Search

A letter to the editor is presented which discusses the immunohistochemical analysis of internal limiting membrane (ILM) using confocal microscopy in stage four idiopathic macular hole surgery.

A letter to the editor is presented which discusses a case of a 42-year-old Sudanese woman with systemic lupus erythematosus who subsequently sustained a combine bilateral central retinal artery and vein occlusion which resulted to visual loss.

Purpose: To compare the anatomic and functional results of primary vitrectomy alone or vitrectomy-scleral buckling for pseudophakic retinal detachment (RD). Vitrectomy permits a detailed view of the peripheral retina, so otherwise undetectable holes or additional small lesions can be found which, left untreated, may cause a residual RD., Patients and Methods: Twenty-four consecutive pseudophakic eyes with pseudophakic RD were operated by vitrectomy and encircling band (Group I) and 27 additional cases were operated on by vitrectomy alone (Group II). Internal subretinal fluid drainage, using liquid perfluoro-n-octane, endolaser, and/or cryocoagulation and fluid-air exchange with SF6 20%, was applied in all cases. Preoperative findings and intraoperative and postoperative complications as well as final results were analyzed., Results: Preoperatively undetected retinal holes were identified in 7 of the 51 eyes and additional retinal holes were found in 21. The mean follow-up was 14 months for Group I and 11.5 months for Group II. The retina was successfully reattached with a single operation in 22 of 24 eyes (92%) in Group I. One eye had a recurrence of RD due to an unsuccessfully treated preexisting retinal tear. Proliferative vitreoretinopathy (PVR) was observed in one case with recurrence of RD. In both cases, a second operation achieved retinal reattachment. In Group II, the retinas were attached with a single operation and visual acuity improved by an average of four or more lines in 62.5% of the vitrectomy-buckling group and in 55.5% of the vitrectomy group. The most frequent complication was a transient hypertony, in 21 cases., Conclusions: Surgical treatment of pseudophakic RD, combining vitrectomy and scleral buckling or vitrectomy alone, achieves very good anatomic and functional results. The advantages include more efficient detection of the peripheral detachment causing retinal lesions, and a lower redetachment rate than after extraocular surgery only.

Purpose: Formation of scarlike epiretinal membranes (ERMs) constitutes potentially the end stage of evolution of proliferative vitreoretinopathy (PVR) and proliferative diabetic retinopathy (PDR). Among various cellular populations, ERMs contain cells with contractile features typical of myofibroblasts. The current study was conducted to investigate the presence of transforming growth factor (TGF)-beta1, TGF-beta receptor II (RII) and ED-A fibronectin (FN), the main inducers of myofibroblastic differentiation in ERMs in PDR and PVR., Methods: Samples of ERM were obtained from 23 patients during microsurgery for PVR or PDR. Electron microscopy, immunohistochemistry, and confocal microscopy with antibodies recognizing beta-smooth muscle (SM) actin, desmin, TGF-beta1, TGF-beta receptors I and II, and ED-A FN were performed., Results: alpha-SM actin was detected in all ERMs, whereas desmin was present in 50% of the cases. ED-A FN was expressed in all ERMs in close relation with alpha-SM actin-positive myofibroblasts. In addition, TGF-beta1 and TGF-beta R II were always present, TGF-beta RII being expressed in both alpha-SM actin-positive and negative fibroblastic cells., Conclusions: Myofibroblast accumulation is a key event in ERM-associated traction retinal detachment occurring during PVR and PDR. The current results suggest that the presence of alpha-SM actin-positive myofibroblasts is probably dependent on the concomitant neoexpression of TGF-beta1, TGF-beta RII, and ED-A FN. The results furnish new data on the mechanism of alpha-SM actin stimulation in fibroblasts in a human pathologic setting.

Purpose: The development of extended areas of nonperfused capillaries after branch vein occlusion (BVO) is correlated to the secondary constriction of the arteriole crossing the occluded area. The decrease in nitric oxide (NO) in tissue that occurs early after BVO accounts for the secondary arteriolar constriction. The present study shows that the administration of an NO donor can reverse the secondary arteriolar vasoconstriction observed after BVO., Methods: Simultaneous preretinal NO profiles and arteriolar diameter measurements were performed in miniature pigs after experimental BVO. The effect of preretinal microinjections of the NO donor sodium nitroprusside (SNP) on the arteriolar diameter was studied., Results: Significant arteriolar vasoconstriction (mean arteriolar diameter, 92.1% +/- 3.3% of control; n = 7; P = 7.4 x 10(-5)) and a simultaneous decrease in the preretinal NO concentration ([NO]) (preretinal [NO], 20% +/- 15.6% of control; n = 5; P = 0.0003) were observed 4 hours after BVO. Microinjection of the NO donor SNP (1 mM applied by puffer) near the constricted retinal arteriole caused a segmental, reversible arteriolar dilation that reached its maximum 20 minutes after the injection (mean arteriolar diameter; 110.8% +/- 7.5% of control; n = 6; P = 0.02) and was completely reversed 60 minutes later (n = 6)., Conclusions: Local administration of NO donors may contribute to the restoration of the retinal arteriolar blood flow after BVO and thus may improve the supply of oxygen and nutrients to the injured tissue.

Purpose: After retinal branch vein occlusion (BVO), the arteriole crossing the occluded territories is often constricted. This constriction persists up to several weeks and is correlated with the development of extended territories of nonperfused capillaries. These are results of an investigation supporting the hypothesis that decrease in the production of nitric oxide (NO) accounts for the observed arteriolar constriction., Methods: Preretinal [NO] was measured using an NO microprobe in the anesthetized miniature pigs, before and during the first 4 hours after experimental branch vein occlusion. Modifications of arteriolar diameter were correlated to preretinal [NO] changes. The retinal arteriolar sensitivity to constitutive NO was checked by applying preretinal puff injections of nitro-L-arginine (L-NA) after both systemic hypoxia and branch vein occlusion., Results: Two hours after branch vein occlusion there was a 73.7 +/- 4% decrease in preretinal [NO] and a simultaneous 25.4 +/- 3.4% decrease in the diameter of the arteriole in the affected territory. Both persisted for at least 4 hours after branch vein occlusion. Applying a puff of L-NA to an arteriole previously dilated by systemic hypoxia induced a vasoconstriction. However, no arteriolar constriction was observed when a puff was applied to an arteriole after branch vein occlusion., Conclusions: These results show that experimental branch vein occlusion induces in the affected retina an impairment in the release of constitutive NO and an arteriolar constriction, which, in turn, contributes to the development of hypoxia in tissue and neuronal swelling and death in the inner retina.

Purpose: Experimental evidence indicates that the retinal microcirculation is mainly controlled by factors released from the tissue surrounding the arterioles. This study explores whether nitric oxide (NO), a possible factor, is released in the retina and controls the arteriolar tone., Methods: Using a NO microprobe, the authors measured [NO] in the preretinal vitreous of miniature pigs as a function of distance from the retinal surface. Additionally, the NO-synthase inhibitor nitro-L-arginine was pressure injected. Finally, the retinal pool size of arginine and its biosynthesis from 14C(U)-glucose were biochemically assessed on retinal tissue and acutely isolated Müller cells., Results: At the retinal surface, [NO] measured 6 to 9 microM, and, in the vitreous, it fell to zero approximately 180 microns away from the retina. Therefore, NO is degraded faster in the vitreous (65 to 80 microM.minute-1) than in aqueous solution. Light flicker stimulation of the dark-adapted retina induced a reversible increase of [NO] (approximately 1.6 microM). Preretinal juxta-arteriolar microinjections of nitro-L-arginine (0.6 mM) induced a segmental and reversible arteriolar vasoconstriction of 45%; in contrast, intravenous infusion of nitro-L-arginine had no measurable effect on arteriolar diameter. The retinal pool size of arginine was small (< or = 200 microM), but there was an important rate of arginine biosynthesis in Müller cells., Conclusions: These results strongly suggest that cells in the retina, other than endothelial cells, produce and release NO, which in turn controls the basal dilating arteriolar tone in the inner retina.

Purpose: The authors investigated the hypothesis that the retinal vasomotor effect of acute hypoxia is mediated by lactate., Methods: Retinal vasomotor arteriolar response was measured in the intact eyes of miniature pigs after systemic administration and after local preretinal juxta-arteriolar microinjection of lactate., Results: Injection of L-lactate (physiologically produced lactate) into the systemic circulation decreased the arterial blood pH but did not dilate the retinal arterioles. By contrast, microinjections of L-lactate (0.5 mol/l, pH 2) into the juxta-arteriolar vitreous induced a reversible segmental vasodilation of 32 +/- 4% (standard deviation). This vasodilation did not depend on periarteriolar pH lowering because microinjections of a 0.5 mol/l L-lactate at neutral pH also dilated segmentally the retinal arterioles (37 +/- 5.5%). The effect of lactate was stereospecific because microinjections of the isomer D-lactate (0.5 mol/l, pH 2) did not affect the arteriolar caliber (P = 0.63). Perfusion of the eye with the cyclo-oxygenase inhibitor indomethacin, through cannulization of the sublingual artery, caused a generalized reversible arteriolar vasoconstriction of 51 +/- 9.8% but did not inhibit the segmental vasodilator effect of locally microinjected L-lactate., Conclusions: It is known that acute hypoxia in the isolated retina causes an increase in lactate production. In the intact eye, there is a retinal vasodilation, which is not inhibited by indomethacin. Hence, it was concluded that retinal, but not blood, lactate is a possible mediator of the acute hypoxia-induced vasodilation.

Laser Doppler velocimetry was performed on retinal vessels of a cat using a linearly polarized He-Ne laser as the incident beam. The diameter of the vessels measured was <120 microm. Measurements show that if double transmission of the laser light through a given retinal vessel can be prevented, the Doppler shift power spectra have the shape theoretically expected from calculations based on a single scattering model and parabolic velocity profile of the red blood cells.