[The effects of prostaglandins on the blood-ocular barrier: II. Blood-retinal barrier (author's transl)].
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Disruption of blood-retinal barrier at the retinal pigment epithelium after systemic urea injection.
Electron microscopic studies were done on the structural alterations of retinal pigment epithelial cells occurring under osmotic stress utilizing rhesus monkeys and lanthanum nitrate as a tracer. Fluorescein fundus angiography revealed leaking points of fluorescein from the choroid to the retina, and various degenerative alterations of the retinal pigment epithelial cells were observed in these leaking areas. Some cells included many vacuoles in their cytoplasm, but diffusion of lanthanum from the choroid to the outer segment of visual cell was obstructed by the tight junctions between the retinal pigment epithelial cells. Other cells were severely damaged with ruptured membranes. Abundant tracer material diffused through the cytoplasm into the subretinal space. Other cells were broken down in an isolated manner and here marked extravasation of lanthanum into the subretinal space was observed.
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Experimental central retinal vascular occlusion. Blood-retinal barrier alterations and retinal lesions.
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Maintenance of the blood-retinal barrier in chronic experimental retinal ischaemia.
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Animals↗
Insulin-sensitive transport of alanine across the blood-retinal barrier [proceedings].
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Alanine↗
The blood-ocular barriers.
The introduction of the concept of blood-ocular barriers in the ophthalmic literature is briefly reviewed. Two main blood-ocular barriers are proposed: the blood-aqueous barrier and the blood-retinal barrier. The blood-aqueous barrier is formed by an epithelial barrier located in the nonpigmented layer of the ciliary epithelium and in the posterior iridial epithelium, and by the endothelium of the iridial vessels. Both these layers have tight junctions of the "leaky" type. The pereability of the blood-aqueous barrier shows a significant degree of pressure-dependent diffusion associated with transport activity, resembling the standing gradient osmotic flow model. The blood-retinal barrier is located at two levels, forming an outer barrier in the retinal pigment epithelium and an inner barrier in the endothelial membrane of the retinal vessels. Both these membranes have tight junctions of the "nonleaky" type. The permeability of the blood-retinal barrier resembles cellular permeability in general, diffusion being directly related to the predominant roles of lipid solubility and transport mechanisms. Finally, the clinical significance of the blood-ocular barrier is analyzed. The metabolism of cornea and lens and the regulation of intraocular fluids are directly influenced by the blood-aqueous barrier. Similarly, an alteration of the blood-retinal barrier appears to play an important role in the development of vascular retinopathies, pigment epitheliopathies, and retinal edema.
Animals↗
Treatment of early diabetic retinopathy with cyclandelate.
In order to assess the effect of cyclandelate on the abnormal permeability of the blood-retinal barrier which occurs in diabetic patients before any other lesions are apparent in the retina a well-controlled, double blind, and paired trial was carried out in 22 patients. The treatments were randomised. The permeability of the blood-retinal barrier was assessed by vitreous fluorophotometry. Each patient was examined before being involved in the trial and then another 3 times with 1 month's interval. The total duration of treatment was 3 months. The results showed that the breakdown of the blood-retinal barrier as evidenced by the degree of abnormal fluorescein penetration into the vitreous suffered a significant decrease in the diabetic patients treated with cyclandelate when compared to the patients submitted to placebo administration, and this effect is particularly apparent in the third month of treatment.
Adult↗
Vitreous fluorophotometry and retinal blood flow studies in proliferative retinopathy.
The permeability of the blood-retinal barrier and retinal blood flow were evaluated by two new fluorophotometric methods in a series of patients with proliferative retinopathy, due either to retinal vein occlusion or to diabetes. A breakdown of the blood-retinal barrier and a decrease in retinal blood flow were observed in these patients. The breakdown of the blood-retinal barrier could be quantitated by vitreous fluorophotometry, which revealed very high concentrations of fluorescein in the vitreous after intravenous administration. The decrease in retinal blood flow appeared to be due mainly to appreciable narrowing of the retinal arteriolar vessels.
Diabetic Retinopathy↗
Experimental macular edema after lens extraction.
Macular edema has been observed frequently in man after cataract extraction, but pathogenic mechanisms remain unclear. Seven eyes of four young adult rhesus monkeys underwent lens extraction. The retinas and maculae of these eyes were examined by ophthalmoscopy fundus photography, fluorescein angiography, light and electron microscopy, and the horseradish peroxidase tracer technique. In the macular region, the blood-retinal barrier at the retinal vasculature was disrupted in three of the seven eyes. All three eyes had had vitreous loss during lens extraction. Horseradish peroxidase was observed both intracellularly and extracellularly in the maculae. In contrast, the blood-retinal barrier at both the retinal pigment epithelium and the retinal vasculature of the peripheral retina in most eyes was intact. We conclude that macular edema secondary to lens extraction is due to disruption of the blood-retinal barrier at the levels of the retinal vasculature and the retinal pigment epithelium.
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Kinetic vitreous fluorophotometry in experimental diabetes.
Kinetic vitreous fluorophotometry was used to measure dynamic alterations in blood-retinal barrier function. Normal hooded rats were compared with diabetic animals before and after insulin treatment. Rats with streptozocin-induced diabetes demonstrated significantly longer (P less than .001) half-periods of fluorescein loss from the vitreous when compared with controls, and insulin treatment significantly reduced (P less than .001) the mean half-period toward control values without normalization of serum glucose. These results suggest that kinetic vitreous fluorophotometry is a good indicator of blood-retinal barrier function and that sufficient amounts of insulin may be more important than normal blood glucose levels in recovery of altered barrier function in diabetes.
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Hypertensive breakdown of cerebral but not of retinal blood vessels in rhesus monkey.
Acute hypertension, induced either by intravenous injection of metaraminol bitartrate (Aramine), infusion of isotonic saline into the common carotid artery, or a combination of both procedures did not in the rhesus monkey lead to breakdown of the blood-retinal barrier. Whereas the cerebral vasculature was made permeable to blood-borne dye at carotid pressure above 160 mm Hg, the retinal blood vessels were intact even at pressures as high as 310 mm Hg. Hypertensive blood-brain barrier opening was associated with neurologic defects and brain edema. The results indicate that the retina is more resistant to acute hypertension than is the brain. The greater resistance in the retina may be due to the high number of contractile, perivascular mural cells counteracting increased intravascular hydrostatic pressure. An alternative or supplementary explanation is that choroidal and retinal blood vessels are better protected from surges in blood pressure than are brain blood vessels. Differences between the innervation of brain and ocular blood vessels could account for this.
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Vitreous fluorophotometry in adult-onset diabetes mellitus.
We studied the breakdown of the blood-retinal barrier in 83 patients with adult-onset diabetes mellitus, by using vitreous fluorophotometry. The patients were in good stable metabolic control and were receiving injectible insulin or oral hypoglycemic agents. Vitreous fluorophotometry readings were abnormally high but similar in both groups of patients, and no significant differences were found between those with and those without early background diabetic retinopathy. Significantly more patients taking oral agents were hypertensive, and significantly fewer of these patients had background retinopathy.
Adult↗
Hemoglobin AIc and red cell oxygen release capacity in relation to early retinal changes in newly discovered overt and chemical diabetics.
The average Hb A1c concentration in consecutive cases of newly discovered nonacidotic diabetics was 11.4% prior to diet and insulin, as compared to 5.5% following prolonged optimal control (p less than 0.001). Hemoglobin A1c was significantly correlated with fasting blood sugar. In a controlled study the average Hb A1c in 30 subjects with chemical diabetes was 5.8% as opposed to 5.3% in controls with normal OGTT (p less than 0.05). Thirty-seven percent of the chemical diabetics had Hb A1c values greater than or equal to 6.5%, while none in the control group showed such high values. Hb A1c in whole blood has increased oxygen affinity. A decrease in red-cell oxygen release was noted in some untreated nonacidotic diabetics, and an adverse effect of insulin on the oxygen release capacity was demonstrated in both newly diagnosed ketoacidotic and nonacidotic diabetics. The importance of this defect in red-cell oxygen-releasing capacity on the function of the microcirculation is discussed. Signs of an early breakdown of the blood-retinal barrier was demonstrated in 20% of the chemical diabetics by fluorescein angiography.
Blood Glucose↗
Early detection of retinal involvement in diabetes by vitreous fluorophotometry.
Vitreous fluorophotometry is a new quantitative method for evaluation of the blood-retinal barrier (BRB). The application of this method to a series of diabetic patients with apparently normal fundi revealed the presence of a significant breakdown of the BRB in the early stages of retinal involvement in diabetes. This alteration of the BRB appears to be the earliest clinically detectable change to occur in the retina in diabetes. Higher vitreous fluorophotometry values, indicating a more marked breakdown of the BRB, occurred in patients who were under worse metabolic control. Higher vitreous fluorophotometry values were also associated with the development of visible retinal lesions.
Diabetes Mellitus↗
A selected review of current retinal research and study.
This paper presents a digest of 50 retinal research projects reported in one British and two American journals from July 1976 through June 1977. The articles reviewed report recent developments pertaining to effects of excessive light on retinal tissue in newborn rats, pathogenesis of cotton-wool spots, control of the blood-retinal barrier in diabetes, infections, macular diseases, variations in retinal pigment epithelium, and retinal detachment.
Adult↗
Studies on ocular blood flow and retinal capillary permeability to sodium in pigs.
A surgical technique was developed in pigs that permits access to the retinal venous plexus surrounding the optic nerve. The effect of surgery on ocular blood flow and capillary permeability was evaluated. Blood flow, determined by the labelled microsphere technique, did not differ significantly between operated and control eyes. Increased intraocular pressure in the operated eye reduced blood flow through the choroid and the anterior uvea in proportion to the reduction in perfusion pressure, while in the retina a smaller reduction in blood flow occurred indicating that autoregulatory mechanisms are involved in the control of retinal blood flow. The capillary permeability to sodium was studied by the single injection technique, using albumin as a reference substance. The fractional initial extractions from the choroidal and the retinal vessels were 0.77 and -0.001 respectively. The absence of a sodium extraction from the retinal vessel indicates that this part of the blood-retinal barrier was intact and that the blood drained by the retinal plexus is not mixed with blood from other sources.
Animals↗
Retinal damage experimentally induced by microwave radiation at 55 mW/cm2.
The action of 550 W/m2 (mean) 3100 MHz pulsed radiation on the rabbit retina in vivo was investigated by fundus photography, blood-retinal barrier tracers, light and electron microscopy, either after a single 1--1.5 h exposure or after a series of repeated 1 h exposures for up to 53 h during about 100 days. The electron microscopic investigation of the repeatedly exposed retinas revealed degenerative changes in the retinal neurons. The neurons appeared depleted of their cytoplasmic constituents and often contained phago-lysosomal structures with myelin bodies. There were many degenerating synaptic boutons. The glial cells displayed reactive changes. These ultrastructural changes could not be demonstrated by the other methods used. A single microwave exposure, followed by an induced 70--100% blood-pressure increase, did not enhance blood-retina barrier permeability to tracers. There was no evidence of blood brain barrier leakage. These studies show that the rabbit eye can be affected by microwave radiation at intensities lower than previously reported.
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Effects of therapy on vitreous fluorophotometry in diabetes mellitus.
Quantitative vitreous fluorophotometry was used to study the alteration of the blood-retinal barrier in 116 patients with diabetes mellitus of adult onset. The patients were in good stable metabolic control on injectable insulin, oral hypoglycaemics, or diet therapy. Vitreous fluorophotometry readings were abnormally high but similar in all three groups and in those with or without early background retinopathy. A higher incidence of systemic hypertension was noted in those patients requiring oral agents compared to those on insulin or diet therapy.
Biological Transport↗