PATHOLOGY OF EXPERIMENTAL PULMONARY BONE MARROW EMBOLISM

The author investigated the morphogenesis of pulmonary arteriosclerosis in rabbits at 2 days to 3 months after the infusion of sliced fresh allogeneic bone marrow (500 mg) into the marginal ear vein of 87 rabbits. After 2 to 7 days, granulation tissue was formed in the embolized bone marrow, and new endothelial cells appeared on the surface resulting in recanalization. By 2 weeks, embolized bone marrow developed into fibrous and fibro-fatty plaques in the arterial wall. Moreover, from 4 weeks on, smooth muscle cells and elastic fibers proliferated in the emboli just beneath the new endothelial lining. The intima of non-embolized small arteries showed circumferential fibroelastosis, as the result of arteritis and followed by proliferation of medial smooth muscle cells, with narrowing of vascular lumen. The medial smooth muscle cells play an important role in the morphogenesis of pulmonary arteriosclerosis in bone marrow embolism. Pulmonary arterial pressure gradually increased 1 month as well as 3 months after the infusion. It Is considered that narrowing of the vascular lumen resulted from post-embolic pulmonary arteriosclerosis may produce persistent pulmonary hypertension.