The basis of pulmonary edema, with emphasis on ultrastructure.
In the normal lung, a delicate interplay of physical forces and structural devices maintains the gas-exchanging membranes hydrated but unflooded. Liquids leaking from the alveolar capillaries are prevented from interfering with gas-exchange by a combination of mechanisms: the alveolar epithelium prevents easy access of liquids into the alveolar space; glycosoaminoglycan "sumps" in the thick portion of the septum bind excess liquid, thereby protecting the gas-exchanging thin portions of the alveolar-capillary barrier from water-logging; gradients of subatmospheric pressure promote the rapid transfer of liquids from the septal "sumps" into a compliant peribronchial space for further disposal by the lymphatic vessels. "Leaky" pulmonary and bronchial microvessels upset the osmotic forces in the interstitial space and interfere with the capacity of the lymphatic system to reabsorb liquids. Accumulation of excess liquids is limited initially to the interstitum. When the capacity of this space to bind liquids is overcome alveolar edema develops.
D000818:Animals; D001980:Bronchi / Q000648:ultrastructure; D001982:Bronchial Diseases / Q000473:pathology; D002199:Capillary Permeability; D006801:Humans; D008168:Lung / Q000378:metabolism / Q000503:physiopathology / Q000648:ultrastructure*; D011650:Pulmonary Alveoli / Q000648:ultrastructure; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology