Studies of the Retinal Capillaries in Relation to Diabetic and Other Retinopathies

Ashton, Norman

doi:10.1136/bjo.47.9.521

Cited by 216 publications

(113 citation statements)

References 16 publications

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“…In diabetic retinopathy both clinical and experimental evidence indicates that capillary closure starts on the arterial part of microcirculatory units (Ashton 1963, Bek 1997a. On the contrary, the cases examined in the present study showed capillary closure to be most prominent on the venous side of microcirculatory units.…”

Section: Discussioncontrasting

confidence: 50%

Capillary closure secondary to retinal vein occlusion, A morphological, histopathological, and immunohistochemical study

Bek

1998

Acta Ophthalmologica Scandinavica

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Section: Discussioncontrasting

confidence: 50%

Capillary closure secondary to retinal vein occlusion, A morphological, histopathological, and immunohistochemical study

Bek

1998

Acta Ophthalmologica Scandinavica

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“…Subsequent to selective perictes loss, the other important histopathological lesions are: endothelial cell proliferation, microaneurysms, and capillary closure [36]. Capillary proliferation was seen in our study, but the total endothelial cell and pericytes count from rats receiving 50% glalactose diet were decreased compared to their counterparts on 50% starch diet.…”

Section: Discussioncontrasting

confidence: 37%

Radiobiological Study of Retinal Microvessel Proliferation in Diabetic-like Rat Model

Mao¹,

Archambeau²,

Baqai³

et al. 2008

TOPHYJ

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Progressive evolution of retinal vascular in diabetic retinopathy leads to blindness in up to 8,000 patients yearly. The major purpose of this investigation was to determine proton radiation dose response of the eye's retinal vasculature in the hypergalactosemia induced rat model of diabetic-like retinopathy and gain insight of possible role of proton radiotherapy in controlling diabetic retinopathy. A single dose range of proton radiation (8, 14, and 20 Gy) was delivered to one eye of each rat at 4 months following induction of hypergalactosemia. The opposite eye of each rat, which was not irradiated, showed normal progression of retinopathy. Stereologic techniques were used to quantify tissue parameters in situ in a retinal digest preparation that allowed unobstructed access to the vasculature. 15 months following 50% galactose diet, characteristic histopathological lesions of retinopathy such as capillary endothelial cell proliferation, capillary closure, capillary microaneurysms, pericyte loss developed in non-irradiated eyes. The endothelial cell densities for rat receiving 50% galactose diet were significantly higher than that of control (p<0.05). Proton irradiation inhibited significant endothelial cell proliferation at dose from 14Gy to 20Gy (p<0.05), yet not diminished pericyte loss at current dose schedule. These findings indicated beneficial effects of proton radiation on hypergalactosemia induced diabetic-like retinopathy. Our study should have an impact on further studies to optimize radiation treatment strategies for diabetic retinopathy.

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“…Our findings suggest that capillary abnormalities play a role in the development of diabetic neuropathy, possibly as an intermediate step between metabolic derangement and pathologic abnormality of nerve fibers. Capillary abnormalities and closure have previously been shown to be involved in diabetic retinopathy (50,51) and nephropathy (52).…”

Section: Discussionmentioning

confidence: 99%

Capillary number and percentage closed in human diabetic sural nerve.

Dyck¹,

Hansen²,

Karnes³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

189

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The number of capillaries per mm2, minimum intercapillary distance, number of endothelial nuclei per capillary section, and percentage of capillaries closed were evaluated in transverse sections of fascicles of 45 control and 36 diabetic sural nerves. All controls and patients were prospectively studied to ascertain their diabetic and neuropathic status. An index of pathology was introduced and it was found to provide a sensitive and reliable measurement of the presence and severity of neuropathy. The number of capillaries and minimum intercapillary distance of diabetic nerves were not significantly different from those of controls (P > 0.05). Diabetic nerves exhibited a small but statistically significant increase in the number of endothelial nuclei per capillary that was positively correlated with the severity of neuropathy. The most striking abnormality was the statistically significant increase in the percentage of capillaries closed in patients with neuropathy as compared to those without neuropathy and controls. Among diabetics, this percentage increased with the severity of neuropathy (P = 0.008). The two capillary abnormalities that have been demonstrated may play a role in the development of diabetic polyneuropathy.Diabetic polyneuropathy, a common complication of diabetes mellitus, is typically expressed as sensory loss, pain, and autonomic dysfunction in the feet and legs (1). Although the mechanisms underlying diabetic neuropathy remain unknown, chronic hyperglycemia may lead to metabolic derangement that directly affects neurons (axons) or Schwann cells or indirectly affects them by first altering another tissue-e.g., vessels. Since a higher rate of atherosclerotic heart disease and peripheral vascular disease occurs among diabetics (2, 3) and since arteriosclerosis with vessel occlusion is reported for vasa nervorum of nerve (4-6), arteriosclerosis has been postulated as a cause of diabetic neuropathy. This hypothesis, however, may not explain the common occurrence of an abnormality of nerve conduction and development of a diffuse neuropathy among diabetic patients who do not manifest peripheral vascular disease (7-10). Attention, therefore, has been focused on metabolic derangements that might affect neurons (or their peripheral axons) or Schwann cells. Among the metabolic mechanisms that have been considered are the following: (i) lipid alterations (11-13); (ii) accumulation of sorbitol and fructose (14, 15); (iii) decreased nerve myo-inositol (16); (iv) increased nonenzymatic glycosylation of protein (17, 18); (v) decrease of Na+,K+-ATPase (19); (vi) increased intraaxonal sodium (20); (vii) alterations in axonal flow (21) and axonal attenuation (22); and (viii) tissue dehydration (23). Since the nerve conduction abnormality is not readily reversed after near normalization of blood glucose for periods of up to 8 months, an irreversible nerve alteration or an intervening pathologic alteration interposed between metabolic derangement and neuropathic dysfunction is inferred (24).A functional...

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Studies of the Retinal Capillaries in Relation to Diabetic and Other Retinopathies

Cited by 216 publications

References 16 publications

Capillary closure secondary to retinal vein occlusion, A morphological, histopathological, and immunohistochemical study

Capillary closure secondary to retinal vein occlusion, A morphological, histopathological, and immunohistochemical study

Radiobiological Study of Retinal Microvessel Proliferation in Diabetic-like Rat Model

Capillary number and percentage closed in human diabetic sural nerve.

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