Structural Changes of the Lungs During Pulmonary Senescence

The aged lung is characterised by airspace enlargement similar to, but not identical with acquired emphysema [4]. Such tissue damage is detected even in non-smokers above 50 years of age as the septa of the lung alveoli are destroyed and the enlarged alveolar structures result in a decreased surface for gas exchange [5 ] (Fig. 6.2). Tobacco smoking, pollution and hereditary factors are all involved in the regulation of emphysema making it difficult to separate the effect of accumulating environmental factors from the process of physiological ageing. Nevertheless, as total tissue mass and the number of capillaries decrease and formation of new alveoli becomes limited breathing difficulty is inevitable. Additional problems are that surfactant production decreases with age [6] increasing the effort needed to expand the lungs

Age-related changes of in the lung alveoli

Fig. 6.2 Age-related changes of in the lung alveoli. The aged lung is characterised by airspace enlargement as the septa of the lung alveoli are destroyed and the enlarged alveolar structures result in a decreased surface for gas exchange. Total lung tissue mass and the number of capillaries decrease with age and formation of new alveoli becomes limited. Additionally surfactant production decreases with age increasing the effort needed to expand the lungs during inhalation

during inhalation in the already reduced thoracic cavity volume where the weakened muscles are unable to thoroughly ventilate. It is therefore no wonder that the decline of lung capacity is detected with age even if no specific disease is diagnosed [7, 8].

As ageing is associated with respiratory muscle strength reduction, coughing becomes difficult making it progressively challenging to eliminate inhaled particles, pollens, microbes, etc. Additionally, ciliary beat frequency (CBF) slows down with age impairing the lungs’ first line of defence: mucociliary clearance [9] as the cilia can no longer repel invading microorganisms and particles. Consequently e.g. bacteria can more easily colonise the airways leading to infections that are frequent in the pulmonary tract of the older adult. In contrast to CBF, mucus production increases with age. Having mucus present in the airways intuitively appears to be beneficial as at baseline the mucus layer is needed to trap and eliminate inhaled particles and to prevent desiccation of airway surfaces. Mucus consists of an assortment of mucins and these high molecular-weight glycoproteins provide viscoelastic, gel-forming and some anti-microbial properties to mucus. Understandably, the precise mucin composition of the mucus is important and whether it changes with age would be of high interest. Currently, however, very little is known about this aspect of mucin secretion. Interestingly, some recent animal studies revealed that while the production of mucus increases with age the ability of bronchial and alveolar cells to effectively produce mucus upon stimuli declines in the older animal [10] making the lungs more vulnerable to environmental factors.

 
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