The lung possesses a unique ability to handle large volumes of blood at a low pressure due to its dual circulation system. It is supplied with two separate blood sources: one for the uptake of oxygen and removal of carbon dioxide from the body (pulmonary circulation) and the other to provide oxygen to the lung tissue (bronchial circulation; Fig. 20.7).

The airway from the terminal bronchiole to the alveolus is illustrated in Figure 20.5. Notably, the terminal bronchiole lacks alveoli. Various major pulmonary diseases collectively referred to as obstructive pulmonary disease affect the conducting airways. These include asthma, bronchiolitis, chronic bronchitis, and cystic fibrosis. Obstruction of airflow in the airways is commonly caused by an increased amount of mucus, airway inflammation, and smooth muscle constriction.

Asthma, a chronic inflammatory disease of the large and small airways, is primarily mediated by lymphocytes and eosinophils. It is associated with increased mucus production and reversible constriction of the airways' smooth muscle (bronchospasm). Bronchiolitis, typically occurring in young infants, is caused by viruses, particularly respiratory syncytial virus.

Chronic bronchitis, often observed in smokers, is characterized by a marked increase in mucus-secreting cells in the airways and excessive mucus production. Cystic fibrosis, an autosomal recessive genetic disease, results from mutations in the Cl- ion channel of the cystic fibrosis transmembrane conductance regulator (CFTR). These mutations lead to a reduction in chloride and water secretion into the mucus covering the epithelial cells, increasing its viscosity. As a consequence, mucus accumulates and chronic pulmonary infections, primarily by Pseudomonas aeruginosa, occur.

It is worth noting that not all important obstructive lung diseases directly affect the airways. Emphysema, an irreversible obstructive lung disease commonly found in smokers, involves the progressive destruction of elastic tissues and loss of alveolar/capillary structure. The mechanisms behind tissue destruction remain unclear but may involve proteolytic enzymes and other toxic compounds present in cigarette smoke. Additionally, emphysema can also develop in non-smokers due to α1-antitrypsin deficiency, a genetic disorder characterized by an inability to regulate proteolytic enzymes, particularly elastase.
The circulation to the lung is unique in its duality and ability to accommodate large volumes of blood at low pressure. The lung has two separate blood supplies, one •Fig. 20.5 The Airway From the Terminal Bronchiole to the Alveo-lus. Notetheabsenceofalveoliintheterminalbronchiole.A,alveolus;RB,respiratorybronchiole;TB,terminalbronchiole.
Theconductingairwaysareinvolvedinseveralmajorpulmonarydiseasescollectivelyreferredtoasobstructive pulmonary disease, includingasthma,bronchiolitis,chronicbronchitis,andcysticfibrosis.Obstructionofairflowthroughtheairwaysiscommonlycausedbyincreasedamountsofmucus,airwayinflammation,andsmoothmuscleconstriction.Asthma isachronicinflammatorydiseaseofthelargeandsmallairways,mediatedpredominantlybylymphocytesandeosinophils,andisassociatedwithincreasedamountsofmucusintheairwaysandwithreversibleconstrictionoftheairwaysmoothmuscle(bronchospasm).Bronchiolitis isadiseaseofthebronchiolesthatusuallyoccurinyounginfantsandiscausedbyviruses,primarilyrespiratory syncytial virus. Chronic bronchitis, adiseasetypicallyofpeoplewhosmoke,isassociatedwithamarkedincreaseinmucus-secretingcellsintheairwaysandanincreaseinmucusproduction.Cystic fibrosis isanautosomalrecessivegeneticdiseasecausedbymutationsintheCl− ionchannelofthecysticfibrosistransmembraneconductanceregulator(CFTR).MutationsintheCFTR genecauseareductioninchlorideandwatersecretionintothemucusoverlyingtheepitheliacells,whichincreasestheviscosityofmucus.Thissituationresultsinmucusaccumulationandchronicpulmonaryinfections,primarilybyPseudomonas aeruginosa.
Notallimportantobstructivelungdiseasesinvolvetheairwaysdirectly.Emphysema isanirreversible,obstructivelungdiseasecommoninpeoplewhosmoke.Thepathogenesisinvolvesaprogressivedestructionoftheelastictissuesinthelungwithalossofalveolar/capillarystructure.Themechanismsoftissuedestructionareunclearbutmayinvolveproteolyticenzymesandothertoxiccompoundsincigarettesmoke.Emphysemaalsooccursinnonsmokingindividualswiththegeneticdisorderα1-antitrypsin deficiency, causedbytheinabilitytoregulateproteolyticenzymes,particularlyelastase.
for the uptake of O2 and removal of CO2 from the body (pulmonary circulation) and the other to supply O2 to lung tissue (bronchial circulation;
Fig. 20.7