Acid administered to rabbits by intrabronchial insufflation causes an immediate and extreme damage of the lung tissue. Within certain limits the degree and extent of the injury vary according to the concentration of the acid. With the greater concentrations death occurs promptly, almost immediately, and the lethal process has associated with it a decreased permeability of the pulmonary vessels. The latter fact has been confirmed by postmortem arterial injections. With weaker solutions the results, grossly and histologically, resemble those noted after influenzal pneumonia and gas poisoning. Thus, there is destruction of the epithelium of the bronchioles, the alveolar ducts, and the alveoli. The extent of the damage to the alveolar walls varies. Exudation occurs into the alveolar, interstitial, perivascular, and peribronchial tissues. Primarily this exudate is serous, but a rapid deposition of fibrin occurs, and later polymorphonuclear leucocytes and erythrocytes accumulate. In different animals, or in different portions of the same lung, there may be consolidations of different types, serofibrinous, hemorrhagic, or purulent, with or without destruction of the alveolar walls. Subsequent changes relate to the organization of the exudate, necrosis, proliferation of the epithelium in the alveoli and bronchi, and, finally, to the regeneration of the pulmonary parenchyma.

Experiments now in progress indicate that similar changes can be induced by various acids, both inorganic and organic. Experiments also show that similar changes are produced in other species of animals but that species differ in their resistance according to the acid and the concentration in which it is employed.

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