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Biomedical subjects

C J Pournaras

Publications and source records attributed to C J Pournaras.

89 records · Page 5Linked to original sources
PubMed1990

[Changes in the concentration of K+ induced by a flash of light in the preretinal vitreous of the anesthesized minipig].

When measured with double-barreled ion-selected microelectrodes, delta K+0 is found to be heterogeneously distributed over the retinal surface. A transient fall (less than or equal to 200 microM) in delta K+0 near an arteriole wall and a transient increase (less than or equal to 500 microM) in zones free of arterioles were observed during light stimulation. In view of these findings the authors assume that the former is due to K+ uptake and transport by perivascular astrocytes, and that the latter is due to K+ siphoning by Müller cells.

Animals↗
PubMed1990

[Experimental venous branch occlusion: change in the preretinal oxygen pressure pO2 by dexamethasone].

Transretinal pO2 profiles were recorded during normoxia and hyperoxia in normal and ischemic retinal regions in anesthetized miniature pigs, using double-barrelled recess-type microelectrodes. In normoxia and hyperoxia, pO2 in the normal region decreased from the inner retina and the choroid toward the midretina, indicating that the choroid cannot supply O2 to the entire normal retina. Preretinal and transretinal pO2 measurements in ischemic regions following laser occlusion of a retinal branch vein showed that in normoxia the direction of pO2 gradients prevents O2 diffusing from the choroid to reach the inner retina. This explains why the ischemic regions remain hypoxic. On the contrary, during hyperoxia the intraretinal pO2 gradient indicates an O2 flux from the choroid to the inner retina, resulting in a marked increase in preretinal pO2 in the affected regions. Hence hyperoxia could be a useful tool for restoring the oxygen supply to the inner, hypoxic retinal layers; unfortunately it cannot be used in clinical practice. Parabulbar injections of dexamethasone induce a transitory increase in preretinal pO2, probably by reducing the outer retinal consumption of O2 and thus allowing O2 which diffuses through the choroid to reach and restore the inner retinal hypoxia; clinical experience has shown that parabulbar dexamethasone injections may be effective in the treatment of venous branch occlusion.

Animals↗
PubMed1989

Diffusion of O2 in the retina of anesthetized miniature pigs in normoxia and hyperoxia.

Intraretinal oxygen tension (pO2) and local electroretinogram (ERG) were simultaneously measured in miniature pigs using double-barreled recess type microelectrodes. Transretinal pO2 profiles were recorded during normoxia and hyperoxia in areas close to (juxta-arteriolar) or far from (intervascular) retinal arterioles. In normoxia, in both areas, the pO2 decreased from the inner retina and the choroid towards the middle of the retina. In the inner retina the gradient of the juxta-arteriolar pO2 profile was steeper than that of the intervascular profile. This characteristic persisted during the breathing of 100% O2. Analysis of the pO2 profiles shows that, even in hyperoxia, the choroid cannot supply O2 to the whole retina. The results also support the conclusions of previous work (Riva, Pournaras and Tsacopoulos, 1986) indicating that in the normal retina it is not the O2 diffusing from the choroid to the retinal arterioles the induces vasoconstriction of these vessels. In the miniature pig this constriction appears to maintain inner retina tissue pO2 at a constant level during hyperoxia. From the pO2 transretinal profiles and previously published choroidal O2 fluxes and pO2 values near retinal vessels an explanatory working hypothesis is formulated according to which O2 consumption (qO2) of the outer retina increases during hyperoxia in the miniature pig.

Animals↗
PubMed1986

Regulation of local oxygen tension and blood flow in the inner retina during hyperoxia.

A study has been undertaken to determine whether local changes in PO2 could be a factor in the regulation of retinal blood flow during 100% O2 breathing. For this purpose we have measured simultaneously in eyes of anesthetized and artificially ventilated miniature pigs the change in local preretinal PO2 and retinal blood flow using O2-sensitive microelectrodes and laser Doppler velocimetry. Although preretinal intervascular PO2 changed little, periarteriolar PO2 increased markedly during 100% O2 breathing. When measured less than 50 microns from the arteriolar wall, the time course of this increase preceded that of the decrease in retinal blood flow. The results indicate that O2 diffusing through the wall of the large retinal arterioles represents the most important component of periarteriolar PO2. This diffusion coupled with the decrease in retinal blood flow could play a major role in the regulation of inner retinal PO2. The data also suggest that diffusional shunting of O2 between retinal arterioles and veins could explain the unexpected increase in venous O2 saturation during 100% O2 breathing that has been previously reported by others. The finding that retinal periarteriolar PO2 is always higher than the PO2 in the outer retina does not support the previously formulated hypothesis that O2 from the choroid is responsible for the constriction of the arterioles during hyperoxia.

Animals↗
PubMed1986

[Vision aids for patients with senile exudative macular degeneration. Comparison of spontaneous fibrovascular scars and scotomas induced by photocoagulation].

Aging exudative macular degeneration frequently results in a fibrovascular scar which entails the loss of central vision. This scar implies an often large and deep scotoma which makes it very difficult for the patient to be fitted with low-vision aids. A Goldmann static perimetry study of retinal sensitivity in the treated areas showed that krypton laser at liminar doses does not induce deep scotomas.

Aged↗
PubMed1985

[The physiopathology of retinal circulation: consequences of acute retinal vascular occlusion].

A constant oxygen supply from the retinal and choroidal vascular system is essential for the maintenance of the retinal electrical activity. Arterial or venous retinal obstruction modifies the hemodynamics in the retinal circulation and produces hypoxia in the affected area. In the case of arterial obstruction, severe hypoxia (anoxia) rapidly (in less than 45 min) produces irreversible cell damage in the inner area of the retina. With venous obstruction, the hypoxia is moderate and the retinal damage is partial. In some cases, hypoxia regresses because the formation of collateral vessels most probably provides adequate perfusion. In cases of irreversible venous obstruction, insufficient formation of collateral vessels results in the development of ischemic regions in the retina and severe hypoxia. In these cases preretinal neovascularization may develop.

Animals↗
PubMed1985

[Retinal vascular occlusion: possibilities of a direct oxygen supply to the hypoxic areas].

Treatment of a retinal vascular occlusion consists in restoration of normal oxygenation to the affected area. An experimentally induced increase in arterial CO2 provokes an increase in preretinal CO2 in a hypoxic retinal area which has developed after venous obstruction, but it is ineffective in anoxic areas of an arterial occlusion. However, clinical application of this treatment offers no benefit for the patient. Hyperoxia caused by respiration of a gas mixture of 5% CO2 and 95% O2 is also ineffective. On the other hand, the results of recent studies in which blood is replaced with fluorocarbon solutions are promising. Finally, it is pointed out that in cases of venous occlusion laser coagulation leads to reoxygenation of the inner hypoxic retina.

Arterial Occlusive Diseases↗
PubMed1985

[Experimental venous thrombosis: preretinal PO2 before and after photocoagulation].

Experimental occlusion of a retinal vein leads to retinopathy in the affected drainage area. In some cases the formation of ischemic regions, where the retina is completely destroyed, is typical for the development of this retinopathy. Laser photocoagulation restores the physiological preretinal oxygen pressure in these hypoxic regions. It is possible that the rise in O2 pressure which has been observed is caused by destruction of pigment epithelium and the photoreceptor layer, as oxygen diffuses freely from the choroid to the inner retina without being consumed by the outer layers.

Animals↗
PubMed1984

[Treatment of exudative hemorrhagic macular degenerations with the krypton laser].

Choroidal neovascularization is considered to be the cause of exudate or subretinal hemorrhage formation in the evolution of different types of macular degeneration (exudative senile macular degeneration, idiopathic macular degeneration, presumed ocular histoplasmosis, angioid streaks, etc. The only curative treatment which has proved to be successful is the destruction of subretinal neovascularisation by photocoagulation. The effect of laser photocoagulation depends on the radiation wavelength emitted and the absorption spectrum of the target tissue. It is for this reason that the red krypton laser is recommended for the destruction of subretinal neovascularizations, its action being restricted to the choroid without inflicting damage on the nerve fiber layer.

Adult↗
PubMedDate not supplied

Regulation of optic nerve head blood flow in normal tension glaucoma patients.

PURPOSE: To investigate the regulation of the optic nerve blood flow (Fonh) in response to an increase of the perfusion pressure (PPm) in normal tension glaucoma (NTG) patients and in age-matched normal volunteers. METHODS: Measurements were performed in 16 eyes of NTG patients and in 10 eyes of age-matched controls. Laser Doppler flowmetry (LDF) was applied to calculate the relative flux of red blood cells at the temporal rim of the optic nerve head (ONH) in response to increases in PPm. PPm was raised through an increase in systemic blood pressure induced by isometric exercise. Before being tested, all patients had 3 weeks of washout of any local medication. RESULTS: In the NTG group, mean ophthalmic arterial blood pressure increased during isometric exercise from 73 to 89 mmHg (22%), resulting in a 29% increase of the PPm. This increase did not induce any significant change in mean Fonh. For the control group, the 28% increase of PPm also did not significantly affect Fonh. There was a trend for a greater increase in vascular resistance during isometric exercise in the NTG than in the normal control group (47% versus 25%). CONCLUSIONS: The LDF parameters, measured in the ONH, did not indicate an abnormal Fonh regulation in response to an increase of the PPm in either normal subjects or NTG patients. The maintenance of constant blood flow is achieved by an increase in local vascular resistance. Our data show a greater percent increase in vascular resistance in the NTG patients compared to the normal subjects for a similar percent increase in PPm in both groups during squatting. This suggests some alteration of the vessel tone regulatory mechanisms in NTG patients.

Aged↗
PubMedDate not supplied

[Diffusion of O2 in the normal and the ischemic retina of miniature pigs].

Transretinal PO2 profiles were recorded during normoxia and hyperoxia in normal and ischemic retinal territories in anesthetized miniature pigs using double barrelled recess type microelectrodes. In normoxia and hyperoxia the PO2 in the normal territory decreased from the inner retina and the choroid towards the mid-retina, indicating that the choroid cannot supply O2 to the whole normal retina. Preretinal and transretinal PO2 measurements in ischemic territories following a laser occlusion of a retinal branch vein demonstrated that in normoxia the direction of PO2 gradients prevents O2 diffusing from the choroid to reach the inner retina. This explains why the ischemic territories are hypoxic. In the contrary, during hyperoxia the intraretinal PO2 gradient indicates an O2 flux from the choroid to the inner retina resulting to marked preretinal PO2 increase at the affected territories. We proposed the hypothesis that in the ischemic retinas the hyperoxia does not induce a rise of the O2 consumption of the outer retina. Hence hyperoxia could be a useful tool to restore the oxygenation of the inner hypoxic retinal layers.

Animals↗
PubMedDate not supplied

[The role of prostaglandins in the regulation of retinal blood flow].

Hypercapnia causes vasodilatation of retinal arterioles. Prostaglandin E1, injected close to retinal arterioles from the vitreal side cause vasodilatation apparently similar to that caused by hypercapnia. An inhibitor of prostaglandin synthase (indomethacin) was injected into the ocular circulation. There was a reversible inhibition of the retinal vasodilatation normally induced by hypercapnia. Indomethacin injected close to retinal arterioles from the vitreal side causes reversible vasoconstriction and inhibits the vasodilatory effect of hypercapnia. It is concluded that prostaglandin E1 satisfies three criteria for a candidate for a mediator of hypercapnia-induced arteriolar dilatation.

Animals↗