idence suggests that the cells also control endothelial proliferation. Together, the two cell types may coordinate "the maintenance of retinal capillary structure and function (Mandarino, 1992, p. 1893)."
In diabetic retinopathy, the retinal capillaries undergo both morphologic and functional alteration. Perhaps the earliest pathophysiologic change involves the loss of pericytes. Subsequent to this loss, the basement membrane thickens and a breakdown in capillary integrity occurs. These changes eventually lead to a dysfunctional ocular-blood barrier and increased permeability (Mames, 1994, p. 241). Such pathologic phenomena are thought to result from chronic metabolic injury. Basement membrane thickening may be caused by nonenzymatic glycosylation and increased cross-linking of extracellular matrix proteins. Further abnormalities may include increased platelet aggregability, decreased red cell deformability, and diminished blood flow. The retina responds to progressive ischemia by growing new capillaries. Existing endothelial cells migrate and proliferate to form new vascular lumens (Mames, 1994, p. 241). Such neovascularization may impair retinal function.
The natural progression of diabetic retinopathy involves five fundamental pathologic processes. It begins with the formation of retinal capillary microaneurysms. Excessive vascular permeability then results in leakage and retinal edema. Thirdly, vascular oc
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