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PubMed1999

Chorioretinal lesions in patients and carriers of chronic granulomatous disease.

OBJECTIVE: To investigate the frequency of retinal lesions in patients with chronic granulomatous disease (CGD) and to seek such lesions in carriers. STUDY DESIGN: Seventy-four individuals from 33 families were recruited; 38 had CGD (30 X-linked and 8 autosomal recessive inheritance). All participants (including 33 control subjects) underwent measurement of visual acuity, anterior segment examination by slit lamp, and dilated funduscopy. RESULTS: Nine of 38 (23.7%) of the affected children had chorioretinal lesions compared with 0 of 33 control subjects. All 9 were known to have X-linked CGD and absent gp91(phox). The "typical" retinal abnormality consisted of "punched out" chorioretinal lesions associated with pigment clumping lying along major retinal vessels. Unexpectedly, 3 XL-CGD asymptomatic carriers also had typical chorioretinal lesions. CONCLUSION: Retinal lesions are relatively common in patients with XL-CGD and may interfere with vision and thus should be sought in such patients.

Adolescent↗
PubMed1980

[Incontinentia pigmenti (Block-Sulzberger syndrome) associated with congenital retinal fold--a long-term 18-year observation].

Report on a case of incontinentia pigmenti presenting with the main characteristics features: patchy hyperpigmentation of the skin, alopecia and dental anomalies. In addition to the rare hyperpigmentation of the lower eyelids, hemiatrophy of the right face and horizontal nystagmus were found. Eye involvement consisted of a congenital retinal fold with retinal vessels draen into and bordered by pigment clumps.--When the patient with 14 total retinal detachment associated with a totally liquefied vitreous occurred and surgical reattachment failed. As a rarity in this case, the full picture of retrolental fibroplasia was not present; it was possible to follow developments over a period of 18 years.

Alopecia↗
PubMed1998

Retinal arterial tone is controlled by a retinal-derived relaxing factor.

The present study provides evidence that retinal tissue may profoundly influence the retinal arterial smooth muscle cell tone by releasing an unknown retinal relaxing factor. Isolated bovine retinal arteries with and without adhering retinal tissue were mounted in a wire myograph for isometric tension recordings. The maximal contraction induced by prostaglandin F2alpha was 0.95+/-0.7 mN (n=6) in the presence and 5.15+/-0.76 mN (n=6) in the absence of adhering retinal tissue. The contractions induced by U-46619, serotonin, and endothelin-1 were similarly blocked in the presence of retinal tissue. The K+ 120 mmol/L-induced contraction was not significantly affected (2.8+/-0.7 mN, n=6, in the presence and 3. 6+/-0.7 mN, n=6, in the absence of retinal tissue). Placing a piece of bovine retinal tissue in the proximity of a contracted (ie, with prostaglandin F2alpha) retinal artery induced a complete relaxation of the retinal vessel, suggesting the involvement of a diffusible chemical vasorelaxant. Also porcine, canine, and ovine retinal tissue completely relaxed the contracted (with prostaglandin F2alpha) bovine retinal artery. Other smooth muscle preparations, including rat mesenteric and renal arteries and rat main bronchi, also relaxed with the application of a piece of bovine retinal tissue. Incubation of bovine retinas in a Krebs-Ringer bicarbonate solution yielded a solution that relaxed isolated precontracted bovine retinal arteries, confirming the involvement of a diffusible chemical messenger. Hexane extraction, heating the solution to 70 degrees C, or treatment with trypsin did not alter the relaxing properties of the incubation solution. The characteristics of the retinal relaxing factor do not correspond with those of nitric oxide, prostanoids, adenosine, acetylcholine, or any other of the known vasoactive neurotransmitters released from the retina. Our results suggest that retinal arterial tone is controlled by a diffusible, hydrophilic, and heat-stable relaxing factor that does not correspond with a known vasoactive molecule formed within the retina.

Animals↗
PubMedDate not supplied

[Amyloidosis of fundus oculi tissues in senile maculopathy (a clinico-morphological study)].

The authors analyze the findings of clinical and morphologic studies of the pathologic changes in fundus oculi tissues of 3 patients who died with senile macular dystrophy, examined in life time by ophthalmoscopic technique with transformed light. The sclera, vascular coating, retina, macula retinae, optic nerve region were thoroughly studied with the use of review histological, histochemical methods, selective test for amyloid, thiazine red fluorescent histochemical method, and thioflavin T fluorescence. In 2 of the 3 cases amyloid degeneration in the presence of amyloid deposits in choroid vessels, arterial plexus vessels round the optic nerve presence of amyloid deposits in choroid vessels, arterial plexus vessels round the optic nerve orifice, in Bruch's membrane and in the sclera. Retinal vessels, optic nerve and its coatings were intact. Further investigations are to follow.

Age Factors↗
PubMed1985

Ocular manifestations of sickle cell disease in Nigerians; experience in Benin City, Nigeria.

The ocular findings in 50 cases of homozygous sickle cell disease are reported. Ocular abnormalities were found in 45 (90%) of them. Conjunctival vascular anomalies, tortuosity of the retinal vessels, particularly the veins and pigmented chorioretinal lesions were the commonest ocular manifestations; central retinal artery occlusion was found in one patient. Angioid streaks, retinitis proliferans and retinal detachment were not observed. Visual acuity was normal in 49 out of 50 patients; the exception was the patient with central artery occlusion.

Adolescent↗
PubMed1983

Progressive chloroquine retinopathy.

Chloroquine retinopathy is a well-documented toxic manifestation of a commonly used systemic medication. The major retinal findings are those of macular retinal pigment epithelial changes, narrowed retinal vessels, and scotomatous visual field defects. The fluorescein angiographic findings are those of a retinal pigment epithelial transmission defect that takes on a bull's-eye configuration. We present a patient who had taken chloroquine for two years while in the military service. Two years after discharge, he was examined and reported to have a mild granular appearance to the macula. Over a period of nine years, progressive decreased central acuity prompted repeated fluorescein angiograms, which revealed a progressive bull's-eye maculopathy compatible with chloroquine retinopathy. Evaluation of offspring failed to reveal any evidence of a hereditary macular dystrophy. To our knowledge, this is the first reported case of delayed onset and progression of chloroquine maculopathy documented by fluorescein angiography.

Chloroquine↗
PubMed2004

Clinical and immunologic aspects of cancer-associated retinopathy.

PURPOSE: To report clinical and immunologic aspects of cancer-associated retinopathy (CAR). DESIGN: Observational consecutive case series. METHODS: A retrospective review was made of 18 consecutive patients with cancer-associated retinopathy who had antiretinal antibody determination by Western blot testing. RESULTS: Clinically, a variety of ophthalmic observations including electroretinography impairment, retinal vessel narrowing, deterioration of visual acuity, visual field changes, and uveitis were frequently observed. As retinal autoantigens in the 18 cases, recoverin was found in all 18 cases (100%), heat shock cognate protein 70 (HSC70) was found in six cases (33%), and other proteins were found in four cases (20%). These antibodies were detected in only 60% of the patients at the initial examination, however, and then became increasingly apparent on the subsequent testing that was performed three times on serum samples obtained sequentially during the following months. CONCLUSION: For diagnosis of cancer-associated retinopathy, the presence of serum autoantibody toward recoverin is essentially required in addition to the characteristic clinical aspects noted above.

Adult↗
PubMed2002

Calculation of the diameter of the central retinal artery from noninvasive measurements in humans.

PURPOSE: The aim of the present study was to calculate the diameter of the central retinal artery from results as obtained with non-invasive techniques in healthy young subjects. METHODS: Twenty-four healthy male subjects participated in this study. Total retinal blood flow was calculated from combined bi-directional laser Doppler velocimetry and measurement of retinal venous diameters using the Zeiss retinal vessel analyzer. Using these techniques red blood cell velocity and vessel diameters of all visible veins entering the optic nerve head were measured and total retinal blood flow was calculated. Blood flow velocity in the central retinal artery was measured with color Doppler imaging. Form these outcome parameters the diameter of the central retinal artery was calculated for each subject individually. RESULTS: In the present study cohort the mean retinal blood flow was 38.1 +/- 9.1 microl/min and the mean flow velocity in the central retinal artery was 6.3 +/- 1.2 cm/s. From these data we calculated a mean diameter of the central retinal artery of 163 +/- 17 microm. CONCLUSIONS: Our results are in good agreement with data obtained from in vitro studies. The data of the present study also indicate that one needs to be careful to interpret velocity data from the central retinal artery in terms of retinal blood flow.

Adult↗
PubMed1998

Increased expression of placenta growth factor in proliferative diabetic retinopathy.

Proliferative diabetic retinopathy is thought to be mediated by the hypoxic regulation of angiogenic growth factors, in particular the vascular endothelial growth factor (VEGF) family. The aim of this study was to determine if placental growth factor (PIGF), a recently identified member of the VEGF family, was expressed in diabetic eyes undergoing preretinal neovascularization. Rabbit anti-PIGF antiserum was raised using a 20-amino acid N-terminal sequence to PIGF and did not cross react with VEGF165. Immunohistochemistry was performed on specimens of normal retina (n = 8), diabetic retina in the absence (n = 7) and presence (n = 4) of proliferative retinopathy, scatter laser-treated diabetic retina (n = 7), excised fibrovascular preretinal membranes (n = 12), and nondiabetic fibrocellular epiretinal (n = 7) membranes. PIGF levels were also determined in vitrectomy specimens from patients with either proliferative diabetic retinopathy or macular hole. PIGF immunoreactivity was intensely localized to the endothelial and perivascular regions of newly formed blood vessels of excised fibrovascular preretinal membranes. Intense localization of PIGF protein was also observed in superficial retinal vessels in diabetic retinae adjacent to neovascular preretinal membranes. Localization of PIGF was weak or absent in diabetic retinae that showed no evidence of neovascular proliferation. PIGF protein was also absent in normal retinae, in diabetic retinae that had received extensive treatment with scatter laser photocoagulation, and in nonvascularized epiretinal membranes. PIGF was present in all diabetic vitreous samples (mean 103 pg/ml) but nondetectable in control samples. These results strongly implicate a role for PIGF in the pathogenesis of proliferative diabetic retinopathy.

Adult↗
PubMed2005

Relation of atherosclerotic changes in retinal arteries to the extent of coronary artery disease.

The aim of this study was to explore the relation between atherosclerosis of the retinal arteries and the extent and severity of coronary artery disease (CAD). In 109 patients, aged 40 to 80 years, who underwent coronary angiography for suspected CAD, the degree of retinal arterial atherosclerosis (stages 1 to 4 according to Scheie) was determined. The fundus examination was done using direct ophthalmoscopy by an ophthalmologist blinded to the extent of the CAD. The CAD extent was evaluated by Gensini score, and coronary angiograms were analyzed by 2 expert observers who had no knowledge of the patients' retinal artery status. The extent and severity of retinal vessel atherosclerosis correlated strongly with the extent and severity of CAD. Thus, atherosclerotic changes in the retinal arteries may be a predictor of the extent of CAD.

Adult↗
PubMed1989

Thrombolytic activity of defibrotide against old venous thrombi.

The age of the thrombus is probably a very important determinant of the outcome of thrombolysis. The clinical potential for rapidly dissolving thrombi by thrombolytic therapy is considerable because restoration of the blood flow can rescue the jeopardized district served by the occluded vessel such as for myocardial infarction, deep vein thrombosis, arterial thrombosis, pulmonary embolism, and occlusion of retinal vessels. Defibrotide was effective against 3-, 7-, or 10-day-old thrombi; its ED50s were 32, 65, or 118 mg/kg-1 hour-1, respectively, suggesting that the age of the thrombus could play a role in the outcome of thrombolysis. A similar pattern was also shown for urokinase.

Animals↗
PubMed2006

Orientation of endothelial cell division is regulated by VEGF signaling during blood vessel formation.

New blood vessel formation requires the coordination of endothelial cell division and the morphogenetic movements of vessel expansion, but it is not known how this integration occurs. Here, we show that endothelial cells regulate division orientation during the earliest stages of blood vessel formation, in response to morphogenetic cues. In embryonic stem (ES) cell-derived vessels that do not experience flow, the plane of endothelial cytokinesis was oriented perpendicular to the vessel long axis. We also demonstrated regulated cleavage orientation in vivo, in flow-exposed forming retinal vessels. Daughter nuclei moved away from the cleavage plane after division, suggesting that regulation of endothelial division orientation effectively extends vessel length in these developing vascular beds. A gain-of-function mutation in VEGF signaling increased randomization of endothelial division orientation, and this effect was rescued by a transgene, indicating that regulation of division orientation is a novel mechanism whereby VEGF signaling affects vessel morphogenesis. Thus, our findings show that endothelial cell division and morphogenesis are integrated in developing vessels by flow-independent mechanisms that involve VEGF signaling, and this cross talk is likely to be critical to proper vessel morphogenesis.

Animals↗
PubMed2006

[Pathogenesis and treatment of myopic foveoschisis].

Myopic foveoschisis (MF) can now be recognized as the result of recent progress in imaging diagnostic technology such as optical coherence tomography (OCT). MF predominantly occurs in highly myopic eyes with posterior staphyloma, and often induces visual loss and/or metamorphopsia. In order to better understand the detailed pathogenesis of MF, we observed 21 myopic eyes after vitrectomy using OCT. Retinal microfolds along the retinal vessels were observed in over 60% of the patients 6 months after surgery. Relative inflexibility of retinal arterioles/venules may be one of the causes for MF. We performed a pilot study (6 eyes of 5 patients) to treat MF by vitrectomy including vitreous cortex removal, internal limiting membrane peeling, and gas tamponade. In all 6 eyes the fovea was reattached and vision improved by more than two lines. This pilot study indicates that vitrectomy is an effective and safe treatment for MF.

Fovea Centralis↗
PubMed1990

PO2 profiles and oxygen consumption in cat retina with an occluded retinal circulation.

If the retinal circulation is occluded, the retina is forced to rely on the choroidal circulation for its oxygen supply. We have measured intraretinal PO2 profiles before, during, and after such an occlusion in cat. Oxygen-sensitive microelectrodes were used to measure intraretinal PO2, and the retinal circulation was occluded by means of a glass probe placed on the retinal vessels at the optic disk. Both air and 100% O2 breathing conditions were investigated. With the retinal circulation occluded, intra-retinal PO2 fell to zero within 60% of the distance through the retina, measured from the choriocapillaris to the internal limiting membrane. With the circulation occluded, but with breathing of 100% O2, PO2 rose throughout the retina so that values within the inner retina were as high or higher than for air breathing with the retinal circulation present. This meant that the whole retina could be supplied with adequate oxygen by breathing with 100% O2 in cat. From these PO2 profiles, oxygen flux and consumption were calculated as a function of distance through the retina. These calculations showed that the outer 20% of the retina had a consumption of 5.45 +/- 2.46 (SD) ml.min-1.100 ml-1 compared with a mean value for the remaining retina of 1.47 +/- 2.66 ml.min-1.100 ml-1. This difference was statistically significant (P less than 0.001) which indicates that there are at least two regions in the retina with different oxygen consumption.

Animals↗
PubMed1995

Retinal oxygen distribution. Its role in the physiopathology of vasoproliferative microangiopathies.

PURPOSE: To study the role of oxygen distribution in the physiopathology of retinal vasoproliferative microangiopathies. METHODS: Experimental retinal branch vein occlusion was induced in miniature pigs, using argon laser photocoagulation. The microvascular modifications, the retinal histologic features, and the retinal oxygen distribution were studied within 48 hours of the occlusion, and 3 weeks later. The retinal oxygen distribution modifications were also studied in ischemic retinal areas treated by scatter argon laser photocoagulation. RESULTS: Impaired regulation and blood flow decrease in the vascular bed that was affected by a retinal branch vein occlusion and tissue hypoxia led to modifications of oxygen delivery resulted in a damage of the neuronal cells, whereas the abnormal permeability of the affected retinal vessel wall induced extracellular edema and disorganization of the inner retina. Three weeks after vein occlusion, retinal neovascularization occurred in ischemic/hypoxic retinas. The "critical PO2" (tissue oxygen partial pressure), which induces neovascularization in miniature pigs has not been determined. Photocoagulation of the ischemic retinal territories induced an increase of preretinal oxygen partial pressure, which is restored to the normal preretinal values. CONCLUSION: A retinal branch vein occlusion in miniature pigs represents a reproducible experimental model of retinal neovascularization. Oxygen partial pressure measurements of the ischemic retina confirmed the hypothesis that tissue hypoxia triggers neovascularization; laser photocoagulation should be applied over the whole ischemic retinal areas to eliminate hypoxia in the inner retina.

Animals↗
PubMed2002

Lipids and nitric oxide in porcine retinal and choroidal blood vessels.

Lipid profiles of porcine retina, and retinal and choroidal vessels were analyzed using the gas chromatography/mass spectrometry (GC/MS) technique. The retina and both isolated retinal and choroidal vessels contained saturated fatty acid stearic acid and polyunsaturated fatty acids, including arachidonic (C20:4, AA), a precursor for vasoactive prostaglandin (PG-2) series, and W-6 docosahexaenoic acids (C22:6, DHA). However, eicosapentaenoic acid (C20:5, EPA), a precursor for PG-3 series, was not detected in these vessels. When stearic acid was used for normalization of tissue sample, the retina contained relatively higher amounts of DHA than AA, retinal vessels had equal amounts of AA and DHA, while choroidal vessels contained higher amounts of AA than DHA. We also examined the endogenous synthesis of vasoactive endothelial-derived factors like PGs and nitric oxide (NO). Since vasoactive angiotensin II (Ang II) releases these products from blood vessels, this polypeptide was used in a porcine retinal circulation model. The porcine retinal central artery was perfused with oxygenated/heparinized physiological salt solution at 37 degrees C. Changes in A1 and A2 arteriolar diameters induced by Ang II were determined in the absence and presence of the nitric oxide synthase inhibitor, l-NO Arginine (LNOA), and cyclooxygenase inhibitor, flurbiprofen (FB). The central retinal artery designated as the first order arteriole A1 and subsequent branch was defined as A2. Luminal diameters of Al and A2 arterioles were 35 +/- 2 am and 10 +/- 1 microm, respectively. Topical Ang II (10(-10) M-10(-6) M) caused small vasoconstrictions in a dose-dependent manner. This response was enhanced after inhibition of PG synthesis by (10-6 M) FB. Ang II induced-constrictions were further enhanced in the presence of NO synthase inhibitor, LNOA (10(-7) M). There was slightly more increase in Ang II-induced vasoconstrictions in the presence of both NO and PG inhibitors, suggesting that NO may cause release of PGs from these vessels. This study demonstrates that the porcine retinal arterioles have the ability to regulate vasoconstriction responses induced by Ang II by synthesis and release of endogenous vasodilating PGs and NO (especially NO); and these substances may play a vital role in porcine retinal circulation.

Angiotensin II↗
PubMed1983

Fluorescein gonioangiography of newly formed vessels in the anterior chamber angle.

Fluorescein gonioangiography was performed in 20 eyes of 20 patients with various ocular disorders such as diabetic retinopathy, retinal vessel occlusion, traumatic angle recession, and granulomatous uveitis. It was clearly demonstrated that newly formed vessels in the anterior chamber angle originated from the ciliary body, and extended predominatingly onto the surface of the angle wall via ciliary body band.

Angiography↗
PubMed2004

Factor XII deficiency: a thrombophilic risk factor for retinal vein occlusion.

PURPOSE: Factor XII deficiency is among the coagulation disorders that have been implicated in major thromboembolic events. However, little is known about an association of this coagulation disorder and retinal vessel occlusion. In the current study, we investigated the prevalence of factor XII deficiency in patients with retinal vein occlusion (RVO) with reference to age and cardiovascular risk factors. DESIGN: Cross-sectional study. METHODS: A cohort of 150 consecutive patients with central or branch retinal vein occlusion and 135 subjects matched for age and gender were prospectively screened for factor XII deficiency. Both cohorts were divided into two subgroups (<= 45 or >45 years), depending on the patients' age at the time of the RVO or a previous thromboembolic event. RESULTS: Overall, factor XII deficiency was found to be present in 14 (9.3%) of 150 patients and in 1 (0.7%) of 135 controls (P =.0009). Patient age <= 45 years at the time of the RVO or a previous thromboembolic event was associated with a high prevalence of factor XII deficiency (18%). By contrast, only 5 (5%) of 100 patients >45 years (P =.016) and none of the young controls (P =.0001) tested positive for factor XII deficiency. The prevalence among patients >45 years was similar to that found in age-matched controls (2%; P =.66). CONCLUSIONS: Our results indicate that factor XII deficiency is highly prevalent in RVO patients <= 45 years of age. By contrast, the prevalence of factor XII deficiency in RVO patients older than 45 years appears to be similar to that seen in healthy individuals.

Adolescent↗