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At least 55 records · Page 3Linked to original sources
PubMed2003

Ophthalmodynamometric assessment of the central retinal vein collapse pressure in eyes with retinal vein stasis or occlusion.

PURPOSE: Using a new Goldmann contact lens associated ophthalmodynamometric device, it was the purpose of the present study to determine the central retinal vein collapse pressure in eyes with retinal vein occlusions or retinal venous stasis. METHODS: The prospective clinical non-interventional comparative study included 19 patients with central retinal vein occlusion ( n=8), branch retinal vein occlusion (n=4), or retinal venous stasis (n=7) and 42 subjects of a control group. With topical anesthesia, a Goldmann contact lens fitted with a pressure sensor was put onto the cornea. Pressure was exerted on the globe by pressing the contact lens, and the pressure value at the time when the central retinal vein started pulsating was noted. RESULTS: Central retinal vein collapse pressure measured 103.6+/-25.4 arbitrary units (AU) in eyes with central retinal vein occlusion what was significantly higher than in the eyes with retinal venous stasis (58.1+/-37.5 AU; p=0.02) and the eyes with branch retinal vein occlusion (43.8+/-25.5 AU; p=0.004). In the latter two groups, the measurements of the central retinal vein collapse pressure were significantly (p<0.001) higher than the measurements in the eyes of the control group (4.2+/-7.8 AU). CONCLUSION: As measured by a new ophthalmodynamometer with direct biomicroscopic visualization of the central retinal vessels during examination, central retinal vein collapse pressure is significantly higher in eyes with central retinal vein occlusion, followed by eyes with branch retinal vein occlusion, eyes with retinal venous stasis and, finally, normal eyes. These findings may have diagnostic and therapeutic implications.

Adult↗
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↗
PubMed1998

Role of retinal vascular endothelial cells in development of CMV retinitis.

PURPOSE: Although cytomegalovirus (CMV) retinitis is known to occur in association with retinal microangiopathy in individuals with marked immunodeficiency, glial cells are believed to be the initial target cells in the development of retinitis. Moreover, it has been hypothesized that CMV gains access to the retinal glia because of altered vascular permeability. In an attempt to address the hypothesis, we studied 30 autopsy eyes of AIDS patients with systemic CMV infection, with or without clinically apparent CMV retinitis. METHODS: The autopsy eyes were processed in three ways. First, dual immunohistochemical studies were done by using anti-CMV antibodies for immediate early, early, and late antigens. The retinal cell types infected with the virus were then determined by using anti-GFAP, anti-VonWillebrand's factor, neuronal specific enolase, and leukocyte marker CD68. Second, selected eyes were processed for in situ hybridization with DNA probe specific to CMV. Third, an eye with clinically apparent CMV retinitis was submitted for electron microscopic examination. RESULTS: At the site of retinal necrosis in those eyes with a clinical diagnosis of CMV retinitis, the immunohistochemical, in situ hybridization, and ultrastructural examinations revealed that CMV was present primarily in the Müller cells and in perivascular glial cells. Adjacent to these infected cells, focal areas of positive staining for CMV antigen were seen in the glial cells, neuronal cells, and retinal pigment epithelial cells. At these sites most of the retinal capillaries were devoid of endothelial cells. Few vessels located at the advancing margin of retinal necrosis showed the presence of viral proteins in the endothelial cells. CONCLUSIONS: The present results indicate that retinal vascular endothelial cells could be the initial target in the development of viral retinitis, with subsequent spread of the infection to perivascular glia, Müller cells, and other retinal cells, including the retinal pigment epithelium.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Management of pseudophakic retinal detachment with undetectable retinal breaks.

BACKGROUND AND OBJECTIVE: Difficulties encountered during the repair of pseudophakic retinal detachment are related to difficulties in peripheral retinal visualization and identification of retinal breaks. The implication of nonvisualized breaks in patients with pseudophakic retinal detachment is associated with lower rates of surgical success. This report decribes the results of a prospective trial to evaluate the efficacy of both scleral buckling surgery in the treatment of pseudophakic retinal detachment with undetected retinal breaks and pars plana vitrectomy techniques in the management of the cases that redetected after primary buckling surgery. PATIENTS AND METHODS: This study represents 25 cases of pseudophakic retinal detachment with undiagnosed retinal breaks. In each case, we performed a scleral buckling that extended over the circumference of the retinal detachment. Pars plana vitrectomy with internal subretinal fluid drainage and long-term tamponade were performed on 7 patients with uncomplicated recurrent retinal detachments after primary buckling surgery. The mean duration of follow up was 32 months. RESULTS: There were 25 eyes (24.5%) of pseudophakic retinal detachment with undiagnosed retinal breaks represented in our pseudophakic retinal detachment cases. Anatomic success was achieved after the initial scleral buckling surgery in 18 eyes (72%). The overall success rate was 92%. The visual acuity was 20/40 or better in 8 patients (32%), 20/80 to 20/40 in 6 patients (24%), 5/200 to 20/80 in 7 patients (28%), and light perception to hand movement in 4 patients (16%). Complications included vitreous hemorrhage, macular pucker, cystoid macular edema, and hypotony with proliferative vitreoretinopathy. CONCLUSION: Scleral buckling surgery in conjunction with cryotherapy is effective in the initial treatment of pseudophakic retinal detachment with undetectable retinal breaks. Pars plana vitrectomy with internal fluid-gas exchange and long-term tamponade can be used to treat these patients with recurrent retinal detachment after primary buckling surgery to get a higher overall success rate.

Adolescent↗
PubMed1982

Anti-retinal autoimmunity and circulating immune complexes in patients with retinal vasculitis.

Sera from 44 patients with isolated retinal vasculitis (RV), 38 patients with retinal vasculitis accompanying systemic inflammatory diseases (RV + SID), and 33 patients with a similar range of systemic inflammatory diseases without eye involvement (SID alone) were assayed for circulating immune complexes (CIC) and for anti-retinal autoantibodies. CIC were present in 41% of patients with isolated RV and 55% of patients with RV + SID, whilst anti-retinal antibodies were present in about 70% of all patients with RV. 42% of those with SID alone had CIC and 30% of those with SID alone had retinal autoantibodies. Titres of anti-retinal antibodies were higher in patients with RV than in those with SID alone. In isolated RV there was an inverse relation between pronounced retinal autoimmunity and the occurrence of CIC--i.e., the more severe autoimmune retinal disease occurred in CIC-negative patients. Most patients with RV + SID tended to have mild or moderate retinal disease accompanied by both retinal autoantibodies and CIC, but severe retinal disease occurred in CIC-positive patients who did not have circulating anti-retinal antibodies. Patients with SID alone had high titres of retinal antibodies only when they were CIC-positive. It is suggested that the formation of CIC, possibly of an idiotype/anti-idiotype nature, may be a compensatory mechanism accompanying anti-retinal autoimmunity and that an imbalance between autoimmunity and immune complex formation may be an important predisposing factor in the development of retinal inflammatory disease.

Antibody Specificity↗
PubMed2005

The association between visual acuity and central retinal thickness in retinitis pigmentosa.

PURPOSE: To determine whether visual acuity is related to central retinal thickness in patients with retinitis pigmentosa. METHODS: Visual acuities were measured with Early Treatment Diabetic Retinopathy Study (ETDRS) charts and optical coherence tomography (OCT3) was used to calculate retinal thicknesses and grade third high-reflectance bands in 162 patients with the typical forms of retinitis pigmentosa who had Snellen visual acuities of 20/20 to 20/200, minimal to no cataracts, and no visible macular cysts. Sixty-five patients were retested within 2 months to estimate the intervisit variability of retinal thickness measurements. RESULTS: ETDRS acuity was best related to retinal thickness measured at fixation and as the average value over the central 1 mm by a second-order polynomial (r(2) = 0.38 and P < 0.001 in both cases). Acuity was maximal for intermediate retinal thickness and appeared to decline for both lesser and greater retinal thicknesses. By linear regression, the decline in acuity for decreasing retinal thickness was steeper in eyes with an absent third high-reflectance band than for eyes with a partially distinct band. No decline was noted in eyes with an intact band. Assessment of intervisit variability of retinal thickness measurements showed 98% confidence limits of +/-17 microm at fixation and +/-11 microm for the central 1 mm. CONCLUSIONS: Both retinal thinning (due to cell loss) and retinal thickening (due to presumed edema) appear to be associated with lower visual acuity in patients with typical retinitis pigmentosa. The definition of the OCT third high-reflectance band may help to predict which patients are more likely to lose visual acuity as retinal thickness declines. An increase or decrease in retinal thickness of more than 17 microm at fixation or 11 microm over the central 1 mm at follow-up can be considered a significant (P < 0.01) change in these patients.

Adolescent↗
PubMed2001

Effects of retinal glial cells on isolated rat retinal ganglion cells.

PURPOSE: The effect of retinal glial cells on retinal ganglion cell (RGC) survival was investigated in cocultures of pure, isolated retinal glial cells with pure, isolated RGCs. METHODS: RGCs from 2-day-old rats were cocultured for 48 hours, avoiding direct contact between cell types, with either nonconfluent retinal glial cells from 3-day-old rats or confluent retinal glial cells from 3-day-old, 12-day-old, or 1-year-old rats. Survival of RGCs was evaluated by flow cytometry. Amino acids were determined in culture medium. The effects of glutamate antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione and MK801, a nitric oxide (NO) scavenger, 2-(4-carboxyphenyl)-4,4,5,5tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO), and an NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), were examined. RESULTS: Nonconfluent retinal glial cells significantly reduced the survival of small and large RGCs, but confluent retinal glial cells reduced the survival of only small RGCs, regardless of the rat's age at the time of retinal glial cell harvesting. Profiles of some amino acids significantly varied, depending on the culture condition. Cocultures of RGCs with nonconfluent retinal glial cells released significantly more glutamate into the medium than cocultures of RGCs with confluent retinal glial cells or RGCs in pure culture. The glutamate antagonists improved the survival of RGCs cocultured with nonconfluent retinal glial cells, especially when the two were administered in combination, and in the case of large RGCs. c-PTIO and L-NAME, also improved the survival of RGCs cocultured with nonconfluent retinal glial cells. CONCLUSIONS: Adverse effects of retinal glial cells on the survival of RGCs varied by size of the RGCs and retinal glial cell confluence. Glutamate and NO may be involved in retinal glial cell-related antisurvival effects.

Animals↗
PubMed2001

Retinal tissue modulates retinal arterial tone through the release of a potent vasodilating factor.

Various intercellular messenger molecules, such as nitric oxide, adenosine and prostanoids, released by perivascular tissue have been implicated in the control of local blood flow. The present work performed in vitro on isolated retinal arteries advances that perivascular retinal tissue releases yet another intercellular messenger molecule exerting a potent vasodilatory influence. In these experiments, isolated bovine retinal arteries (mounted in a wire-myograph) incompletely cleaned of retinal tissue contracted weaker in response to prostaglandin F2 alpha, than arteries without retinal tissue. This also applied for thromboxane-, endothelin-, and serotonin-induced contractions. Apposition of a piece of retinal tissue elicited a complete and reversible relaxation of a bovine retinal artery contracted with prostaglandin F2 alpha, suggesting that the inhibitory effect of adherent retinal tissue is mediated by a diffusible relaxing factor. Incubation of a bovine retina for 6 hours (37 degrees C, O2/CO2 95%/5%) yielded a solution which induced a relaxation of the retinal artery contracted with prostaglandin F2 alpha, further confirming the involvement of a diffusible chemical substance. The inhibitory effect of adherent retinal tissue on the contractile tone of isolated bovine retinal arteries could not be attributed to the release of NO, prostaglandins or adenosine. Nor did the characteristics of this factor correspond to any of the known vasoactive mediators formed within the retina. Further experiments demonstrated that the release of this elusive factor is probably linked to the oxygen tension, since hypoxia induced a vasodilation of preparations with adherent retinal tissue whereas preparations without retinal tissue were not affected by the change in oxygenation. The present work reveals a new form of intercellular communication in which (a) factor(s) derived from the retina profoundly relax(es) the smooth muscle cells of retinal arteries and hence modulate(s) retinal blood flow. The identity of this (these) factor(s) and the mechanisms by which this (these) factor(s) induce(s) vasodilation remain as yet to be determined.

Animals↗
PubMed1997

Specific retinal diacylglycerol and protein kinase C beta isoform modulation mimics abnormal retinal hemodynamics in diabetic rats.

PURPOSE: Elevation of diacylglycerol (DAG) and protein kinase C (PKC) levels in diabetic vascular tissue is associated with abnormalities of retinal and renal hemodynamics. The object of this study was to determine whether direct elevation of retinal DAG levels, in the absence of diabetes or hyperglycemia, can mimic the hemodynamic abnormalities normally observed in diabetic rats. Retinal DAG levels were elevated using an inhibitor of DAG kinase that converts DAG to phosphatidic acid. The effectiveness of a specific PKC-beta isoform inhibitor introduced directly into the retinas of diabetic rats in reversing diabetes-related abnormal retinal hemodynamics was also investigated. METHODS: For retinal blood flow studies, diacylglycerol kinase (DGK) inhibitor R59949, at various concentrations, was injected into the vitreous of nondiabetic Sprague-Dawley rats (n = 33), and a PKC-beta isoform-selective inhibitor LY333531 was injected into the vitreous of rats with streptozotocin (STZ)-induced diabetes of 2 weeks' duration (n = 21). Retinal hemodynamic changes were quantitated using video-based fluorescein angiography. Total DAG levels were assayed from five nondiabetic rat retinas after DGK inhibition and retinal PKC activities were assayed from six diabetic rat retinas after PKC-beta inhibition. RESULTS: DGK inhibitor R59949 injected into the vitreous dose dependently increased the mean circulation time (MCT) and decreased retinal blood flow (EC50 = 10(-8) M). After 30 minutes, 10(-5) M R59949 induced a 1.7-fold increase in total retinal DAG levels, compared with the levels in vehicle-injected eyes, an increase in MCT from 0.87 +/- 0.05 seconds to 1.44 +/- 0.12 seconds (P < 0.01) and a decrease in retinal blood flow from 105.3 +/- 6.5 pixel2/second to 64.1 +/- 5 pixel2/second (P < 0.01). The effect of R59949 was sustained for 60 minutes after injection. These retinal hemodynamic parameters after DGK inhibition were comparable to those measured at baseline in rats with STZ-induced diabetes of 2 weeks' duration (MCT = 1.38 +/- 0.20 seconds; retinal blood flow = 68 +/- 11.2 pixel2/second). Intravitreal injection of the PKC-beta inhibitor (LY333531) at 10(-5) M in diabetic rats decreased by a factor of 1.6 the diabetes-related increased PKC activation, decreased the prolonged MCT (0.98 +/- 0.13 seconds; P < 0.01) and increased retinal blood flow (93.4 +/- 14.2 pixel2/second; P < 0.01). The measured retinal circulatory parameters after PKC inhibition in the retina were comparable to those measured at baseline in the nondiabetic rats. CONCLUSIONS: These results provide direct evidence that DAG elevation and subsequent PKC-beta isoform activation are the primary biochemical sequelae responsible for the development of the abnormal retinal hemodynamics observed in diabetic rats.

Animals↗
PubMed1997

Intravitreal sustained release of VEGF causes retinal neovascularization in rabbits and breakdown of the blood-retinal barrier in rabbits and primates.

Vascular endothelial growth factor (VEGF) has been identified as a possible mediator of retinal neovascularisation (NV), but it is not certain if VEGF alone is sufficient to cause retinal NV. We sought to investigate this issue by implanting ethylene-vinyl acetate copolymer pellets that slowly release VEGF into the vitreous cavity of rabbits and primates. Eyes were examined by indirect ophthalmoscopy, fundus photography, and fluorescein angiography and then animals were killed at various time points and immunocytochemical and ultrastructural evaluations were carried out. Seven days after implantation of a pellet containing 30 micrograms of human recombinant VEGF into the vitreous cavity of rabbits, retinal blood vessels became dilated and tortuous, and between days 14 and 21, retinal NV was noted in all eyes. Fluorescein angiography showed profuse leakage of dye from the anomalous vessels. Immunohistochemical staining for proliferating cell nuclear antigen (PCNA) showed positively staining nuclei in many of the endothelial cells of new blood vessels on the surface of the retina. Six eyes implanted with control pellets containing vehicle and two eyes implanted with pellets containing 30 micrograms of human serum albumin alone showed no retinal vascular abnormalities. Implantation of pellets containing 100 micrograms of VEGF into the vitreous cavity of primates resulted in iris NV and retinal vascular dilation and tortuosity very much like that seen in humans with ischemic retinopathies. Immunohistochemical staining for serum albumin showed widespread severe breakdown of the blood-retinal barrier (BRB). Histology showed dilated thin-walled retinal vessels, but unequivocal retinal NV could not be identified and staining for PCNA was negative. These findings indicate that sustained intravitreal release of VEGF causes widespread retinal vascular dilation and breakdown of the BRB. Retinal NV seems to require persistent high levels of VEGF at the retinal surface and can be achieved in rabbits providing a potentially useful model of retinal NV, but is difficult to achieve in primates. The extensive VEGF-induced disruption of the blood-retinal barrier suggests that VEGF antagonists may provide a new therapy for patients with ischemic retinopathies and macular edema.

Animals↗
PubMed2000

Alterations of the blood-retinal barrier and retinal thickness in preclinical retinopathy in subjects with type 2 diabetes.

OBJECTIVE: To identify alterations of the blood-retinal barrier by mapping retinal fluorescein leakage into the vitreous and changes in retinal thickness occurring in the macular region in preclinical diabetic retinopathy. METHODS: Ten eyes from 10 patients with type 2 diabetes and no lesions visible on fundus photography (level 10 of Wisconsin grading) were examined with the retinal leakage analyzer (RLA) (Confocal Scanning Laser Ophthalmoscope [modified]; Carl Zeiss Inc, Thornwood, NY) and the retinal thickness analyzer (RTA) (Talia Technology, Mevaseret Zion, Israel). The maps of retinal leakage and retinal thickness were aligned and integrated in the same image to correlate leakage with thickness. Data from the group of individuals with diabetes were compared with those of a healthy control population (N = 14; mean age, 48 years; range, 42-55 years) and used to establish reference maps for the RLA and RTA. RESULTS: Areas of abnormally increased fluorescein leakage were detected in 9 of 10 eyes examined. The increased leakage in 6 (67%) of 9 eyes reached values higher than 40% more than the mean +2 SD RLA control value. Areas of abnormally increased thickness were found in 7 of 10 eyes examined. For the most part, the increases in retinal thickness were not severe (ie, <15% increase in 5 eyes and an 18% increase in 1 eye). The eyes with the most extensive leakage (cases 1, 3, and 9) showed relatively good coincidence between the location of the areas of increased leakage and the location of the areas of increased thickness. In 4 eyes (cases 2, 5, 7, and 8), no such correlation was apparent. The 3 remaining eyes showed little coincidence between these locations. Characteristically, the latter 3 eyes had areas of abnormally increased thickness that were much larger than the areas of increased fluorescein leakage, which were relatively moderate or absent of any leakage. CONCLUSIONS: Localized sites of increased fluorescein leakage and zones of increased retinal thickness were found in most eyes in a series of 10 eyes in the preretinopathy stage from 10 patients with type 2 diabetes. Increases in retinal thickness may be observed that do not coincide with sites of retinal leakage. Two types of increased retinal thickness may, therefore, be present in the preretinopathy stage of diabetic retinopathy, one directly associated with an alteration of the blood-retinal barrier, and another occurring without apparent breakdown of blood-retinal barrier.

Adult↗
PubMed1998

Retinal blood flow measurements in branch retinal vein occlusion using scanning laser Doppler flowmetry.

PURPOSE: To determine capillary blood flow measurements in eyes with branch retinal vein occlusion using a scanning laser Doppler flowmeter. METHODS: Retinal capillary blood flow in branch retinal vein occlusion areas and corresponding ipsilateral nonbranch retinal vein occlusion areas, 11 equivalent areas of the contralateral fellow eye of 12 consecutive untreated branch retinal vein occlusion patients, and 16 eyes of 11 age-matched normal control subjects were measured with scanning laser Doppler flowmetry. A template consisting of eight squares, each with a field of 100 x 100 microm (10 x 10 pixel) with space interval of 500 microm equidistant horizontally and vertically was used to obtain blood flow measurements in all subjects. Mean blood volume, flow, and velocity were obtained by averaging the mean values measured in each field. We avoided measurement over large retinal vessels to prevent the aliasing artifact of blood cells from moving faster than the sampling frequency. RESULTS: Branch retinal vein occlusion areas have significantly decreased microvascular blood volume (P = .0009), flow (P = .02), and velocity (P = .016) compared with ipsilateral nonbranch retinal vein occlusion areas in the same eye. Branch retinal vein occlusion areas also have decreased blood volume (P = .001), flow (P = .0042), and velocity (P = .0044) compared with areas of contralateral fellow eyes of branch retinal vein occlusion subjects. Branch retinal vein occlusion areas have significantly decreased blood volume (P = .0012), flow (P = .008), and velocity (P = .02) compared with age-matched normal areas. CONCLUSION: Average retinal blood volume, flow, and velocity in areas of branch retinal vein occlusion are significantly lower than in healthy retinas. The ability to noninvasively measure hemodynamic changes in the retinal capillary bed may be relevant to development of new therapies for retinovascular disease.

Aged↗
PubMedDate not supplied

Treating cytomegalovirus retinitis-related retinal detachment by combining silicone oil tamponade and ganciclovir implant.

BACKGROUND AND OBJECTIVE: With the efficacy of pars plana vitrectomy and silicone oil infusion in treating cytomegalovirus (CMV) retinitis-related retinal detachment and the success of the ganciclovir implant in controlling CMV retinitis, we sought to evaluate the possible benefits of combining these two procedures in one surgical operation. PATIENTS AND METHODS: A retrospective review of 10 patients was conducted. Each patient was diagnosed with a CMV retinitis-related retinal detachment and treated with pars plana vitrectomy and silicone oil infusion, with simultaneous placement of a ganciclovir implant. Parameters evaluated included location of retinal detachment, reattachment rate, pre- and post-operative Snellen visual acuity, pre- and post-operative CMV retinitis activity and location, and complications of the combined procedure. RESULTS: Overall anatomic reattachment was achieved in all 10 patients. Four patients presented with macular involvement of their retinal detachments. Three of these patients experienced significant post-operative improvement in visual acuity. Surgery preserved visual acuity in the 6 patients who presented with macula attached. Best postoperative acuity was better than or equal to 20/100 in 7 (70%) patients. All 3 CMV retinitis patients with inactive retinitis preoperatively remained free of retinitis for the duration of follow up. At last follow up, 8/10 (80%) showed no active CMV retinitis and no patients experienced progression of their retinitis. CONCLUSIONS: Results of this series indicate that patients benefit from excellent anatomic reattachment rates, preservation or improvement of visual acuity in most cases, and extended control of their CMV retinitis. Combining the two procedures appears viable. Further study is warranted to assess definitive anatomic and functional outcomes resulting from this new technique.

Antiviral Agents↗
PubMed2003

Effects of sildenafil on retinal blood flow and flicker-induced retinal vasodilatation in healthy subjects.

PURPOSE: Sildenafil is a specific inhibitor of phosphodiesterase V, which is widely used for the treatment of erectile dysfunction. Sildenafil has been shown to induce vasodilation in several vascular beds by inhibiting the cGMP breakdown. The present study was conducted to investigate whether sildenafil increases blood flow in the human retina. METHODS: In a randomized, double-masked, placebo-controlled, two-way crossover study in 12 healthy male volunteers the effects of a single dose of 100 mg sildenafil were studied. Subjects received sildenafil or placebo on two different study days. After administration, retinal hemodynamic parameters were measured every 20 minutes. Retinal vessel diameters and retinal blood velocity were assessed with the retinal vessel analyzer and bidirectional laser Doppler flowmetry, respectively. In addition, the response of retinal vessel diameters to stimulation with diffuse flicker light was studied. Blood pressure and intraocular pressure were measured with noninvasive techniques. RESULTS: Sildenafil had no effect on mean arterial pressure, pulse rate, intraocular pressure, retinal blood velocity, or retinal arterial diameter. However, a significant increase in retinal venous diameters (4.7% +/- 3.2%; P=0.0028 versus placebo) and retinal blood flow 15.7% +/- 18.0%; P=0.029 versus placebo) was observed. Sildenafil had no effect on flicker-induced vasodilation in retinal arteries or veins. CONCLUSIONS: The data indicate that sildenafil increases retinal venous diameters and retinal blood flow in healthy subjects. By contrast, it does not affect intraocular pressure and flicker-induced retinal vasodilation. Further studies are needed to elucidate whether this drug may be therapeutically used in retinal ischemic disease.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2004

Directed retinal nerve cell growth for use in a retinal prosthesis interface.

PURPOSE: Retinal prosthetic devices that use microelectrode arrays to stimulate retinal nerve cells may provide a viable treatment for degenerative retinal diseases. Current devices are based on electrical field-effect stimulation of remaining functional neural elements. However, the distance between target neurons and electrodes limits the potential density of electrodes and the ability to stimulate specific types of retinal neurons that contribute to visual perceptions. This study was conducted to investigate the use of microcontact printing (muCP) to direct cultured or explant retinal ganglion cell (RGC) neurites to precise and close stimulation positions and to evaluate the cell types that grow from a retinal explant. METHODS: RGCs and whole retinal explants were isolated from postnatal day-7 Sprague-Dawley rats using immunopanning purification and microdissection, respectively. Aligned muCP was used to direct the growth of RGC neurites from pure cultures (n=105) and retinal explants (n=64) along laminin patterns and to individual microelectrodes. Immunofluorescence stains (n=39) were used to determine the cell types that grew out from the retinal explants. RESULTS: RGC neurite growth was directed reproducibly along aligned laminin micropatterns to individual microelectrodes in pure RGC cultures and from full-thickness explanted rat retinas in 92% of experiments, neurites from pure RGC cultures extended along the laminin lines with an average length of 263 +/- 118 microm (SD; n=27) after 24 hours. Neurites from retinal explants extended in more than 80% of experiments and were observed to grow to an average length of 279 +/- 78 microm (n=64) after 2 days in culture. These neurites grew up to 3 mm after 1 month of culture on the laminin micropatterns. Immunohistochemical stains demonstrated that extended processes from both RGCs and glial cells grew out of retinal explants onto stamped laminin lines. CONCLUSIONS: Using muCP to pattern surfaces with growth factors, individual neuronal processes from pure RGC culture and whole retinal explants can be directed to discrete sites on a microelectronic chip surface. By directing RGC neurite processes to specific sites, single cell stimulation becomes possible. This may allow discrete populations of retinal neurons to be addressed so that physiologic retinal processing of visual information can be achieved.

Animals↗