Alveolar pharmacology

At the cellular level, eosinophils, mast cells, alveolar macrophages, lymphocytes and neutrophils recruited to the airways of asthmatics produce a variety of inflammatory mediators, such as histamine, kinins, neuropeptides, and leukotrienes, which lead to airway smooth muscle constriction and obstruction of airflow, and the perpetuation of airway inflammation [20, 21]. An understanding of the inflammatory processes and the molecular pathways of these mediators has led to the development and widespread use of several pharmacologic agents that mitigate airway inflammation and bronchoconstriction. 

Lung compliance in vivo Ciliary beat assays in vitro Mucus level assays in vitro Alveolar Type II cell surfactant secretion assay in vitro Pharmacological profiling — binding or functional assays at receptors, enzymes, ion channels, transporters... 

Clinical pharmacology Alpha-1 antitrypsin deficiency is a chronic, hereditary, usually fatal, autosomal recessive disorder in which a low concentration of alphai-proteinase inhibitor is associated with slowly progressive, severe, panacinar emphysema that most often manifests itself in the third to fourth decades of fife. The pathogenesis of development of emphysema in alpha-1 antitrypsin deficiency is believed to be due to a chronic biochemical imbalance between elastase and alphai-proteinase inhibitor (the principal inhibitor of neutrophil elastase), which is deficient in alpha-1 antitrypsin disease. As a result it is believed that alveolar structures are unprotected from chronic exposure to elastase released from a chronic low-level burden of neutrophils in the lower respiratory tract, resulting in progressive degradation... 

Kanapilly G. M. (1977) Alveolar microenvironment and its relationship to the retention and transport into the blood of aerosols deposited in the alveoli. Health Phys. 32, 89-100. Kawanishi S. (1995) Role of active oxygen species in metal-induced DNA damage. In Toxicology of Metals—Biochemical Aspects (eds. R. A. Goyer and M. G. Cherian). Handbook of Experimental Pharmacology, Springer, Berlin, vol. 115, pp. 349-372. 

The MAC is defined as the lowest alveolar anesthetic gas to air percentage that will yield pharmacologic effects. An anesthetic with a high MAC thus requires a large amount of anesthetic to induce anesthesia, while a drug with a low MAC requires a lower amount to yield the same effect. 

Zissel G, Ernst M, Schlaak M, et al. Pharmacological modulation of the IFNgamma-induced accessory function of alveolar macrophages and peripheral blood monocytes. Inflamm Res 1999 48(12) 662-668. 

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