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At least 865 records · Page 48Linked to original sources
PubMed2000

[Autoregulation of retinal arterioles in patients with diabetes mellitus and normal probands].

BACKGROUND: Measurement of myogenic autoregulation of retinal arterioles was demonstrated by the use of the Retinal-Vessel-Analyzer (Carl Zeiss, Jena). The purpose of the presented study was to find a significant difference of this myogenic response in a group of healthy individuals vs. a group of patients with pathologic conditions. PATIENTS AND METHODS: As a group of patients with known pathology in microcirculation patients with type 1 diabetes were chosen. By isometric exercise an identical rise in mean arterial blood-pressure was provoked in 20 patients with type-1 diabetes and 20 matched healthy volunteers. The myogenic response of retinal arterioles was measured in both groups by the use of the Retinal-Vessel-Analyzer. The Wilcoxon test was used for statistical analysis within the two groups whereas both groups were compared with each other by the use of the Mann-Whitney test. RESULTS: Having the same age and same blood-pressure rise (p = 0.624) a significant better myogenic response was found in the healthy subjects vs. the diabetic group (p = 0.008). In the diabetic group no correlation was found between myogenic response and duration of diabetes (p = 0.982) or HbA1c values (p = 0.83). CONCLUSIONS: In this study significant loss of autoregulation in patients with type 1 diabetes is demonstrated. By the use of the Retinal-Vessel-Analyzer noninvasive testing of the function of autoregulation of retinal arterioles is possible. This method might prove to be of great value in early detection of diabetic vessel pathology.

Adolescent↗
PubMed1987

Angiotensin binding sites in bovine and human retinal blood vessels.

Blood vessels isolated from bovine and human retinas have sites that specifically bind 3H-angiotensin II (3H-Ag II) with an apparent dissociation constant (Kd) of 14 nM and a capacity of binding (Bmax) of 0.82 pmol/g. The binding sites for 3H-Ag II appear to be influenced by guanine nucleotides (GTP) and cations (Mg2+ and Na+) in a way that resembles angiotensin II receptors in other tissues. The physiologic effect of blood-borne or locally-formed angiotensin II on retinal blood flow remains to be defined.

Angiotensin II↗
PubMed1988

Changes in oxygen tension and effects on cyclooxygenase metabolites: III. Decrease of retinal prostacyclin in kittens exposed to hyperoxia.

The acute phase of oxygen-induced retinopathy is associated with vasoconstriction and occlusion of the retinal vessels. Because this acute vasoobliterative phase could be due to the inhibition in retinal vessels of the production of the potent vasodilator and antithrombotic metabolite prostacyclin, animal experiments were performed to assess this possibility. Eight litters of 27 kittens (four to six days of age) were used. Control kittens were left in room air; hyperoxic kittens were placed in 80% oxygen for 48 hours; recovery kittens were returned to room air for 24 hours following hyperoxic exposure. Following treatments, the animals were killed, retinas isolated, and prostaglandin formation assessed. Retinal tissues produced 6-keto-prostaglandin F1 alpha, prostaglandin F2 alpha, prostaglandin E2, and thromboxane B2 from exogenous arachidonate. A significant (approximately 33%) reduction in retinal 6-keto-prostaglandin F1 alpha (the end product of prostacyclin) was observed both in the hyperoxic and recovery litter mates when compared with controls. Both of the experimental groups also demonstrated a reduction in total retinal prostanoids that paralleled the changes observed in prostacyclin, suggesting that the biochemical effect of hyperoxia on retinal vascular arachidonic acid metabolism occurred at the level of cyclooxygenase. A decrease in the local production of prostacyclin during hyperoxia is consistent with the histologic retinal changes observed during the acute phase of oxygen-induced retinopathy.

6-Ketoprostaglandin F1 alpha↗
PubMed2001

Ocular changes after intravitreal injection of methanol, formaldehyde, or formate in rabbits.

We evaluated the effects of intravitreal injection of methanol, formaldehyde, or formate on rabbit eyes. One hundred microl of 1% methanol, 1% or 0.1% formaldehyde, or 1% formate was injected in the vitreous cavity of the right eyes of rabbits. The eyes were examined by biomicroscopy and ophthalmoscopy weekly. One month after injection, the eyes were enucleated and examined histologically. One week after treatment the animals that received 0.1% formaldehyde showed retinal vessel dilation, and the rabbits that received 1% formaldehyde showed mild posterior subcapsular cataract and retinal vessel dilation and haemorrhages. One month after treatment, the animals that received 0.1% or 1% formaldehyde developed mild posterior subcapsular cataract and retinal lesions. Animals that received 1% methanol or 1% formate showed nearly normal optical media and fundi. Histologically disorganized retina and optic nerve were seen in eyes that received 0.1% or 1% formaldehyde. Eyes that received 1% methanol or 1% formate appeared histologically normal. Our findings indicate that intravitreal injection of formaldehyde causes retinal and optic nerve damage, while methanol and formate are not or less toxic to ocular tissues.

Animals↗
PubMed1991

Dietary treatment of atherosclerosis abolishes hyperresponsiveness of retinal blood vessels to serotonin in monkeys.

BACKGROUND AND PURPOSE: Atherosclerosis alters vascular responses of the eye to serotonin. Augmented vasoconstrictor responses in the retina to serotonin are associated with functional impairment and may contribute to amaurosis fugax. The goal of this study was to test the hypothesis that dietary treatment of atherosclerosis restores vascular responses of the eye toward normal. METHODS: We measured blood flow to the retina using microspheres in six normal monkeys, five atherosclerotic monkeys, and five atherosclerotic monkeys that were fed a normal (regression) diet for 18 months. RESULTS: Infusion of 8 and 40 micrograms.min-1.kg-1 serotonin into the left atrium had little effect on blood flow to the retina in normal monkeys. In contrast, the high dose of serotonin reduced blood flow to the retina by a mean +/- SEM of 81 +/- 9% (p less than 0.05) in atherosclerotic monkeys. In monkeys that were fed the regression diet, serotonin had no effect on blood flow to the retina. CONCLUSIONS: Regression of atherosclerosis abolishes augmented responses of the retinal circulation to serotonin.

Animals↗
PubMed2002

Inter-eye differences in chronic open-angle glaucoma patients with unilateral disc hemorrhages.

OBJECTIVE: Flame-shaped optic disc hemorrhages are a hallmark of glaucomatous optic neuropathy. The purpose of this study was to evaluate which parameters differ between companion eyes with and without an optic disc hemorrhage in patients with chronic open-angle glaucoma. DESIGN: Comparative (companion eye) observational case series. PATIENTS: The study included 99 white patients with bilateral chronic open-angle glaucoma and unilateral flame-shaped optic disc hemorrhages. METHODS: All patients underwent qualitative and morphometric evaluation of color stereo optic disc photographs. MAIN OUTCOME MEASURES: Size and shape of the optic disc, neuroretinal rim and parapapillary atrophy, diameter of the retinal vessels, intraocular pressure measurements, and both mean value and loss variance value of the visual field examination. RESULTS: In an intraindividual inter-eye comparison, the eyes with disc hemorrhages and the contralateral eyes without disc bleeding did not vary significantly (P > 0.20) in size and shape of the optic disc and neuroretinal rim, optic cup depth, size of alpha and beta zone of parapapillary atrophy, retinal vessel diameter, intraocular pressure measurements, refractive error, and perimetric indices. CONCLUSIONS: In bilateral chronic open-angle glaucoma, the development of unilateral optic disc hemorrhages does not depend on inter-eye differences in size and shape of the optic disc, neuroretinal rim and parapapillary atrophy, diameter of the retinal vessels, intraocular pressure measurements, or visual field loss.

Adolescent↗
PubMed2000

[Noise field findings in 24 patients with coronary heart disease].

PURPOSE: In earlier studies it was shown that patients with vascular disturbances (e.g. sudden hearing loss) had white-noise field campimetry abnormalities despite normal visual fields. The aim of this study was to clarify whether patients with coronary heart disease (CHD) have such disturbances in the white-noise field campimetry, too. PATIENTS AND METHODS: Twenty-four patients (m:f = 23:1; mean age 58 +/- 9 years) with an angiographically documented CHD and 30 healthy controls (m:f = 29:1; mean age 54 +/- 7 years) were examined. In order to evaluate the morphological and functional ocular status, we examined the following parameters: morphological status, visual acuity, intraocular pressure, perimetry (Tübinger Automatic Perimeter 2000 ct, Oculus) and white-noise field campimetry (Tübinger Electronic Campimeter, Oculus). RESULTS: Fifteen patients had had a cardiac infarction. Twenty-one patients, but only 6 controls had alterations in perilimbal vessels of the conjunctiva and sixteen patients had a tortuousity of retinal vessels. The visual acuity, the intraocular pressure, the cup/disc ratio and the visual fields were within normal ranges. However, twenty patients and 5 controls were abnormal in the white-noise field campimetry. DISCUSSION: Although patients with CHD appeared unaffected in the standard eye examinations, the disturbances in the white-noise field campimetry indicated a functional visual impairment. Together with the changes in the perilimbal vessels of the conjunctiva and the retinal vessels, a disturbed ocular microcirculation as the underlaying cause could be discussed.

Adult↗
PubMed2005

A novel protocol of retrograde cerebral perfusion with intermittent pressure augmentation for brain protection.

OBJECTIVES: We examined a novel protocol of retrograde cerebral perfusion with intermittent pressure augmentation to improve the clinical usefulness of this procedure, in a canine model, because a high retrograde cerebral perfusion pressure may be required to open cerebral vessels. METHODS: Eighteen dogs (25.2 +/- 4.1 kg) were randomly divided into the following 3 groups: circulatory arrest group (circulatory arrest alone), conventional-retrograde cerebral perfusion group (conventional retrograde cerebral perfusion at 25 mm Hg), and intermittent-retrograde cerebral perfusion group (retrograde cerebral perfusion at 15 mm Hg with intermittent pressure augmentation to 45 mm Hg). The animals were cooled down to 26 degrees C under cardiopulmonary bypass and underwent 60 minutes of circulatory arrest with or without retrograde cerebral perfusion in accordance with the protocol described. They were weaned from cardiopulmonary bypass after rewarming and observed for 12 hours after the procedures. The retinal vessels were observed as a means of noninvasive direct visualization of the cerebral vascular system. The level of Tau proteins in the cerebrospinal fluid was measured as a marker of neuronal damage. RESULTS: While the retinal vessels were fully distended with blood (100%) at a retrograde cerebral perfusion pressure of 45 mm Hg in the intermittent-retrograde cerebral perfusion group, full distension of the retinal vessels was not observed in the conventional-retrograde cerebral perfusion group (67%). The level of Tau proteins, measured 12 hours after the operation, was lower in the intermittent-retrograde cerebral perfusion group (247 +/- 70 pg/mL) than in the circulatory arrest group (1313 +/- 463 pg/mL; P < .05) or the conventional-retrograde cerebral perfusion group (1449 +/- 693 pg/mL; P < .05). Histopathologic examination revealed that the most effective brain protection was obtained in the intermittent-retrograde cerebral perfusion group (P < .05). CONCLUSIONS: Intermittent-retrograde cerebral perfusion effectively opens up cerebral vessels to allow adequate blood supply to the brain, thereby minimizing brain damage. This novel method may protect the cerebral system effectively from ischemia during circulatory arrest.

Animals↗
PubMed1981

Chorioretinal dysplasia in young subjects with Wagner's hereditary vitreoretinal degeneration.

Six young patients from three pedigrees with Wagner's disease were submitted to fluorescein angiography of the peripheral fundus. All eyes showed aberrant areas, characterized by: 1. localization principally in equatorial region of temporal half of the fundus. 2. whitish appearance of neuroretina with sharp demarcations. 3. absence of retinal vasculature. 4. marked atrophy of choriocapillaris and retinal pigment epithelium. 5. abnormal deflections of retinal vessels at the posterior margin of these areas. Arguments are presented in support of the hypothesis that these areas were dysplastic and not degenerative. The difference with lattice degeneration, another wellknown finding in Wagner's disease, is that retinal vasculature never developed in the dysplastic peripheral areas. It is probable that hypoplasia of the choroid has led to a too inferior structure of the overlying retina to permit development of retinal vessels. The frequent occurrence of retinal breaks in young patients with Wagner's disease, especially in the temporal periphery, seems to be a consequence of the poor condition of the retina in these dysplastic areas caused by the inferior development of both retinal and choroidal vasculature.

Adolescent↗
PubMed1999

Automated localisation of the optic disc, fovea, and retinal blood vessels from digital colour fundus images.

AIM: To recognise automatically the main components of the fundus on digital colour images. METHODS: The main features of a fundus retinal image were defined as the optic disc, fovea, and blood vessels. Methods are described for their automatic recognition and location. 112 retinal images were preprocessed via adaptive, local, contrast enhancement. The optic discs were located by identifying the area with the highest variation in intensity of adjacent pixels. Blood vessels were identified by means of a multilayer perceptron neural net, for which the inputs were derived from a principal component analysis (PCA) of the image and edge detection of the first component of PCA. The foveas were identified using matching correlation together with characteristics typical of a fovea-for example, darkest area in the neighbourhood of the optic disc. The main components of the image were identified by an experienced ophthalmologist for comparison with computerised methods. RESULTS: The sensitivity and specificity of the recognition of each retinal main component was as follows: 99.1% and 99.1% for the optic disc; 83.3% and 91.0% for blood vessels; 80.4% and 99.1% for the fovea. CONCLUSIONS: In this study the optic disc, blood vessels, and fovea were accurately detected. The identification of the normal components of the retinal image will aid the future detection of diseases in these regions. In diabetic retinopathy, for example, an image could be analysed for retinopathy with reference to sight threatening complications such as disc neovascularisation, vascular changes, or foveal exudation.

Algorithms↗
PubMed2003

Human T-cell lymphotropic virus type 1-associated retinal vasculitis in children.

PURPOSE: To describe predominant retinal vasculitis in children carrying human T-cell lymphotropic virus type 1 (HTLV-1). METHODS: The authors examined clinical records of patients with HTLV-1-associated uveitis between 1987 and 2001 in Kagoshima University Hospital and reviewed cases of extensive, smoldering retinal vasculitis. RESULTS: Three previously healthy teenagers noted mild visual symptoms and presented with extensive sheathing of retinal vessels, complicated by mild anterior segment inflammation. The retinal vascular disease responded poorly to systemic corticosteroids, had a smoldering course with persistent sheathing of retinal vessels, and eventually resulted in diffuse chorioretinal degeneration. Results of laboratory studies were unremarkable except for the presence of serum antibodies to HTLV-1. One patient developed HTLV-1-associated myelopathy 11 years after the onset of ocular disease. CONCLUSIONS: The retinal vasculitis differed from the retinal vascular changes commonly seen in HTLV-1-associated uveitis. The authors suggest a clinical disease HTLV-1-associated retinal vasculitis that affects young HTLV-1 carriers, characterized by smoldering retinal vasculitis with ultimate retinal degeneration.

Adolescent↗
PubMed2006

Noninvasive evaluation of wall shear stress on retinal microcirculation in humans.

PURPOSE: To evaluate wall shear stress (WSS) on retinal microcirculation noninvasively. METHODS: Retinal vessel diameter (D) and mean centerline blood velocity (V(max, mean)) were measured in the retinal arterioles and venules at first- and second-order branches in 13 subjects using laser Doppler velocimetry (LDV). Retinal blood flow (RBF) and wall shear rate (WSR) were calculated using these two parameters. Blood viscosity at the calculated shear rate was also measured using a cone-plate viscometer. WSS was calculated as the product of the WSR and the blood viscosity. RESULTS: In the first-order branches, the averaged D, V(max, mean), RBF, and WSR(mean) were 108 +/- 13 microm, 41 +/- 10 mm/s, 11 +/- 4 microL/min, and 1539 +/- 383 s(-1) in the arterioles and 147 +/- 13 microm, 23 +/- 3 mm/s, 12 +/- 4 microL/min, and 632 +/- 73 s(-1) in the venules, respectively. The apparent blood viscosities at the measured shear rates were 3.5 +/- 0.3 centipoise (cP) in the arterioles and 3.8 +/- 0.4 cP in the venules. Therefore, the averaged WSS was 54 +/- 13 dyne/cm2 in the arterioles and 24 +/- 4 dyne/cm2 in the venules. The WSS in the second-order arterioles was significantly lower than that in the first-order branches (P = 0.002), but the WSS in the first-order venules was similar to that in the second-order venules. CONCLUSIONS: The authors demonstrated that the WSS in the retinal vessels could be evaluated noninvasively in humans using LDV and cone-plate viscometry. This system may be useful for further clinical investigation of the role of shear stress in the pathogenesis of various retinal disorders.

Adult↗
PubMed1984

Microvascular aspects of acquired immune deficiency syndrome retinopathy.

Twelve of 13 patients with the acquired immune deficiency syndrome exhibited ophthalmoscopically detectable retinal findings, including cotton-wool spots, hemorrhages, Roth spots, and microvascular changes. When we used fluorescein angiography, we detected focal nonperfusion and microvascular changes in all 13 of our patients. Most patients had no visual complaints unless they had cytomegalovirus involvement of the optic papilla or the central retina. One patient lost central visual acuity from loss of perfusion in a portion of his perifoveal capillary net. Histopathologic studies demonstrated the loss of retinal capillary cells and focal occlusions of small vessels. Retinal vessel walls were also thickened with PAS-positive material.

Acquired Immunodeficiency Syndrome↗
PubMed1985

[Simultaneous photography or angiography of anterior and posterior eye segments in experimental animals].

Simultaneous photographic or angiographic studies of the anterior and posterior segments requires a considerable reduction in the respective parts of the negatives; this can be avoided by simultaneous study of the one segment ipsilaterally and the other contralaterally (this can also be performed vice versa). Differences and common properties of the eyes of rabbits and miniature pigs and the human eye are described. Apart from the monkey eye, the pig eye is most readily comparable with the human eye as regards vasotopographic and vasomorphologic conditions. In addition, the courses of angiographies in the eyes of experimental animals were observed; measurements of fluorescein inflow and circulation times in the anterior and posterior segments in miniature pigs are presented. These were subjected to significance tests: only the difference in the inflow and outflow of the dye in retinal vessels was found to be statistically highly significant. The difference in inflow between choroidal and retinal vessels was not significant, though this may have been due to an error of measurement. The techniques and measurements described represent the basis of observation in miniature pigs with experimentally induced hypertension.

Animals↗
PubMed1999

Hyperoxia causes decreased expression of vascular endothelial growth factor and endothelial cell apoptosis in adult retina.

Mice or humans with photoreceptor degenerations experience permeability and dropout of retinal capillaries. Loss of photoreceptors results in decreased oxygen usage and thinning of the retina with increased oxygen delivery to the inner retina. To investigate the possibility that increased tissue oxygen plays a role in the vascular damage, we exposed adult mice to hyperoxia, which also increases oxygen in the retina. After 1, 2, or 3 weeks of hyperoxia, there was a statistically significant decrease in retinal vascular density that was not reversible, and endothelial cell apoptosis was demonstrated by TUNEL staining. Mice exposed to hyperoxia and mice with photoreceptor degeneration both showed decreased expression of VEGF in the retina. After complete or near-complete degeneration of photoreceptors, there was increased expression of VEGF in RPE cells, which may explain the association of photoreceptor degeneration and neovascularization in or around the RPE. Increased expression of VEGF in photoreceptors of transgenic mice failed to prevent hyperoxia-induced retinal capillary dropout. These data suggest that increased oxygen in the retina, either by increased inspired oxygen or by photoreceptor degeneration, results in endothelial cell death and dropout of capillaries. Decreased expression of VEGF may be a contributing factor, but the situation may be more complicated for mature retinal vessels than it is for immature vessels, because VEGF replacement does not rescue mature retinal vessels, suggesting that other factors may also be involved.

Animals↗
PubMed1997

Retinal leukocyte behavior in experimental autoimmune uveoretinitis of rats.

In vivo retinal leukocyte behavior in the experimental autoimmune uveoretinitis (EAU) of rats was investigated using acridine orange digital fluorography. The technique employed high resolution images obtained from a scanning laser ophthalmoscope (SLO) subsequent to staining with the fluorescent nuclear dye, acridine orange. Two weeks after immunization with synthetic peptides of retinal soluble antigen (S-Ag), acridine orange was intravenously injected, and fundus images were generated by SLO. Many rolling leukocytes were observed along the venous walls as slowly moving fluorescent dots; moreover, leukocytes infiltrating into the vitreous cavity were also noted especially over the retinal veins, but not over the retinal arteries. In addition, major retinal vessels were significantly dilated. The diameters of the retinal veins at a distance of 1 disc diameter away from the center of the optic disc were 49.8+/-4.5 micron for the normal rats and 88.2+/-3.6 micron for the EAU rats, respectively (P<0.001). Similarly, the diameters of retinal arteries were 32.6+/-3.7 micron for the normal rats, 53.8+/-1.5 micron for the EAU rats, respectively (P<0.01). The dilation was more prominent in the veins than in the arteries. These results suggest that it is possible to visualize the retinal involvement of EAU in vivo. The results also suggest that leukocyte-endothelial interaction and extravascular infiltration in the retinal venous vasculature may play significant roles in the early stages of posterior segment inflammation in EAU.

Acridine Orange↗