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At least 649 records · Page 36Linked to original sources
PubMed2005

[The influence of the estrogens on a retinal blood vessels].

PURPOSE: To define the influence of the estrogens on a retinal blood vessels. MATERIAL AND METHODS: 20 healthy women, mean age 23.5 +/- 1.55 with normal laboratory investigations and with regular fundus and blood vessels appearance, participated in our study. Fundus examination was performed with fundus camera Canon NF 505 and with HRT II. The measurements were made before estrogens application (300 microg dermal plasters) and 36 hours after the application in 4th and 6th day of a period. RESULTS: The difference between the size of the retinal vessels before and after estrogens application was significant in all cases. In the main branches the increase of a vessel's diameter was 4.4% to 11.22% (mean 7.61% +/- 3.210%), p<0.05. The increase in a smaller branches of central retinal artery balanced from 1.2% to 9.2% (mean 5.47 +/- 4.11%), p<0.05. CONCLUSIONS: Estrogens have a great vasodilatation effect on a retinal blood vessels. The level of the dilatation after the estrogens' application is about 8% in main branches and about 5% in a smaller vessels.

Adult↗
PubMed2003

The diameters of the human retinal branch vessels do not change in darkness.

PURPOSE: To examine whether the diameters of retinal branch vessels of the human eye change during dark and light adaptation. METHODS: Images (S-VHS recordings) were obtained of the peripapillary region in 11 eyes of 11 healthy young adults (seven women, four men; mean age, 26.4 years). The images were made under a sequence of different illumination conditions (light, 30 minutes of darkness, light) with a scanning laser ophthalmoscope (SLO), using near-infrared illumination (785 nm). The recordings were then analyzed with a retinal vessel analyzer (RVA), and the caliber changes of one branch artery and one vein were measured in each eye. RESULTS: For arteries, the changes of diameter under different illumination conditions showed no clear trend, and comparisons between the different time sections revealed no statistically significant changes (P = 0.933; repeated measures ANOVA). There was a slight dilation (average, 0.9%; range, -3.9% to +5.1%) in darkness, and a return to baseline (range, -2.9% to + 2.9%) on restoring normal illumination. Veins during darkness showed a small but fairly consistent constriction (average, 1.5%; range -5.4% to +3.9%; significant P = 0.05), again returning to baseline (range, -2.1% to +2.6%) in normal light. CONCLUSIONS: The small changes of retinal branch vessel diameters under different light conditions probably have little influence on the possible changes of retinal blood flow in healthy subjects.

Adult↗
PubMedDate not supplied

Retinal oximetry using intravitreal illumination.

PURPOSE: To demonstrate spectroscopic retinal oximetry measurements on arteries and veins in swine using intravitreal illumination. Retinal arterial and venous saturations are measured for a range of inspired O2 levels after pars plana vitrectomy. METHODS: Pars plana vitrectomy and intravitreal manipulations were performed on two female American Yorkshire domestic swine. Light from a scanning monochromator was coupled into a fiberoptic intraocular illuminator inserted into the vitreous. The retinal vessels were illuminated obliquely, minimizing vessel glints. Multispectral images of the retinal vasculature were obtained as the swine's arterial blood oxygen saturation was decreased from 100% to 67% in decrements of approximately 10%. Retinal vessel spectra were used to calculate oxygen saturation in selected arteries and veins. Arterial oxygen saturations were calibrated using blood gas analysis on blood drawn from a Swan-Ganz catheter placed in the femoral artery. RESULTS: Oblique illumination of retinal vessels using an intravitreal fiberoptic illuminator provided a substantial reduction in the central vessel glint usually seen in fundus images, thus simplifying the analysis of spectral data. The vessel shadows were displaced from the vessel image simplifying the light paths in the eye. Using a full spectral analysis simplified by the light path reductions, we calculated retinal vessel saturations. The reduction of glint allowed for increased accuracy in measuring retinal vessel spectral optical density. Abnormally low retinal venous oxygen saturations were observed shortly after pars plana vitrectomy. CONCLUSIONS: Retinal oximetry using intravitreal illumination has been demonstrated. As a research tool, intravitreal illumination addresses several difficulties encountered when performing retinal oximetry with transcorneal illumination.

Animals↗
PubMed2001

Study of the distribution of retinal blood vessels in buffaloes (Bos bubalis).

The distribution of retinal blood vessels in the eye of buffalo was studied macroscopically and microscopically in twenty-two eyes of healthy animals. After macroscopic observation, 12 of 22 eyes were used for histological study. Ten eyes were stained with hematoxylin and eosin and two eyes with PAS stain. The present findings revealed that the eye of the buffalo was characterized by the complex network of retinal blood vessels (holangiotic or euangiotic). The central retinal artery and vein pierced the eye through the optic disc and gave off several branches. There were four pairs of primary vessels that were named dorsal, ventral, nasal and temporal retinal arteries and veins. The veins anastmosed with each other at the optic disc to form a somewhat circle. Three patterns of the distribution of blood vessels were described. The distribution of the arteries and veins was the same.

Animals↗
PubMed2005

Inhaled carbon monoxide increases retinal and choroidal blood flow in healthy humans.

PURPOSE: It has been hypothesized that carbon monoxide (CO) acts as an important vascular paracrine factor and plays a role in blood flow regulation in several tissues. The present study investigated the effect of inhaled CO on retinal and choroidal blood flow. METHODS: Fifteen healthy male volunteers were studied in a randomized, double-masked, placebo-controlled design with washout periods of at least 1 week between study days. CO in a dose of 500 ppm or placebo (synthetic air without CO) was inhaled for 60 minutes. Ocular hemodynamics were measured at baseline and at 30 and 60 minutes after start of inhalation. Retinal vessel diameters were measured with a retinal vessel analyzer. RBC velocity was assessed using bidirectional laser Doppler velocimetry. Retinal blood flow was calculated based on retinal vessel diameters and RBC velocity. Fundus pulsation amplitude (FPA) was measured using laser interferometry, and submacular choroidal blood flow using laser Doppler flowmetry. RESULTS: Breathing of CO significantly increased carboxyhemoglobine, from 1.2 +/- 0.5% to 8.5 +/- 0.9% and 9.4 +/- 0.6% at the two time points, respectively (P < 0.01). The diameter of retinal arteries increased by +3.5 +/- 3.8% and +4.2 +/- 3.9% (P < 0.01) in response to CO inhalation. In retinal veins, CO also induced an increase in diameter of +4.3 +/- 3.0% and +4.8 +/- 5.0%, respectively (P < 0.01). By contrast, placebo did not influence retinal vessel diameter. RBC velocity tended to increase during CO inhalation (+8 +/- 22%), but this effect did not reach the level of significance (P = 0.1). Calculated retinal blood flow increased significantly by +12 +/- 5% (P < 0.02). FPA increased after breathing CO by +20 +/- 20% and +26 +/- 21% at the two time points, respectively (P < 0.01). Subfoveal choroidal blood flow increased by +14 +/- 9% and +15 +/- 9% during breathing of CO (P < 0.01). CONCLUSIONS: This experiment demonstrated that retinal and choroidal blood flow increase during inhalation of CO. Whether this increase is caused by tissue hypoxia or a yet unknown mechanism has to be clarified.

Administration, Inhalation↗
PubMed1989

Electroretinography and electro-oculography to localize abnormalities in early-stage inflammatory eye disease.

Electrophysiological investigations were performed in patients with inflammatory eye disease characterized by the presence of vitreous cells. The eyes were classified into four categories on the basis of fluorescein angiography: 1) no fluorescein leakage from retinal vessels, 2) fluorescein leakage from peripheral retinal vessels, 3) fluorescein leakage from the disc or macular vessels, and 4) fluorescein leakage from retinal vessels associated with pigment epithelial and choroidal changes. The electro-oculogram light rise was abnormally increased in the eyes in category 1, but it progressively declined for those in the other categories. The ratio of the b-wave (postreceptoral component) and a-wave (receptoral component) of the flash electroretinogram was unchanged in all categories, but the electroretinographic amplitudes progressively declined from a somewhat supernormal level in category 1 to subnormal in the other categories. Thus, in inflammatory eye disease, changes in the electrical potentials arising in the pigment epithelium and photoreceptors are the earliest detectable signs. Some biochemical changes in the choroid, pigment epithelium, and the photoreceptors appear to take place before any pathological changes in these structures or in the retinal vessels are detectable by ophthalmoscopy or fluorescein angiography.

Adult↗
PubMed1991

[3H]mepyramine binding sites, histamine H1-receptors, in bovine retinal blood vessels.

The presence of histamine H1-receptors in the bovine retinal blood vessels was studied with a [3H]mepyramine binding assay. The membranes of purified vessels obtained from bovine retinas showed specific [3H]mepyramine binding sites with a dissociation constant (KD) of 2.78 +/- 0.32 nM. This was similar to values obtained from the retinal neuronal fractions. The binding capacity (Bmax) was 53.8 +/- 1.7 fmol/mg protein, which was about a half that of the retinal neuronal fractions (108.9 +/- 3.1 fmol/mg protein). Some H1-antagonists proved to be potent competitors for [3H]mepyramine binding sites in bovine retinal blood vessels. These results indicate that histamine H1-receptors exist in the retinal blood vessels which may be involved in the physiological and the pathological responses of blood circulation in retinas.

Animals↗
PubMed1988

Macular grid photocoagulation. An experimental study on the primate retina.

We studied the effect of macular grid photocoagulation on the retinal vessels, retina, retinal pigment epithelium, and choroid of normal cynomolgus monkeys. Argon blue-green laser photocoagulation, similar to that employed for treating macular edema due to branch retinal vein occlusion, resulted in a decreased retinal capillary area at both one and five months after treatment. The photoreceptors and retinal pigment epithelium between laser lesions were altered at three days after treatment, but their appearance returned to normal by five months. The significance of these findings is discussed with regard to resolution of macular edema and improvement in vision following grid photocoagulation.

Animals↗
PubMed1994

Hypertension and retinopathy, arteriolar narrowing, and arteriovenous nicking in a population.

OBJECTIVE: To investigate the relationship of various retinal lesions to systemic hypertension in the population-based Beaver Dam Eye Study. DESIGN: In this cross-sectional population-based study, blood pressure was measured using standardized protocols. Using standardized protocols, stereoscopic color fundus photographs were graded in a masked fashion to determine the presence of retinopathy (defined as retinal microaneurysms only, blot hemorrhages only, hemorrhages and/or microaneurysms, cotton-wool spots, hard exudates, intraretinal microvascular abnormalities, venous beading, and retinal new vessels), retinal arteriolar narrowing, and arteriovenous nicking. PARTICIPANTS: Subjects aged 43 through 84 years who lived in Beaver Dam, Wis, between 1987 and 1988 were examined between 1988 and 1990. People with diabetes or retinal vascular occlusions were excluded. RESULTS: Retinopathy was present in 336 subjects (7.8%), arteriolar narrowing in 582 subjects (13.5%), and arteriovenous nicking in 95 subjects (2.2%) in the nondiabetic population. Hypertension was associated with increased frequency of retinopathy, arteriolar narrowing, and arteriovenous nicking. After adjusting for age, hypertension was associated with the presence of retinopathy (in men: relative risk [RR], 1.47; 95% confidence interval [CI], 1.10 to 1.96; in women: RR, 1.69; 95% CI, 1.26 to 2.27), arteriolar narrowing (in men: RR, 1.34; 95% CI, 1.03 to 1.74; in women: RR, 1.37; 95% CI, 1.14 to 1.64), and arteriovenous nicking (in men: RR, 1.87; 95% CI, 0.99 to 3.54; in women: RR, 1.65; 95% CI, 1.00 to 2.73). Retinopathy, arteriolar narrowing, and arteriovenous nicking were more frequent in those subjects whose blood pressure was elevated despite use of antihypertensive medications compared with those subjects whose blood pressure was controlled with antihypertensive medications or those who were normotensive. CONCLUSIONS: These data suggest that retinopathy and retinal arteriolar narrowing are common in people with hypertension. Further longitudinal study is necessary to evaluate the public health significance of these retinal lesions regarding possibly increased risk of renal and cardiovascular disease.

Adult↗
PubMed2001

VEGF-initiated blood-retinal barrier breakdown in early diabetes.

PURPOSE: The objectives of this study were to (1) determine whether endogenous vascular endothelial growth factor (VEGF) triggers diabetic blood-retinal barrier breakdown, and (2) identify the site as well as phenotype of the hyperpermeable diabetic retinal vessels. METHODS: Retinal VEGF mRNA levels were quantified in 1-week diabetic rats using the RNase protection assay. VEGF bioactivity was blocked via the systemic administration of a highly specific VEGF-neutralizing soluble Flt/F(c) construct (VEGF TrapA(40)). An inactive IL6 receptor/F(c) construct (IL6R Trap) was used as an isotype control. Blood-retinal barrier breakdown was quantified using the Evans blue technique and was spatially localized with fluorescent microspheres. RESULTS: Retinal VEGF mRNA levels in 1-week diabetic animals were 3.2-fold higher than in nondiabetic controls (P < 0.0001). Similarly, retinal vascular permeability in 8-day diabetic animals was 1.8-fold higher than in normal nondiabetic controls (P < 0.05). Diabetes-induced blood-retinal barrier breakdown was dose-dependently inhibited with VEGF TrapA(40), with 25 mg/kg producing complete inhibition of the diabetes-induced increases (P < 0.05). Blood-retinal barrier breakdown in diabetic animals treated with solvent alone or IL6R Trap did not differ significantly from untreated diabetic animals (P > 0.05). Spatially, early blood-retinal barrier breakdown was localized to the retinal venules and capillaries of the superficial retinal vasculature. CONCLUSIONS: Early blood-retinal barrier breakdown in experimental diabetes is VEGF dependent and is restricted, in part, to the venules and capillaries of the superficial inner retinal vasculature. VEGF inhibition should prove a useful therapeutic approach in the treatment of early diabetic blood-retinal barrier breakdown.

Animals↗
PubMed1992

Oxygen-induced retinopathy in the rat. Vitamins C and E as potential therapies.

Oxygen-induced retinopathy (OIR) was produced by subjecting newborn albino rats to a 60% oxygen atmosphere for 14 days before they were killed and retinal analysis was done. The extent of OIR was measured by estimating the severity of retinal vasoobliteration in ink-perfused flat-mounted retinas. This was done with the aid of a digitizing camera and an image-analysis system designed to create binary images of the retinal blood vessels. Retinal levels of several antioxidant molecules also were measured. Alpha-tocopherol and ascorbic acid were reduced in oxygen-exposed rats by 34% and 20%, respectively, compared with room air-raised control animals. Retinal glutathione reductase, S-transferase, and peroxidase showed no differences between oxygen-treated and -untreated rats. Attempts to increase the newborn rats' retinal ascorbic acid by administering daily subcutaneous injections (5 g/kg body weight) to the mother rats were unsuccessful. However, the level of retinal alpha-tocopherol of newborn rats could be altered by dietary manipulation of the mothers. The mothers were fed diets containing either 1 g alpha-tocopherol acetate/kg food or none, starting 21-25 days before the birth of their litters and lasting throughout the exposure period. This treatment resulted in three- to fourfold differences in the retinal alpha-tocopherol levels of the pups. The combination of dietary and oxygen treatments also resulted in significant differences in retinal glutathione peroxidase activity, with the vitamin E-deprived, oxygen-exposed group having highest levels. Newborn rats both supplemented with and deprived of alpha-tocopherol had less vasoobliteration than did those nursed by mothers fed rat chow.

Animals↗
PubMed2004

Intravenously administered histamine increases choroidal but not retinal blood flow.

PURPOSE: To determine the effect of intravenously administered histamine on both retinal and choroidal blood flow in humans. METHODS: A randomized, double-masked, two-way crossover study was performed in 14 healthy volunteers. Placebo or histamine was administered intravenously in stepwise increasing doses (0.08 microg/kg/min, 0.16 microg/kg/min, and 0.32 microg/kg/min). Retinal vessel diameters were measured with a retinal vessel analyzer, and retinal venous blood speed was assessed by bi-directional laser Doppler velocimetry. Using these parameters retinal blood flow was calculated. Subfoveal and pulsatile choroidal blood flow were measured with laser Doppler flowmetry and laser interferometry, respectively. RESULTS: After infusion of histamine pulsatile choroidal blood flow increased by 5 +/- 3%, 9 +/- 8%, and 14 +/- 7% (P = 0.001, ANOVA) and subfoveolar choroidal blood flow by 8 +/- 11%, 13 +/- 11%, and 13 +/- 12% (P = 0.003, ANOVA). Retinal arterial and venous vessel diameter significantly increased by 3 +/- 4%, 2 +/- 4%, and 3 +/- 5% (P = 0.047, ANOVA) and 1 +/- 2%, 3 +/- 2%, and 3 +/- 2% (P = 0.015, ANOVA), respectively. Red blood cell velocity in major retinal veins tended to decrease by -9 +/- 12%, -9 +/- 20%, and -13 +/- 12%, but this effect did not reach levels of significance. Calculated retinal blood flow was not changed by administration of histamine (-7 +/- 14%, -4 +/- 20%, and -8 +/- 12%, P = 0.28, ANOVA). CONCLUSIONS: Intravenous histamine in the selected doses increased choroidal blood flow. Retinal vessels showed a small diameter increase, whereas red blood cell speed decreased, resulting in an unchanged total retinal blood flow. This may result from local differences in the receptor distribution in the posterior part of the eye.

Adult↗
PubMed1997

Retinal large vessel oxygen saturations correlate with early blood loss and hypoxia in anesthetized swine.

BACKGROUND: Noninvasive monitoring would likely improve trauma care. Using laser technology, we monitored the oxygen saturation in retinal vessels during exsanguination and hypoxia. METHODS: Seven anesthetized swine were bled at 0.4 mL/kg/min for 40 minutes. During exsanguination, retinal venous saturation (SrvO2) was measured using an eye oximeter, and central venous saturation (SvO2) was measured using a fiber-optic catheter. After the shed blood was reinfused, the FiO2 was progressively decreased from 0.97 to 0.07. Femoral artery oxygen saturation (SaO2) and retinal artery oxygen saturation (SraO2) were measured at each increment. RESULTS: During exsanguination, SrvO2 correlated with blood loss (r = -0.93) and SvO2 (r = 0.94). SraO2 correlated with SaO2 during incremental hypoxia (R2 = 0.93 +/- 0.15). CONCLUSIONS: In this model of exsanguination, retinal venous oxygen saturation correlates with blood volume and with central venous oxygen saturation. The SraO2 correlates with SaO2 during graded hypoxia. Use of an eye oximeter to noninvasively monitor trauma patients appears promising and warrants further study.

Anesthesia↗
PubMed1987

Retinal vascular endothelium expresses fibronectin and class II histocompatibility complex antigens in experimental autoimmune uveitis.

To analyze the role of the retinal vascular endothelial cells in the development of experimental autoimmune uveitis (EAU), we studied the presence of Ia antigen and FN in retinal vessels of Lewis rats immunized with retinal S antigen. Immunopathologic studies were performed on frozen tissues obtained during various stages of the disease. Our results show that Ia antigen was not present in the normal rat retina, and there was very little FN present in a few retinal vessels. One to two days prior to the histologic and clinical onset of EAU, FN was found to be increased in the retinal vessels. Ia antigen was found to be present in the retinal vessels coincident with the first signs of cellular infiltration. During the stage of maximal cellular infiltration, FN was present diffusely throughout the retina, as well as in the subretinal space, and Ia antigen was found diffusely in the cellular infiltrate. Therefore, FN and Ia antigen reflect the immunomodulation of vascular endothelial cells in EAU, which may be very important in the pathogenesis of retinal S antigen-induced uveitis. Two possible mechanisms for the role of the activation of the retinal vascular endothelium in the development of retinal inflammation in uveitis are discussed.

Animals↗
PubMed1983

Insulin receptors in calf and human retinal blood vessels.

A system for isolation of capillaries from the retina has been adapted to biochemical studies in vitro. Insulin receptors were identified in human and calf retinal blood vessels. Binding of 125I insulin by calf retinal blood vessels takes place through high affinity (low capacity) and low affinity (high capacity) receptor sites. Insulin binding is inhibited by glucagon, and cGMP and proinsulin. Dissociation of insulin receptor protein or lipid with Triton X-100 or phospholipase results in significant decreases in 125I insulin binding by retinal blood vessels. Dissociation of insulin bound occurs only at 0 degrees C which may be due to rapid internalization of insulin at higher temperatures. Activities of cAMP and cGMP phosphodiesterases and cyclase of retinal vessels were not significantly changed by incubation with insulin. At high concentrations in the media human growth hormone stimulates and then inhibits I125 insulin binding by retinal capillaries.

Aged↗
PubMed2003

Regulation of human retinal blood flow by endothelin-1.

There is evidence from in vitro and animal studies that endothelin is a major regulator of retinal blood flow. We set out to characterize the role of the endothelin-system in the blood flow control of the human retina. Two studies in healthy subjects were performed. The study design was randomized, placebo-controlled, double-masked, balanced, two-way crossover in protocol A and three way-way crossover in protocol B. In protocol A 18 healthy male subjects received intravenous endothelin-1 (ET-1) in a dose of 2.5 ng kg (-1)min(-1) for 30 min or placebo on two different study days and retinal vessel diameters were measured. In protocol B 12 healthy male subjects received ET-1 in stepwise increasing doses of 0, 1.25, 2.5 and 5 ng kg (-1)min(-1) (each infusion step over 20 min) in co-infusion with the specific ET(A)-receptor antagonist BQ123 (60 microg min (-1)) or placebo or BQ123 alone investigating retinal vessel diameters, retinal blood velocity and retinal blood flow. Measurements of retinal vessel size were done with the Zeiss retinal vessel analyzer. Measurements of blood velocities were done with bi-directional laser Doppler velocimetry. From these measurements retinal blood flow was calculated. In protocol A exogenous ET-1 tended to decrease retinal arterial diameter, but this effect was not significant versus placebo. No effect on retinal venous diameter was seen. In protocol B retinal venous blood velocity and retinal blood flow was significantly reduced after administration of exogenous ET-1. These effects were significantly blunted when BQ-123 was co-administered. By contrast, BQ-123 alone had no effect on retinal hemodynamic parameters. Concluding, BQ123 antagonizes the effects of exogenously administered ET-1 on retinal blood flow in healthy subjects. In addition, the results of the present study are compatible with the hypothesis that ET-1 exerts its vasoconstrictor effects in the retina mainly on the microvessels.

Adult↗