Disease relevance of Retinal Vessels

• We prevented retinal vessel development by raising newborn mice in a high-oxygen atmosphere, which leads, paradoxically, to retinal hypoxia (confirmed by using the oxygen-sensing reagent EF5) [1].
• Immunohistochemistry and in situ hybridization demonstrate expression of PDGF in ganglion cells and cells of retinal blood vessels [2].
• Rats with experimental galactosaemia develop a diabetic-like retinopathy in the absence of other metabolic abnormalities characteristic of diabetes mellitus; basement membrane thickening is measurable in their retinal vessels after 7 months of galactose feeding [3].
• RESULTS: Fluorescein angiography, funduscopic examination, and ADPase preparations showed dilated and tortuous retinal vessels, pigmentary changes, incomplete vascularization of peripheral retina, vitreous hemorrhage, and persistence of massive intravitreal neovascularization [4].
• These results suggest that retinal circulatory abnormalities are found before observable retinopathy development in GK rats and that there may be some mechanism causing a reduction in SBF without changing major retinal vessel diameters at an early stage in non-insulin-dependent diabetes mellitus (NIDDM) [5].

High impact information on Retinal Vessels

• At 5 days postpartum (P5), VEGFR-1 protein was colocalized with retinal vessels, whereas VEGFR-2 was detected only in the neural retina [6].
• At the same time, the retinal vessels of the diabetic animals develop a resistance to the vasodilatory activity of monobutyrin [7].
• An up-regulation of beta1-integrin and FN was observed in the retinal vessels in the mouse model of hypoxia-induced retinal angiogenesis [8].
• Instead, Dp71 is localized to the inner limiting membrane (ILM) and to retinal blood vessels [9].
• Expression of the high affinity flk-1 receptor for VEGF was demonstrated in newly formed retinal vessels, confirming that the secreted VEGF acts on the vessels, in a paracrine fashion [10].

Chemical compound and disease context of Retinal Vessels

• METHODS: Growth of retinal vessels in the neonatal rat retina was examined in three conditions: normal development, cyclic hyperoxia, and normoxia (1 day 70% to 75% oxygen, 1 day room air for up to seven cycles from birth, and room air for up to 16 days), and direct hypoxia (10% oxygen from postnatal day 3 [P3]) [11].
• Strong labeling of the CRT was seen in the photoreceptor inner segments in all species studied and labeling of a variety of inner neuronal cells (amacrine, bipolar, and ganglion cells), the retinal nerve fibers and sites of creatine transport into the retina (retinal pigment epithelium, inner retinal blood vessels, and perivascular astrocytes) [12].
• During the experiment, body weight, calcaemia and phosphataemia were measured; retinal blood vessel calibre was observed by ophthalmoscopic examination of the ocular fundus [13].
• We studied the effects of the yellow (577 nm), orange (595 nm) and red (630 nm) dye lasers, the argon blue-green (488, 514.5 nm) and green (514.5 nm) lasers, and the krypton red (647 nm) laser on experimentally produced serous and hemorrhagic retinal detachments and on retinal vessels in rabbits [14].
• An investigation has been made of the effect of acute decompression sickness upon the permeability of the cerebral, iridic, and retinal vessels of the rat, with sodium-fluorescein as intravenous tracer [15].

Biological context of Retinal Vessels

• Angiotensin binding sites in bovine and human retinal blood vessels [16].
• Our results showed an active transport of fluorescein in the rabbit retinal vessels coupled with net fluid flux from outside the vessels into the lumen [17].
• Fluorescein angiography revealed normal vascular patency of the retinal vessels after vitrectomy [18].
• Vasoactive doses of Ang II (10(-10) M to 10(-4) M) caused a dose-dependent increase in the release of NO and PGI2 from isolated bovine retinal vessels, indicating that the increase in EDRF may nullify direct Ang II-induced vasoconstriction [19].
• Compared with prior published data, these findings represent the first direct human evidence of both bioavailability of RBX to retinal vessels and amelioration of diabetes-induced retinal hemodynamic abnormalities by an oral PKC beta inhibitor [20].

Anatomical context of Retinal Vessels

• Adhesion of blood leukocytes to retinal endothelial cells in vivo was significantly raised 48 h before the appearance of clinical disease, and this correlated with the increased expression of CD54 on retinal vessels [21].
• RESULTS: Oatp2 immunoreactivity was abundantly present at the apical microvilli of the rat retinal pigment epithelium and to a lesser degree in small retinal vessels [22].
• We conclude, as demonstrated by these methods, that MSG retards development of the retinal vessels but does not affect development of the blood-retinal barriers [23].
• 1. The most prominent labeling of the Kir4.1 protein was found in the endfoot membranes of Müller glial cells facing the vitreous body and surrounding retinal blood vessels [24].
• Krypton laser radiation (green and, to an even greater extent, yellow) produced measurably greater effects on retinal vessels and adjacent structures than on deeper retinal levels; argon laser radiation (green) produced greater effects on the pigment epithelium [25].

Associations of Retinal Vessels with chemical compounds

• Retinal vessel diameters and risk of impaired fasting glucose or diabetes: the Rotterdam study [26].
• Clinically, based on ophthalmoscopy and fluorescein angiography, retinal vessels were normal [27].
• Dietary treatment of atherosclerosis abolishes hyperresponsiveness of retinal blood vessels to serotonin in monkeys [28].
• PURPOSE: Previous studies in humans have demonstrated that oxygen (O2) reduces retinal vessel caliber and blood flow, whereas carbon dioxide (CO2) usually has opposite effects [29].
• CONCLUSIONS: The present data confirm that histamine increases ChBF and retinal vessel diameters in healthy subjects [30].

Gene context of Retinal Vessels

• Mice with targeted disruption of the Fgf2 gene had no detectable expression of FGF2 in the retina by Western blot, but retinal vessels were not different in appearance or total area from wild-type mice [31].
• PURPOSE: The authors used histochemical analysis to determine whether increased vascular endothelial growth factor (VEGF) immunoreactivity in diabetic retinal vessels is related to increased vascular permeability, as indicated by human serum albumin (HSA) immunostaining, or to presumed retinal hypoxia as demonstrated by decreased vascularity [32].
• The location of monocarboxylate transporter-2 on glial foot processes surrounding retinal vessels suggests that this transporter is also important in blood-retinal lactate exchange [33].
• Histology showed dilated thin-walled retinal vessels, but unequivocal retinal NV could not be identified and staining for PCNA was negative [34].
• Strong NOS immunoreactivity was seen in the endothelium of choroidal and retinal vessels [35].

Analytical, diagnostic and therapeutic context of Retinal Vessels

• The fluid flux from bath to lumen across the retinal vessels, which was 6.3 +/- 1.0 nl/min/mm for perfusion rates of 6.6 +/- 0.2 nl/min, was temperature-dependent and was coupled to the fluorescein transport [17].
• Immunoreactive MCP-1 and MIP-1alpha were detected in the GCL, INL, and the retinal vessels 24 hours after reperfusion [36].
• Angiotensin II-induced constrictions are masked by bovine retinal vessels [19].
• Enzyme immunoassays were used to measure the release of cGMP (an index of NO release) and 6-keto-PG-F1alpha (a stable metabolite of PGI2) from isolated bovine retinal vessels [19].
• The ECM of unfixed frozen human retinal blood vessels was examined by indirect immunofluorescence using antibodies raised against collagen types I, II, III, IV, and V as well as the structural glycoproteins laminin and fibronectin [37].

References