Lung tissues of rats from two different age groups (2-12 and 16-26 months of age) were studied by both light and electron microscopy. Proliferation of granular pneumocytes in pulmonary alveolar lining was a frequent occurrence in older rats. Lungs of older rats showed not only an increase in number of granular pneumocytes, but also a remarkable increase of lamellar bodies and other forms of lipid vacuoles in individual granular pneumocytes. Spontaneously-occurring nodular lesions characterized by the accumulation of macrophages in the alveolar spaces were accompanied by desquamation and proliferation of granular pneumocytes. These lesions developed only in the lungs of rats older than l7 months of age. Such lessions in lungs of old rats were similar in many respects to desquamative interstitial pneumonitis of human lungs. Atrophy of alveolar walls and emphysematous areas seen in senile rats was characterized by irregular cytoplasmic breakdown of Type I alveolar lining epithelial cells. Obliteration of capillaries by spontaneously-occurring thrombus formation or a herniated cytoplasm of the septal cell and collagen fibers was considered to be a cause of atrophy of alveolar walk. Degeneration and actual breakdown of endothe1ial cytoplasm of puImonary capillaries enhanced herniation of the septal tissue. Vacuolar degeneration of epithelial cytoplasm was occasionally observed, but only in rats older than 20 months of age. The basement membrane of pulmonary alveolar walls was often thicker in old rats than in younger rats. Hyperplasia of granular pneumocytes invariably accompanied large septal cells, some of which contained many of the organelles found in granular pneumocytes.
Aging* ; Animal ; Female ; Macrophages/cytology* ; Male ; Pulmonary Alveoli/anatomy & histology* ; Pulmonary Alveoli/cytology ; Rats