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C J Pournaras

Publications and source records attributed to C J Pournaras.

At least 55 records · Page 3Linked to original sources

[Myofibroblasts and retinal fibrovascular membranes].

INTRODUCTION: Epiretinal tissue proliferations occurring during the evolution of ischemic microangiopathies or preretinal diseases are tough to cause retinal detachment by traction mechanisms. Cellular migration/proliferations and finally contraction are tough to be the pathogenic element. Myofibroblasts are contractile cells having features intermediate between those of the fibroblasts and smooth muscle. We conducted a study to explore whether such cells are present in preretinal membranes. MATERIALS AND METHODS: 8 membranes, preelevated during vitrectomy for proliferative vitreoretinopathy or diabetic proliferative vitreoretinopathy, were analysed with immunostaining technique searching for alpha-actine smooth muscle, desmine, which are specific markers for myofibroblasts and TGF-beta1, that is considered as the mean factor promoting the transformation of fibroblasts into myofibroblasts. RESULTS: All the histological preparation showed abundant staining with antibody against alpha-actine smooth muscle, desmine and TGF-beta1. CONCLUSIONS: Myofibroblasts are one of the major cellular element of preretinal membranes. They are scattered throughout the membrane and seem to account for their contractile properties.

Actins↗

Effect of nitroprusside on arteriolar constriction after retinal branch vein occlusion.

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.

Animals↗

[Surgery of idiopathic epiretinal membranes: functional results and complications].

PURPOSE: Surgery has been successful in removing epiretinal membranes from the macula allowing some improvement in vision in 80 to 90% of patients, however complications are relatively frequent. We conducted a retrospective study to evaluate the rate of peri- and postoperative complications and their influence on functional outcome of eyes having been operated for idiopathic epiretinal membranes. MATERIAL AND METHODS: Preoperative findings, intraoperative and postoperative complications as well as outcome in 40 consecutive cases of idiopathic epiretinal membranes operated by the same retina surgeon were analyzed. RESULTS: In all cases the epiretinal membranes were successfully removed from the fovea. The mean visual acuity increased from 0.36 +/- 0.2 to 0.54 +/- 0.3, (p < 0.05) postoperatively. Peroperative complications included intraoperative hemorrhage (18%) and retinal tears (10%). Postoperatively progressive nuclear sclerosis was observed in 75% of the cases and retinal tears causing detachments in 10%. CONCLUSIONS: Performing surgery for ERMs is worthwhile on eyes with major decreased visual acuity (< 0.25) as on eyes with metamorphopsia but only moderately reduced vision. Postoperative complications are frequent but can usually be managed successfully. Of them only retinal detachment involving the macula is of worse prognosis on the final functional outcome.

Aged↗

Systemic hyperoxia decreases vascular endothelial growth factor gene expression in ischemic primate retina.

OBJECTIVES: To determine whether systemic hyperoxia can reverse retinal hypoxia and decrease vascular endothelial growth factor (VEGF) gene expression in ischemic nonhuman primate retina. METHODS: Six eyes of 3 cynomolgus monkeys were studied. Retinal ischemia was induced via laser vein occlusion and confirmed with fluorescein angiography. Animals were randomly assigned to treatment with either 21% or 100% inhaled oxygen. Arterial PO2 was monitored while systemic acid-base status was maintained. An oxygen microelectrode on a micromanipulator was used to measure preretinal oxygen concentrations in ischemic and nonischemic retina in situ. RNA was isolated from fresh whole retinas, and VEGF messenger RNA levels were quantified with Northern blotting. RESULTS: The preretinal PO2 in ischemic retina was less than the PO2 in nonischemic retina in animals breathing 21% oxygen (intervascular zone PO2, 14.3+/-0.53 vs 21.8+/-0.55 mm Hg; P=.002). After 8 hours of systemic hyperoxia (arterial PO2, 512+/-18 mm Hg), the preretinal PO2 in ischemic retina increased to 166.2+/-15.6 mm Hg (21.8% oxygen) and retinal VEGF messenger RNA levels were reduced by an average of 55%. CONCLUSIONS: These data demonstrate that systemic hyperoxia can lower retinal VEGF gene expression and reoxygenate ischemic adult primate retina.

Animals↗

Distribution and regulation of the optic nerve head tissue PO2.

We investigated the distribution and regulation of the optic nerve head (ONH) tissue partial pressure of oxygen (PO2) under various stimuli and the role of the nitric oxide in the ONH circulation. Tissue PO2 was measured using double-barreled recess microelectrodes in the intact eyes of miniature pigs during normoxia, hyperoxia, hypoxia, variations of systemic blood pressure, and after inhibition of the endothelial nitric oxide synthesis by the administration of nitro-L-arginine. Measurements were performed in front of the ONH at intervascular and juxta-arteriolar areas and at a depth of 50 and 200 microm within the ONH at the center and the rim. During normoxia, PO2 was heterogeneously distributed in the ONH, higher close to the arterioles than in intervascular areas. Hyperoxia induced a significant increase of juxta-arteriolar tissue PO2, while in intervascular areas no change was noticed. Hypoxia did not modify intervascular tissue PO2 at 200 microm depth within the ONH. Variations of the systemic blood pressure did not induce any significant change in ONH tissue PO2. Similarly, no modification was noticed after the administration of nitro-L-arginine. There is a remarkable autoregulatory capacity of the ONH circulation that may compensate for parameters such as hyperoxia, hypoxia, and variations of the systemic blood pressure. Endothelially derived nitric oxide inhibition does not modify the ONH tissue PO2, probably because the tissue PO2 is stabilized by compensatory regulation.

Animals↗

Continuous measurements of intra-vascular pO2 in the pig optic nerve head.

BACKGROUND: The measurement of oxygen concentration in the microvasculature of a tissue is important for the understanding of oxygen delivery. MATERIAL AND METHODS: A technique was developed to measure in a continuous manner the partial pressure of oxygen (pO2) in the optic nerve microvasculature of the minipig. This technique is based on the quenching by oxygen of the phosphorescence emitted by a dye that is injected intravenously. It provides measurements of the intra-vascular pO2 and was applied simultaneously with measurements of the extra-vascular pO2 with microelectrodes and blood flow by laser Doppler flowmetry. RESULTS: We demonstrate for the first that the optic nerve head intra-vascular pO2 increases during dark adaptation. Furthermore no change in extra-vascular pO2 and blood flow could be detected. CONCLUSIONS: Based on Krogh's model, these results suggest that oxygen consumption by the optic nerve head tissue increases during dark adaptation.

Animals↗

Decreased nitric oxide production accounts for secondary arteriolar constriction after retinal branch vein occlusion.

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.

Animals↗

[Treatment of full-thickness macular holes by vitreoretinal surgery].

PURPOSE: To assess the benefit of vitreous surgery in treating patients with full thickness macular holes (stages II to IV from Gass), we report anatomic and visual statements before and after operation in a series of 12 consecutive eyes (3 holes stage II and 9 holes stage III). METHODS: Visual acuity and anatomical status of the eye before and after the operation were retrospectively reviewed. Surgery included vitrectomy with care to remove the posterior cortical vitreous and relief of all tangential tractions at the posterior pole, retinal tamponade with intraocular gas and face down position for one week. RESULTS: Postoperatively anatomic success was achieved in 83% cases. Mean preoperative as postoperative visual acuity was 0.4, but postoperative visual acuity was improved at least one line in 66% cases. A secondary cataract was observed in 42% cases within 3 months postoperatively and a transient postoperative intraocular hypertonia (30 to 50 mm Hg) was found in 83% cases within 3 days after the operation. It could be successfully treated in each case with diamox p.o. No case of retinal ischemia was observed. CONCLUSIONS: Macular hole surgery provides retinal reattachement and meaningful improvement in visual acuity in selected cases. Vitreous surgery is the treatment of choice for constitued macular holes.

Aged↗

[Early alterations in release of nitrogen monoxide by the retinal after experimental venous occlusion].

PURPOSE: We present hereby some results indicating that there is a significant decrease in the release of NO by the retina immediately after branch-venous occlusion (BVO). METHODS: Using an NO microprobe we measured (NO) in the preretinal vitreous of miniature pigs before and two hours aRer bvo. Conventional and electronic microscopy were performed on the affected retina. RESULTS: At the retinal surface (NO) was reduced to 25% of the previous value two hours after BVO, at the same time significative oedema of the inner retina was observed. CONCLUSIONS: Immediately after BVO there is a significative decrease in the amount of NO released by the affected retina, parallel to the first evidences of an oedema of the inner retinal layers.

Animals↗

[Morphology of early retinal lesions after experimental venous occlusion].

PURPOSE: Study of early hystological lesions after experimental branch venous occlusion (BVO) in miniature pigs. MATERIALS AND METHODS: The retina was taken 1, 2, 4, 6 and 8 hours after BVO with green argon laser for examination with conventional and electronic microscopy. RESULTS: 1 hour after occlusion an extracellular focal oedema is observable in the ganglion cells optic nerve fibers and cells of inner plexiform layer; 2 hours after occlusion there is also an extracellular oedema of the external plexiform layer as intracellular oedema of the inner nuclear layer, 4 hours after occlusion the extracellular oedema is more diffuse especially in the ganglion cells, inner nuclear and optic nerve fibers layers. Cytoplasmic vacuolisation, nuclear pycnosis and ruptured cell membrane layers are observed; 8 hours after occlusion both intra and extracellular oedema are observable throughout the inner retina. CONCLUSIONS: After BVO histological lesions are found within one hour only following the occlusion, apoptosis and cell necrosis are present as soon as 4 hours after experimental BVO.

Animals↗

[Intraocular surgery for secondary retinal detachment in proliferative vitreoretinopathy].

BACKGROUND: Proliferative vitreoretinopathy (PVR) is defined as the growth and contraction of cellular membranes within the vitreous cavity and on both surfaces of the retina following rhegmatogenous retinal detachment. This process is extremely important as these membranes exert traction and may cause recurrent detachment by reopening otherwise successfully treated retinal breaks or create new retinal breaks. We present the results of a small retrospectively series of 63 cases operated in the University of Geneva Eye Clinic, between 1990 and 1993. Surgical procedure, anatomical results, visual acuity have been reviewed. SUBJECTS AND METHODS: Surgical technique, number of surgical procedures, anatomical result and final visual acuity, have been reviewed in each case. Subjects have been divided into two groups depending on the degree of PVR (stage B or C). All patients have been operated combining extra- and intraocular microsurgical technique (scleral buckling, extended vitrectomy, perfluorodecaline, peroperative tamponade, endolaser photocoagulation, retinectomy and gaz or silicone oil tamponade). RESULTS: In the group presenting a stage-B PVR, the retina was reattached in 79% of cases, but only in 47% of the stage-C cases after one surgical procedure. The functional results showed only 31% of cases with a visual acuity superior to 0.4 in the stage-B group and 28% in the stage-C one. In all the stage-B cases that needed further surgical procedure, the retina could be definitely reattached, but in 9% cases of the stage-C group the retina remained detached and in 18% of the same group permanent silicone oil tamponade was necessary to maintain the retina reattached. CONCLUSION: Significant evolution has been observed in microsurgical endoocular surgery in the last ten years, allowing a significant improvement in the anatomical results. Stage-B PVR could be efficiently treated by one surgical procedure in more than 2/3 of cases strongly suggesting the use of endoocular microsurgery as a first intention procedure for retinal detachment complicated by stage-B PVR. An initial stage-C PVR is associated with a poorer anatomical and functional result because of an increased risk of recurrent PVR.

Female↗

[Constitutional release of nitrogen monoxide (NO) by the retina of the minipig is a major determinant of arteriolar basic tonus in the internal retina].

PURPOSE: NO is a nonpolar gas, which diffuses across cell membranes in an isotropic fashion. In relatively large arteries NO has been identified as the endothelium-derived releasing factor and the current hypothesis is that NO controls the vascular tone. We are investigating an alternative hypothesis proposing that the retinal tissues surrounding the arterioles contribute in the process of NO production. METHODS: We performed flicker light stimulation in anesthetized minipigs (hypnodyl 100 mg/hr, tubocurarine 0.1 mg/hr und N2O) in steady-state of normoxia-normocapnia. An NO-microprobe mounted on a micromanipulator was introduced into the eye through the pars plana and positioned on the preretinal space in a zone free of visible vessels. Preretinal NO gradient and recording of NO release variations in response to flicker light stimulation were performed so as periarteriolar microinjections of nitro-L-arginine. RESULTS: When advancing the NO-probe from the vitreous towards the retina we recorded an NO-gradient corresponding to an efflux of 7.1 pMol x min-1 x cm-2 (N = 9). With the microprobe positioned close to the retina and after 60 min dark adaptation we recorded a mean increase in NO release of 1.59 muMol +/- 0.13 SE. After periarteriolar microinjection of nitro-Larginine we recorded a transitory reversible vasoconstriction. CONCLUSIONS: These results indicate that a process occurring in the extravascular tissue of the retina modulates the production of NO and that constitutional NO release by the retina is a major determinant of the basal retinal arteriolar tone.

Animals↗

Nitric oxide controls arteriolar tone in the retina of the miniature pig.

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.

Animals↗

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↗

[Rhegmatogenous retinal detachment operated by extraocular implants. Apropos of 74 cases].

In a series of 88 cases of rhegmatogenous retinal detachments, 14 have been treated by vitrectomy and 74 by scleral buckling with or without intraocular gas tamponade. In 69 cases of the second group (93%) the retina was reattached with an extraocular intervention although 10 cases needed a second intervention. The 5 remaining cases (7%) needed a vitrectomy because of PVR. The reason for failure of extraocular technique is usually related to undertreatment of retinal tears.

Diabetic Retinopathy↗

[Candida chorioretinitis: current therapeutic approach].

BACKGROUND: Candida endophthalmitis may occur either during systemic Candida infection (candidemia), particularly in immunocompromised hosts or as a single manifestation in drug abusers. PATIENT AND METHODS: One case of endogenous candida endophthalmitis (ECE) in a patient with systemic candidiasis and four cases of drug abusers are presented. Well confined inflammatory lesions in retina and choroid were adequately treated with systemic Amphotericin B administration, whereas lesion extension beyond the internal limiting membrane towards the vitreous required surgical management, to remove epiretinal fibrovascular tissue, and intravitreal Amphotericin B injection. CONCLUSION: In all cases, treatment resulted to regression of the lesions, however visual function recovery depends on location of chorioretinal lesions.

Adult↗

[The role of nitric oxide in retinal vasomotor regulation].

Nitric oxide (NO) is one of the most important messenger molecules dilating blood vessels in response to neurotransmitters and serving itself as a neurotransmitter in the brain. We explored its role in the retinal vascular regulation using a sensitive and specific NO microsensor and local perivascular microinjections of NO-synthase inhibitor (nitro-L-arginine in the intact eye of anesthetized miniature pigs. Our findings suggest that NO release is involved in the regulation of basal vascular tone in the inner retina. In contrast hypercapnia and hypoxia induce vasodilatation in an NO independent mechanism.

Animals↗