Ultrastructrual studies on choroidal vessels in streptozotocin-diabetic and spontaneously hypertensive rats.

Seven spontaneously hypertensive rats (SHR) and 14 Wistar inbred Kyoto strain rats (WKR) were used. Seven WKR were made diabetic by a single intravenous injection of streptozotocin (50 mg/kg body weight); the seven untreated WKR served as controls. The choroidal vessels of all rats were observed by electron microscopy after 12 months. The choroidal capillaries of control rats showed focal accumulation of basement (BM) in the subendothelial space. Two distinct types of BM lesions were noted: homogeneous thickening and sparse, interlacing branches, or ramifications, of BM. Increased BM caused indentations in the vascular wall. In diabetic rats, BM of capillaries, small arteries, and small veins showed arabesque ramification of BM which represented advanced forms of the sparse, interlacing ramifications seen in normal controls. Contiguous lesions of ramified BM, separated by narrow cytoplasmic processes projecting from the endothelial cells, resembled a scalloped border. In hypertensive rats, the arabesque ramifications were most conspicuous in the small veins. Homogeneous thickening of BM was noted in choroidal capillaries, small arteries, and small veins of SHR, although ramified BM was seen adjacent to it. Endothelial cell proliferation was seen in the small arteries of diabetic and hypertensive rats. The cytoplasm of endothelial cells at the lesion of proliferation was broadened, and cell nuclei appeared cubic or spherical. Consequently, the arterial lumina were narrowed. Complete occlusion was seldom seen in the choroidal arteries of diabetic rats, but it was observed in small arteries of SHR, accompanited by hypertrophy of medial smooth muscle cells and endothelial proliferation. Basement membrane accumulation and endothelial proliferation were common to both groups of rats, but the overall effect of pathological changes was more profound in hyptertension than in diabetes.