Biomedical subjects

C J Pournaras

Publications and source records attributed to C J Pournaras.

At least 73 records · Page 4Linked to original sources

PubMed1994

[Prognostic factors in surgical treatment of epiretinal membranes].

BACKGROUND: Macular epiretinal membranes, whether idiopathic or secondary to vitreo-retinal pathology may result in a lowering of central vision and/or metamorphopsia following a distortion of retinal tissue. Although an adequate surgical peeling procedure is known to result in a functional improvement, the criteria for patient selection for such intervention are, as yet not clearly established. METHODS AND RESULTS: In order to establish prognostic indicators of a good visual recovery, we studied 25 cases of epiretinal membrane. Our results showed an improvement in visual acuity of 2 or more Snellen lines among 34% of our patients, regardless of their initial visual acuity. The duration of symptoms prior to intervention was found to be a prognostic factor whereas the presence of macular edema detected preoperatively on fluorescein angiography had no effect on the final visual outcome. CONCLUSION: A common post-operative complication came to our attention: secondary opacification of the crystalline lens.

Cataract↗

PubMed1993

Pathogenetic mechanisms in combined cilioretinal artery and retinal vein occlusion: a reappraisal.

We examined nine patients who presented cilioretinal artery occlusion (CLRAO) associated with retinal vein occlusion (RVO). CLRAO was probably secondary to the raised intraluminal resistance consequent to the RVO in patients showing initially a delayed filling of the cilioretinal artery in fluorescein angiography. Interestingly, these patients presented an ophthalmoscopically more severe form of RVO and had systemic predisposing factors for a RVO. In patients presenting a physiological perfusion of the cilioretinal artery in fluorescein angiography, RVO was a self limited disease and etiologic factors were not found. This may suggest that in these patients the CLRAO probably occurred simultaneously with the RVO after a decrease in perfusion pressure in both retinal and cilioretinal arterial systems. In this combined vaso-occlusive retinopathy the vulnerability of cilioretinal arteries can be explained either by the absence of autoregulation or by their lower perfusion pressure gradient in comparison with retinal arteries.

Adolescent↗

PubMed1993

Microinjection of L-lactate in the preretinal vitreous induces segmental vasodilation in the inner retina of miniature pigs.

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.

Animals↗

PubMed1992

[Uveitis complicating posterior segment neovascularization. Six cases].

Subretinal or preretinal neovascularisation may be occasionally observed during the evolution of certain forms of uveitis. Subretinal neovascularisation commonly begins at the level of the chorioretinal uveitic scars. Consequently, the alteration of the retinal pigment epithelium-Bruch's membrane-choriocapillaris complex is the apparent cause. Laser photocoagulation of the neovascular front, when indicated, is the treatment of choice. In contrast, preretinal neovascularisation is observed at the active stage of uveitis. Fluorescein angiography findings suggest that it is probably correlated with the importance of inflammation since in most of the cases there is no retinal ischemia. Therefore, in order to obtain a regression of the neovascular tufts the treatment should be directed against the inflammatory process. In this study the authors report five cases of subretinal neovascularisation which developed at the level of chorioretinal post-inflammatory scars and one case of papillary neovascularisation which occurred during the active stage of an unilateral intermediate uveitis and in which new vessels regressed completely following systemic steroid treatment.

Adolescent↗

PubMed1992

[Peeling of epiretinal macular membranes. Results and conclusions of the Geneva Clinic].

Epiretinal macular membranes can cause a lowering of visual acuity and may even lead to a total loss of foveal function in the absence of surgical procedure. The only surgical treatment is vitreo-retinal surgery with peeling of the membrane. In Geneva, we studied 23 patients, all of whom were operated for epiretinal membrane even though visual acuity was greater as 0.2, 10 membranes were idiopathic et 13 secondary. Six patients from this second group had recently undergone cataract surgery. The results were good: 83% of the patients showed an improvement in post-operative visual acuity and 60% gained 2 or more lines on the Snellen scale. The main factors for prognosis were preoperative macular cystoid edema and duration before surgery. The principal post-operative complication encountered was a secondary opacification of the lens with, to a lesser extent, cystoid edema of the macula.

Cataract Extraction↗

PubMed1992

[Profile of pO2. I. Profile of transretinal pO2 in hypoxia].

Transretinal PO2 measurements during systemic hypoxia, made during variations of the PO2 by steps of 10 mmHg between 120 and 30 mmHg, have shown that the PO2 values measured at the inner-retina up to half the thickness of the retina remained stable. On the other hand, those measured at the choroid and at the outer-retina decreased in a linear manner according to the variations of PaO2. These results suggest a regulation in the retinal blood flow, allowing the PO2 to remain stable for the different steps of hypoxia studied. On the other hand, the values measured at the choroid and at the outer-retina showed the absence of regulation in the choroidal blood flow during hypoxia. Systemic hypoxia may affect the metabolism of the photoreceptors and the pigmentary epithelium.

Animals↗

PubMed1992

[Metabolic factors of vasomotor regulation of the inner retina].

Lactic acid, the end metabolic product of anaerobic glycolysis is probably the mediator of the hypoxia induced vasodilation on retinal arterioles. In this study we explored the mechanisms of the retinal vasomotor effect of this metabolite by performing preretinal juxtaarteriolar pulsatile pressure microinjections on the intact eye of anesthetized and artificially ventilated miniature pigs. Microinjections of the levorotatory isomer L-lactic acid (pH: 2) induced a local maximal dilation of retinal arterioles. This vasodilator effect, like that of systemic hypoxia, was not mediated by the release of prostaglandins. Preretinal pulsatile pressure juxtaarteriolar microinjections of neutral-pH solution of L-lactic acid also induced a segmental retinal arteriolar dilation. In contrast, microinjections of the dextrorotatory isomer D-lactic acid (pH: 2, solution), which is not produced by the retina, did not affect significantly the arteriolar diameter. Consequently, the vasodilator effect of lactic acid does not depend on periarteriolar pH modification and probably interferes with retinal metabolism since only the natural levorotatory metabolite is recognized.

Animals↗

PubMed1992

[Regulation of papillary pO2].

PO2 measurements using a double barelled recess type microelectrodes were measured in the optic nerve head of miniature pigs during systemic hyperoxia (100% oxygen breathing) and variations of the systemic blood pressure by intravenous injection of Adrenaline or trinitrine. During either systemic hyperoxia, or progressive variations of blood pressure, the intervascular PO2 remained stable. These results suggest a regulation of the tissue PO2 of the optic nerve head, as the retina does, at constant values.

Animals↗

PubMed1992

[Profile of pO2. Regulation of papillary pO2].

Animals↗

PubMed1991

New ocular micromanipulator for measurements of retinal and vitreous physiologic parameters in the mammalian eye.

A new ocular micromanipulator for introducing a microelectrode into the mammalian eye is described. Included is a technical description of the device, incorporating arched tracks and DC motors to provide for angular motion around a scleral entrance point. Applications for in vivo measurements of local PO2 in the retina and vitreous of miniature pigs and cats are shown. The new design features of this micromanipulator allow for smooth microelectrode movements over large retinal areas, facilitating the rapid collection of data in many different areas of the retina and vitreous.

Animals↗

PubMed1991

[Retinal vascular occlusion in a young patient with hemostatic abnormalities].

Retinal vascular occlusion (RVO) in the young patient without vascular parietal disease have been encountered in different pathologic states, coagulopathy being frequent. We started a prospective study in Geneva to find out the hypercoagulable states responsible for RVO. We give suggestions to the paraclinical investigations to perform. We discuss the primary and secondary hypercoagulable states in the light of two patients who had coagulation abnormalities.

Adult↗

PubMed1991

[Occlusion of a cilioretinal artery associated with occlusion of the central retinal vein].

Cilioretinal artery occlusion (CLRAO) may be occasionally associated with central retinal vein occlusion (CRVO). This combined retinal vascular pathology is described in 5 patients. In this clinical setting the vulnerability of cilioretinal vessels can be explained by the difference in regulatory mechanisms between choroidal and retinal blood flow. The type of CRVO may predict whether the CLRAO is primary or secondary to the CRVO.

Adult↗

PubMed1991

[Regulation of PO2 in the area of the optic papilla of the minipig in hyperoxia].

PO2 measurements using a double barrelled recess type microelectrodes were measured in the optic nerve head of miniature pigs in normoxia and hyperoxia. Although periarteriolar PO2 increased markedly during systemic hyperoxia (100% oxygen breathing), the intervascular PO2 remained stable under hyperoxia. These results suggest a regulation of the tissue PO2 of the optic nerve head, as the retina does, at constant values during hyperoxia.

Animals↗

PubMed1990

[Eyelid injuries].

The eyelids not only protect the ocular globe, but also keep it wet and transparent. In the case of a palpebral wound the survival of the ocular globe is perhaps at stake. Corrective reconstruction of a palpebral wound must be considered as quickly as possible in order to restore eyelid shape and mobility. A facial emergency must be treated along the lines of an immediate reconstruction. A completely successful restoration must see to the prevention of complications associated, on one hand to poor adaptation of the wounded edge engendering a deformed eyelid, a coloboma at the free edge, malpositioning (entropion or ectropion), or an acquired ptosis. On the other hand, stenosis of the lacrymal canaliculus will lead to epiphora. Both complications present later difficulties for treatment.

Eyelids↗

PubMed1990

Diffusion of O2 in normal and ischemic retinas of anesthetized miniature pigs in normoxia and hyperoxia.

Transretinal PO2 profiles were recorded with O2-sensitive microelectrodes in the normal retina and in ischemic retinal foci induced by the occlusion of a retinal branch vein with argon laser photocoagulation in anesthetized miniature pigs. In the normal retina there are two PO2 gradients: one from the inner retina and the other from the choroid, both directed toward the middle of the retina. Both PO2 gradients persisted during hyperoxia. Thus, even in hyperoxia, the choroid does not supply the whole thickness of the normal retina with O2. Preretinal and transretinal PO2 measurements in ischemic inner retinal foci showed the existence of two PO2 gradients in steady-state systemic normoxia, as did those in the normal retina. This finding indicates that even in ischemia the choroid does not supply O2 to the inner retina; as a result, tissue hypoxia is maintained. During systemic hyperoxia, the intraretinal PO2 measurements in the ischemic foci showed only one gradient going from the choroid toward the inner retina. This gradient indicates that under these conditions, the choroid can supply O2 to the entire thickness of the ischemic retina. Extending a previously formulated hypothesis, we propose that in the ischemic retina as opposed to the normal retina, hyperoxia does not induce an increase in the O2 consumption of the outer retina. This suggestion could explain the rise in PO2 in the inner ischemic retina during hyperoxia.

Animals↗

PubMed1990

Rhythmic changes in velocity, volume, and flow of blood in the optic nerve head tissue.

Using laser Doppler flowmetry, slow variations in velocity, volume, and flux of red blood cells in the optic nerve head (ONH), choroid, and retina of the anesthetized minipig have been demonstrated. The variations of velocity and volume were highly regular and vigorous in the ONH and had frequencies ranging from 2.5 to 4.5 cycles/min. The flux variations were smaller or absent due to a phase shift of approximately 180 degrees between the volume and velocity changes. The volume fluctuations were synchronized to those of the PO2 measured in the vitreous, at approximately 50 microns from the surface of the ONH tissue. The fluctuations were less regular in the choroidal and the retinal vessels and their frequencies were higher than those in the ONH. The lack of correlation between the fluctuations in the ONH and those in the retinal and choroidal vessels points toward a local mechanism. The changes in blood volume in the ONH, the phase shift between volume and velocity changes, and the predominance of venules at the surface of the ONH are three factors suggesting that this mechanism involves a change in the diameter of the venules rather than in the arterioles.

Animals↗

PubMed1990

Scatter photocoagulation restores tissue hypoxia in experimental vasoproliferative microangiopathy in miniature pigs.

Experimental retinal branch vein occlusion using argon laser photocoagulation in miniature pigs induced the development of ischemic retinal territories associated with preretinal neovascularization. Preretinal partial pressure of oxygen (PO2) measurements on the ischemic territories, using O2-sensitive microelectrodes, established that the ischemic retinal areas were hypoxic. Scatter photocoagulation of these ischemic hypoxic territories restores the local PO2 to the normal values within 2 weeks. Hence, the reported inhibitory effect of photocoagulation on the development of retinal neovascularization could be due to a reversal effect on tissue hypoxia.

Animals↗

PubMed1990

Experimental retinal branch vein occlusion in miniature pigs induces local tissue hypoxia and vasoproliferative microangiopathy.

In miniature pigs, retinal veins were experimentally occluded using argon laser coagulation. Microvascular modifications leading to retinal hemorrhages and retinal edema were observed some hours after the occlusion. These lesions resolved progressively within 3 weeks after the occlusion, but in most cases ischemic retinal territories persisted. Preretinal partial pressure of oxygen (PO2) measurements, using double barrelled O2-sensitive microelectrodes, showed that all the ischemic areas were indeed hypoxic. In half of the experiments, preretinal and intravitreal new vessels grew on the ischemic territories. Tissue hypoxia appears to be a key step in triggering neovascularization. However, the critical level of hypoxia was not determined.

Animals↗