Vascular changes involved in pulmonary hemorrhage of stroke-prone spontaneously hypertensive rats.

The frequency of pulmonary hemorrhagic lesions in stroke-prone spontaneously hypertensive rats (SHRSP) was higher in older than in younger rats. Hemoglobin and protein contents in pulmonary lavage fluid which may indicate alveolar hemorrhage showed an increase with the progress of age, but the difference of hemorrhagic levels was much more in older rats than that of younger ones. A strong relationship between hemoglobin and protein contents of pulmonary lavage fluid was observed. Morphologically, the most striking feature was fibrinoid degeneration of the vascular walls in the center of hemorrhagic lesions of the lung, not only in the capillaries but also in small arteries. In the early stage of hemorrhage, endothelial discontinuity exhibited intraluminal fibrin deposits in this area of the vessels. Erythrocytes and polygonal deposits of fibrin could also be seen within the same vascular walls. In the advanced stage, subendothelial spaces and medial layers of vascular walls contained an electron-dense amorphous material which was consisted to be a degradation product of fibrinogen. The occurrence of this substance was thought to be induced by the hemodynamic effects of hypertension, the results of increased permeability and the accumulation of blood components. From these results, we suggest that fibrinoid degeneration due to abnormal cellular permeability associated with hypertension in SHRSP may be in some way linked to the development of pulmonary hemorrhage.