1987
DOI: 10.2337/diabetes.36.7.813
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Increased vascular permeability in spontaneously diabetic BB/W rats and in rats with mild versus severe streptozocin-induced diabetes. Prevention by aldose reductase inhibitors and castration

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Cited by 95 publications
(62 citation statements)
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“…Whether androgen, estrogen and progesterone receptor mRNAs in other ocular tissues are translated and mediate the action of these hormones on meibomian gland lipid production, intraocular pressure, aqueous outflow, lens permeability and retinal/uveal vascular permeability (Kambert 1968;Knepper 1986;Sullivan et al 1998b;Williamson et al 1987), or on glaucoma, lens opacities, amblyopia, pseudo-myopia and diabetic retinopathy (Guttridge 1994;Haffner et al 1990;Hitawari 1963;Kambert 1968;Klein 1994;Knepper 1986) remains to be determined. Similarly, it has yet to be definitively established whether these sex steroid receptors play a significant role in the: [a] diverse ocular changes that occur during the menstrual cycle, menopause and pregnancy (Guttridge 1994;Imafidon & Imafidon 1992;Imafidon et al 1993;Millodot & Lamont 1974;Qureshi 1997;Ruben 1966;Serrander & Peek 1993); [b] gender-related differences in meibomian gland lipid release, corneal wetting time, corneal epithelial mitotic rate, conjunctival goblet cell density, lens epithelial cell number, intraocular pressure and visual acuity (Chew et al 1993;GuggenmoosHolzmann et al 1989;Klein et al 1991;Moore et al 1987;Norn 1969;Qureshi 1997;Tsai et al 1985); or [c] gender-associated variations in the incidence of dry eye syndromes, glaucoma, cataracts, agerelated maculopathy, macular holes, macular degeneration, retinal detachment diabetic retinopathy and visual impairment (Caffery et al 1998;Guttridge 1994;Guyer and Gragoudas 1994;Hiller et al 1986;Kahn et al 1977;Klein et al 1984…”
Section: Discussionmentioning
confidence: 99%
“…Whether androgen, estrogen and progesterone receptor mRNAs in other ocular tissues are translated and mediate the action of these hormones on meibomian gland lipid production, intraocular pressure, aqueous outflow, lens permeability and retinal/uveal vascular permeability (Kambert 1968;Knepper 1986;Sullivan et al 1998b;Williamson et al 1987), or on glaucoma, lens opacities, amblyopia, pseudo-myopia and diabetic retinopathy (Guttridge 1994;Haffner et al 1990;Hitawari 1963;Kambert 1968;Klein 1994;Knepper 1986) remains to be determined. Similarly, it has yet to be definitively established whether these sex steroid receptors play a significant role in the: [a] diverse ocular changes that occur during the menstrual cycle, menopause and pregnancy (Guttridge 1994;Imafidon & Imafidon 1992;Imafidon et al 1993;Millodot & Lamont 1974;Qureshi 1997;Ruben 1966;Serrander & Peek 1993); [b] gender-related differences in meibomian gland lipid release, corneal wetting time, corneal epithelial mitotic rate, conjunctival goblet cell density, lens epithelial cell number, intraocular pressure and visual acuity (Chew et al 1993;GuggenmoosHolzmann et al 1989;Klein et al 1991;Moore et al 1987;Norn 1969;Qureshi 1997;Tsai et al 1985); or [c] gender-associated variations in the incidence of dry eye syndromes, glaucoma, cataracts, agerelated maculopathy, macular holes, macular degeneration, retinal detachment diabetic retinopathy and visual impairment (Caffery et al 1998;Guttridge 1994;Guyer and Gragoudas 1994;Hiller et al 1986;Kahn et al 1977;Klein et al 1984…”
Section: Discussionmentioning
confidence: 99%
“…Although diabetes in the rodent model is not associated with proliferative retinopathy it does develop increased retinal vascular permeability [27,48,49] in association with increased retinal VEGF expression [21,50]. In adult primates intravitreal injections of VEGF leads to many of the changes associated with non-proliferative diabetic including oedema, microaneurysms and intraretinal haemorrhages [51] suggesting that VEGF has a key role in non-proliferative as well as proliferative retinopathy.…”
Section: Discussionmentioning
confidence: 99%
“…The coronary venular P a of STZ-diabetic animals was demonstrated to be significantly elevated compared to non-diabetic controls four weeks after the onset of diabetes [42]. Biobreeding rats (a model of type II diabetes) and STZ-induced diabetic rats had elevated albumin permeation as measured by 125 I-albumin in the vasculature of eyes, sciatic nerve, aorta, and kidney, those tissues predisposed to diabetic vascular disease in humans [43]. No evidence of increased albumin permeation was noted in heart, brain, testes or skeletal muscle [43].…”
Section: Factors?mentioning
confidence: 99%