Vitreous Fluorophotometry in Rats With Streptozocin-Induced Diabetes

Ak, Vine; Am, Kisly; Betz, A. Lorris; Wf, Howatt

doi:10.1001/archopht.1984.01040030877038

Cited by 11 publications

(6 citation statements)

References 7 publications

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“…Diabetic and galactosaemic rats develop many complications similar to human diabetics, including BRB failure (Jones et al, 1979;Krupin et al, 1979;Ishibashi et al, 1980;Tso et aI., 1980;Jones et al, 1982;Blair et al, 1984;Vine et aL, 1984;Caldwell et al, 1985;Lightman et al, 1987;Williamson et al, 1987). Based upon electron-microscopic immunocytochemical staining for albumin to determine the method of extravasation in the retinas of these experimental animals, the nature of the BRB breakdown appears to be primarily due to increased focal permeability of the RVE and RPE cells, allowing serum proteins to transgress the barrier and infiltrate the retina (Vinores et aI., 1990b).…”

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confidence: 43%

Electron microscopic immunocytochemical demonstration of blood-retinal barrier breakdown in human diabetics and its association with aldose reductase in retinal vascular endothelium and retinal pigment epithelium

et al. 1993

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Light-microscopic immunohistochemical staining for albumin has been used to localize sites of blood-retinal barrier (BRB) breakdown in ocular disorders, but the mechanism for BRB compromise cannot be resolved at this level. Using eyes up to 2 days post-mortem from normal patients or from patients with diabetic retinopathy, or other disorders known to cause BRB failure, electron-microscopic immunocytochemistry reveals focal breakdown of the inner BRB, comprised of the retinal vascular endothelium (RVE), which appears to be mediated by diffuse permeation of the RVE cells and by vesicular transport. Permeation of the retinal pigmented epithelial (RPE) cells that comprise the outer BRB also occurs, but there is no evidence of opening of tight junctions between RVE or RPE in any of the disorders evaluated. Increased aldose reductase (AR) expression in the RVE and RPE cells of diabetics as well as in the perivascular retinal astrocytes, which interact with RVE cells to establish the inner BRB, suggests that AR activity and the subsequent intracellular accumulation of sorbitol in these cell types may impair the function of the BRB in diabetes.

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confidence: 43%

Electron microscopic immunocytochemical demonstration of blood-retinal barrier breakdown in human diabetics and its association with aldose reductase in retinal vascular endothelium and retinal pigment epithelium

et al. 1993

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“…Our study shows that retinal vascular permeability, as measured by VFP, increased significantly in the STZ-induced diabetic rats compared with control rats. This finding agrees with the results of previous studies in which retinal vascular permeability also increased at an early stage of experimentally-induced diabetes [4,5,15,24].…”

Section: Discussionmentioning

confidence: 45%

Constitutive nitric oxide synthase is associated with retinal vascular permeability in early diabetic rats

et al. 2001

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Diabetes can result in retinopathy, which causes vision loss and blindness. Abnormalities of retinal vascular permeability precede the appearance of clinical retinopathy and could provide information about its pathogenesis. Increased retinal vascular permeability induced by retinal vascular disorders cause macular oedema [1], which decreases visual acuity and is difficult to cure clinically. Abnormal retinal vascular permeability caused by the breakdown of the blood-retinal barrier (BRB) was found in patients with diabetes and animals with experimentally induced diabetes using vitreous fluorophotometry (VFP) [2±5].Vascular endothelial growth factor (VEGF) is a major vascular permeability factor increasing retinal Diabetologia (2001) Abstract Aims/hypothesis. We investigated the association between vascular permeability and constitutive nitric oxide synthase in rats with diabetes for a short duration (2 weeks). Methods. Retinal vascular permeability was evaluated in rats with diabetes induced by streptozotocin using vitreous fluorophotometry and a small animal adapter. We carried out in situ hybridization and semi-quantitative reverse transcription±polymerase chain reaction to study the expression of endogenous constitutive nitric oxide synthase mRNA in diabetic retinas. We also examined changes in the protein expression of constitutive nitric oxide synthase in diabetic retinas using immunohistochemistry and Western blotting. Results. Retinal vascular permeability was significantly higher in diabetic rats (median, 1.09 arbitrary unit) compared with control rats (median, 0.69 arbitrary unit) (p < 0.05). The expression of both neuronal nitric oxide synthase (NOS) and endothelial nitric oxide synthase mRNA was higher in diabetic retinas than in the retinas of control rats as determined by in situ hybridization and reverse transcriptionpolymerase chain reaction. Immunohistochemistry and Western blotting also showed that neuronal nitric oxide synthase increased in diabetic retinas. The immunohistochemistry of endothelial nitric oxide synthase indicated that non-vessel tissues increased in diabetic retinas while retinal vessels weakened. Western blotting showed that the amount of endothelial nitric oxide synthase increased. Conclusion/interpretation. These results suggest that increases in both constitutive NOSs (nNOS and eNOS) could be associated with retinal vascular permeability and that NOS is associated with clinical vascular dysfunction in the early stages of diabetes.[ Diabetologia (2001

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“…The mortality rate was low (2 of 24) due to short duration of anesthesia and type of anesthetic used [5,6,13,18,22]. Although many sites have been tested for fluorescein injection (tail vein [20], femoral vein [6,19]), we found the external jugular vein to be the most accessible. Full pupillary dilatation is mandatory for proper VFP records.…”

Section: Discussionsupporting

confidence: 39%

“…Insulin either affects the decompensated retinal endothelial cells directly [5] or indirectly by normalization of blood glucose level [22], or improvement of diabetic acidosis [15,16]. The last possibility is questionable since Vine et al [20] did not find significant difference in blood pH between normal and diabetic rats.…”

Section: Introductionsupporting

confidence: 38%

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Effect of piroxicam on the blood-retina barrier in experimentally induced diabetes in rats

et al. 1991

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The effect of piroxicam on the blood-retina barrier was evaluated in rats with experimentally induced diabetes. Diabetes was induced in rats by intraperitoneal injection of streptozocin (STZ). Diabetic rats were divided into two equal groups: those treated with piroxicam, a long-acting platelet inhibitor, and an untreated control group. Vitreous fluorophotometry (VFP) was performed both before and two weeks after induction of diabetes and piroxicam intake. Streptozocin-induced diabetes caused an alteration in the blood-retinal barrier evidenced by an increase in vitreous fluorescein concentration in diabetic rats compared with normal rats. Piroxicam intake did not lead to significant change in vitreous fluorescein concentrations. However, the examination had to be terminated at two weeks because of cataract formation. The piroxicam treated group showed less incidence of lens opacity formation (59.1% compared to 81.8% in the untreated group, p = 0.0006). Piroxicam administration appears to protect the diabetic rat eye against lens opacification.

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Vitreous Fluorophotometry in Rats With Streptozocin-Induced Diabetes

Cited by 11 publications

References 7 publications

Electron microscopic immunocytochemical demonstration of blood-retinal barrier breakdown in human diabetics and its association with aldose reductase in retinal vascular endothelium and retinal pigment epithelium

Electron microscopic immunocytochemical demonstration of blood-retinal barrier breakdown in human diabetics and its association with aldose reductase in retinal vascular endothelium and retinal pigment epithelium

Constitutive nitric oxide synthase is associated with retinal vascular permeability in early diabetic rats

Effect of piroxicam on the blood-retina barrier in experimentally induced diabetes in rats

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