Objective To investingate the ultrastructural changes of retinal pigment epithelium(RPE) and its permeability in spontaneously hypertensive rats(SHR)and explore the relation between these changes and hypertensive retinopathy.MethodsThe ultrastructure of RPE cells in the SHR aged five,six,seven months wasobserved with transmission electronmicroscope and compared to its normotensive control strain(WKY) with the same age.Then,lanthanum tracer procedures were carried out to investigate pathological changes of the blood-retinal barrier.Results (1)In SHR the main pathological changes involved swelling of mitochondria,enlargement of endoplasmic reticula,decrease of RPE cell infolding,and sparseness of microvilli.These degenerations were more serious in older rats with higher blood pressure.(2)The breakdown of outer blood-retinal barrier with permeation of lanthanum tracers were evident in SHR aged six or seven month,however,in WKY and five-month SHR the traces were prevented from passing by tight junctions.ConclusionThe degeneration of RPE owing to ischemia and anoxia arises in early periosd of hypertensive retinopathy.The pathological changes of ultrastructure and permeability might interact with the damage of visual cells and play a main role in the hypertensive retinopathy.
Objective To investigate the pathological spectrum of hypertensive retinopathy. Methods Systemic hypertension was produced experimentally in SD rats by partially constricting the right renal artery and removing the left kidney.The eyes obtained from hypertensive animals at 2 weeks,1,2,4months were examined by means of light microscopy,immunohistochemical staining,electron microscopy and histochemical electron microscopy and compared with the control group. Results 1.From 2 months after surgery,thickening of retinal capillary basement membrane(RBM)became apparent.2.From then on,RBM showed an increased staining reaction for type Ⅳcollagen and laminin,while staining reaction of RBM for fibronectin in hypertensive rats was negative at any stages.The number of anionic sites within the RBM was gradually reduced following the development of hypertension and it was definitely decreased at 4 months. 3.A few deteriorated endothelial cells were lifted focally from the RBM with subendothelial swelling in retinal vessels at 2 weeks,and the pericytes exhibited edema and deterioration at 4 months. Conclusions Detachment of the endothelial cells from the RBM,thickening of the RBM companied with the reduction of anionic sites and deterioration of pericytes may be responsible for hypertensive retinopathy. (Chin J Ocul Fundus Dis, 1999, 15: 163-166)
Hypertensive retinopathy (HR) often coexist with carotid lesions in hypertensive patients. Carotid lesions are closely associated with cardiovascular and cerebrovascular diseases, as well as end events, offering early important evidence to screening high risk patients. HR has significant value to predict target organ damage (TOD) of hypertension including carotid lesion. In addition, hypertensive retinopathy and carotid lesions-related ischemic ocular diseases will cause serious vision function damage. This article is going to summarize the value and correlation between hypertensive retinopathy and carotid lesions in terms of clinical manifestations, pathological physiological mechanism and target organ damage.