The pulmonary vascular pathology of experimental radiation pneumonitis

Dogs exposed by inhalation to an aerosol of fused aluminosilicate particles containing the radionuclide yttrium 90 developed radiation pneumonitis. The aerosol had a mean aerodynamic diameter of 0.8 to 1.2 mu with a sigma(g) of 1.6 to 1.9. The 36 dogs included in this report received initial lung burdens of 590 to 5200 muCi (90)Y/kg body weight and died at 7.5 to 237 days after exposure with total cumulative radiation doses to lung of 9300 to 70,000 rads. Vascular lesions in the lungs were marked. Early changes included edema of vessel walls with leukocytic infiltration, dilation of perivascular lymphatic channels, and occasional periarterial lymphangiectasia. Splitting and reduplication of the elastica were occasionally visible. The most striking inflammatory vascular changes were vasculitis and fibrinoid necrosis, which involved bronchial and pulmonary vessels at some-what different times. Such lesions were often segmental and included fibrinoid necrosis and a variable leukocytic infiltrate in and around the actively involved lesions. Vasculitis was most commonly seen in small muscular arterioles, but veins and venules also occasionally exhibited similar inflammatory lesions. Progressive vascular inflammation led to extensive intimal proliferative lesions and fibromuscular hypertrophy with eventual fibrous accumulation around blood vessels, obliterative intimal and medial thickening, and luminal narrowing. Such changes eventually formed the morphologic basis for increased pulmonary vascular resistance and the development of cardiac dilation and hypertrophy reflecting pulmonary hypertension.