This chapter focuses on airway blood flow (Qaw) in asthma and chronic obstructive pulmonary disease (COPD), with a brief discussion of the normal airway circulation as background. Since the blood circulation typically participates in inflammatory processes at the tissue level, the vasculature of the tracheobronchial tree can be expected to undergo structural and functional changes in asthma and COPD, conditions that are associated with airway inflammation. There are distinct differences in the vascular abnormalities between asthma and COPD. The purpose of this chapter is to review the pathophysiological role of the tracheobronchial circulation in asthma and COPD and the vascular effects of pharmacologic interventions. The airway circulation, which derives its blood from the systemic circulation, is the principal vascular supply to the airway wall. Bronchial arteries usually arise from the aorta or intercostal arteries and form a peribronchial plexus surrounding the bronchial wall. Under physiological conditions, total bronchial blood flow comprises 0.5-1% of cardiac output. The major part of blood flow is distributed to the subepithelial tissues where the microvasculature comprises 10-20% of tissue volume. Subepithelial blood flow (Qaw) has been reported to range between 30 and 95 ml min-1 100 g wet tissue-1 in different species including in humans. Allergic and non-allergic inflammation is considered a major factor in the vascular changes that have been associated with asthma. The inflammatory mechanisms include the complex actions of inflammatory cells and mediators, neurotransmitters, and neuropeptides on vascular endothelial and smooth muscle cells. The main vascular manifestations are hyperemia, hyperpermeability, and edema formation.
|Original language||English (US)|
|Title of host publication||Asthma and COPD|
|Number of pages||8|
|State||Published - Dec 1 2009|
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