Pathogenesis of hypertensive retinopathy. An experimental study in the monkey.

Garner, A; Ashton, Norman; Tripathi, Ramesh C.; Kohner, Eva M.; Bulpitt, C. J.; Dollery, C. T.

doi:10.1136/bjo.59.1.3

Cited by 134 publications

(76 citation statements)

References 31 publications

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“…If blood pressure further increases, then fibrinoid necrosis of the muscle cells in the arteriolar wall can occur at localized vulnerable points, possibly through the breakdown of the blood-retina barrier, allowing insudation of plasma into the vessel wall and deposition of fibrin. 26 Therefore, an alternative interpretation of our findings may be that some of the arteriolar wall signs, such as focal arteriolar narrowing, could be secondary to acute blood pressure elevation or to a more recent, further elevation of blood pressure in patients with ICH. Patients with deep ICH had significantly higher admission blood pressure levels than patients with nonlacunar stroke subtypes (Table 1).…”

Section: Discussionmentioning

confidence: 79%

Retinal Microvascular Signs May Provide Clues to the Underlying Vasculopathy in Patients With Deep Intracerebral Hemorrhage

Baker

Hand²,

Liew³

et al. 2010

Stroke

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Background and Purpose-Deep intracerebral hemorrhage (ICH) and lacunar infarcts are the result of small vessel disease, whereas nonlacunar infarcts are often caused by large artery atherosclerosis or cardiac embolism. We hypothesized that patients with deep ICH and lacunar infarcts have similar retinal microvascular signs and that these differ from those seen in patients with nonlacunar infarcts. Methods-We studied patients with acute stroke and classified their stroke as deep ICH, lacunar infarction, or nonlacunar infarction. In a masked fashion we assessed retinal photographs for quantitative and qualitative evidence of microvascular damage. Results-We recruited 630 patients (51 had deep ICH, 93 had lacunar infarction, and 486 had nonlacunar infarction).Patients with deep ICH were more likely than those with nonlacunar infarcts to have severe focal narrowing of the retinal arterioles (OR, 3.7), severe arteriovenous nicking (OR, 2.6), and quantitatively narrower retinal arterioles and wider retinal venules. Retinal microvascular signs were similar in patients with deep ICH and lacunar infarction. Conclusions-Patients

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Section: Discussionmentioning

confidence: 79%

Retinal Microvascular Signs May Provide Clues to the Underlying Vasculopathy in Patients With Deep Intracerebral Hemorrhage

Baker

Hand²,

Liew³

et al. 2010

Stroke

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“…Increased vascular plasma protein deposition and vascular occlusion such as that observed in the SHR model produce retinal neuroinfarcts that occur both in hypertensive and in diabetic primates and humans [18,19].…”

Section: Discussionmentioning

confidence: 99%

Aminoguanidine inhibits the development of accelerated diabetic retinopathy in the spontaneous hypertensive rat

Hammes¹,

Brownlee²,

Edelstein³

et al. 1994

Diabetologia

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Summary Arterial hypertension has been identified as a major secondary risk factor for diabetic retinopathy. However, the mechanisms by which hypertension worsens retinopathy are unknown. Inhibition of advanced glycation product formation prevents the development of experimental diabetic retinopathy in normotensive diabetic rats. In this study the effect of hypertension on the rate of diabetic retinopathy development and the formation of arteriolar thrombosis was evaluated. We also evaluated the effect of aminoguanidine, an inhibitor of advanced glycation end product formation on retinal pathology of diabetic hypertensive rats. After 26 weeks of diabetes, hypertension accelerated the development of retinopathy despite a lower mean blood glucose level than in the non-hypertensive group (diabetic spontaneous hypertensive rats (SHR) 16.00 + 6.83 mmol/l; diabetic normotensive Wistar Kyoto rats (WKY) 34.9 + 3.64 mmol/1; p < 0.0001). Diabetic SHR had nearly twice as many acellular capillaries as diabetic WKY (SHR diabetic: 91.9 + 7.5 acellular capillaries per mm 2 of retinal area vs WKY diabetic: 53.7 + 8.5 acellular capillaries per mm 2 of retinal area), and a 3.8-fold increase in the number of arteriolar microthromboses (SHR diabetic 23504 + 5523 gm 2 vs SHR non-diabetic 6228 + 2707 gm2). Aminoguanidine treatment of SHR diabetic rats reduced the number of acellular capillaries by 50 %, and completely prevented both arteriolar deposition of PASpositive material and abnormal microthrombus formation. These data suggest that hypertension-induced deposition of glycated proteins in the retinal vasculature plays a central role in the acceleration of diabetic retinopathy by hypertension. [Diabetologia (1994) 37: 32-35] Key words Diabetic retinopathy, rat model, hypertension, SHR, aminoguanidine, glycation.Over the past few years, hypertension has been identified as a major secondary risk factor for diabetic microvascular complications [1][2][3]. Hypertension accelerates the progression of diabetic nephropathy, and antihypertensive treatment has been shown to reduce declining renal function even in normotensive diabetic subjects [4].Systolic hypertension is also a risk factor for diabetic retinopathy [5][6][7] and in patients with unilateral carotid The mechanisms by which hypertension worsens diabetic retinopathy are unknown. In non-hypertensive diabetic animals, inhibition of advanced glycation product formation (AGE) by aminoguanidine prevents the development of experimental diabetic retinopathy [9]. Since AGEs induce a procoagulatory state in endothelial cells in vitro [10], we hypothesized that increased deposition of glycated plasma proteins in the microvasculature of hypertensive diabetic animals would accelerate diabetic retinopathy by inducing microvascular thrombus formation.In order to test this hypothesis, we examined the effect of aminoguanidine treatment on the retinal pathology of diabetic spontaneously hypertensive rats.

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“…Decorrente destas alterações vasculares, são observados os outros achados da RH: manchas algodonosas, exsudato duro, hemorragia retiniana e o papiledema (27)(28)(29) .…”

Section: Fisiopatologia E Histopatologia Da Retinopatia Hipertensivaunclassified

Retinopatia hipertensiva: revisão

Silva¹,

Silva²,

Herkenhoff³

2002

Arq. Bras. Oftalmol.

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Pathogenesis of hypertensive retinopathy. An experimental study in the monkey.

Cited by 134 publications

References 31 publications

Retinal Microvascular Signs May Provide Clues to the Underlying Vasculopathy in Patients With Deep Intracerebral Hemorrhage

Retinal Microvascular Signs May Provide Clues to the Underlying Vasculopathy in Patients With Deep Intracerebral Hemorrhage

Aminoguanidine inhibits the development of accelerated diabetic retinopathy in the spontaneous hypertensive rat

Retinopatia hipertensiva: revisão

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