational bronchoconstriction could influence mucus clearance during a cough in two major ways, by determining: 1) the location and extent of airway collapse and 2) the lung volume at which collapse occurs. Without smooth muscle action, cough effectiveness would be limited to the central airways at low lung volumes. With bronchoconstriction, a few generations out of the tree, dynamic compression mouthward would be more extensive and easier to produce (flow limitation can be velocity enhancing!).
My overall conclusion is that airway smooth muscle's utility is at least twofold; in both instances it assists mucus clearance.
REFERENCES
This article has been cited by other articles:
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  W. Mitzner A further comment on Point:Counterpoint "Airway smooth muscle is/is not useful" J Appl Physiol, March 1, 2008; 104(3): 902 - 902. [Full Text] [PDF]
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J. H. T. Bates How should airway smooth muscle be punished for causing asthma? J Appl Physiol, March 1, 2008; 104(3): 575 - 576. [Full Text] [PDF]
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 Y. Bosse, A. Sobieszek, P. D. Pare, and C. Y. Seow Length Adaptation of Airway Smooth Muscle Proceedings of the ATS, January 1, 2008; 5(1): 62 - 67. [Abstract] [Full Text] [PDF]
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L. E. Ford Comment on Point:Counterpoint: "Airway smooth muscle is/is not useful" J Appl Physiol, June 1, 2007; 102(6): 2407 - 2407. [Full Text] [PDF]
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