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PubMed2002

Blockade of nitric-oxide synthase reduces choroidal neovascularization.

Nitric oxide (NO) promotes retinal and choroidal neovascularization, although different isoforms of nitric-oxide synthetase (NOS) are critical in each. Deficiency of endothelial NOS (eNOS) suppresses retinal but not choroidal neovascularization, whereas deficiency of neuronal NOS (nNOS) or inducible NOS (iNOS) suppresses choroidal, but not retinal neovascularization. In this study, we investigated the effect of N(G)-monomethyl-L-arginine (L-NMMA), a nonspecific NOS inhibitor, in three models of ocular neovascularization. Oral administration of L-NMMA caused significant inhibition of choroidal neovascularization in mice with laser-induced rupture of Bruch's membrane and significantly inhibited subretinal neovascularization in transgenic mice with expression of vascular endothelial growth factor (VEGF) in photoreceptors (rho/VEGF mice) but did not inhibit retinal neovascularization in mice with ischemic retinopathy. By extensive mating among mice deficient in NOS isoforms, triple homozygous mutant mice deficient in all three NOS isoforms were produced. These mice had marked suppression of choroidal neovascularization at sites of rupture of Bruch's membrane and near-complete suppression of subretinal neovascularization in rho/VEGF mice but showed no difference in ischemia-induced retinal neovascularization compared with wild-type mice. These data indicate that NO is an important stimulator of choroidal neovascularization and that reduction of NO by pharmacologic or genetic means is a good treatment strategy. However, the situation is more complex for ischemia-induced retinal neovascularization for which NO produced in endothelial cells by eNOS is stimulatory, but NO produced in other retinal cells by iNOS and/or nNOS is inhibitory. Selective inhibitors of eNOS may be needed for treatment of retinal neovascularization.

Animals↗
PubMed1991

Uniform cell-autonomous tumorigenesis of the choroid plexus by papovavirus large T antigens.

The simian virus 40 (SV40) large tumor antigen (T antigen) under its natural regulatory elements induces choroid plexus papillomas in transgenic mice. Because these tumors develop focally after several months, it has been suggested that secondary cellular alterations are required to induce a tumor in this tissue. In contrast to SV40, the related lymphotropic papovavirus early region induces rapid nonfocal choroid plexus neoplasia in transgenic mice. Here, using hybrid gene constructs, we showed that T antigen from either virus in in fact sufficient to induce these tumors. Their abilities to induce proliferative abnormalities in other tissues, such as kidney and thymus, were also indistinguishable. Differences in the rate of choroid plexus tumorigenesis reflected differences in the control regions of the two viruses, rather than differences in T antigen per se. Under SV40 regulation, expression was limited to a fraction of the choroid plexus cells prior to the formation of focal tumors. When SV40 T antigen was placed under lymphotropic papovavirus control, in contrast, expression was generally uniform in the choroid plexus and rapid expansion of the tissue ensued. We found a direct relationship between T-antigen expression, morphological transformation, and proliferation of the choroid plexus epithelial cells. Analysis of mosaic transgenic mice indicated further that T antigen exerts its mitogenic effect cell autonomously. These studies form the foundation for elucidating the role of various T-antigen subactivities in tumorigenesis.

Animals↗
PubMed2004

Response of choroidal blood flow to carbogen breathing in smokers and non-smokers.

AIM: To investigate a potential difference in ocular vascular reactivity during carbogen breathing in optic nerve head, choroid, and retina between healthy smokers and non-smokers. METHODS: 25 (13 smokers and 12 non-smokers) healthy male volunteers participated in this observer masked, two cohort study. During inhalation of carbogen (5% CO(2) and 95% O(2)) over 10 minutes measurements were taken using laser Doppler flowmetry to assess submacular choroidal and optic nerve head blood flow, laser interferometry to assess fundus pulsation amplitudes, and retinal vessel analyser (RVA) to assess retinal vessel diameters. RESULTS: At baseline choroidal blood flow was higher (p = 0.018, ANOVA) in smokers than in non-smokers. During administration of carbogen the response in choroidal blood flow was significantly different between the two groups: there was an increase in non-smokers after carbogen breathing (p = 0.048) compared with relatively stable blood flow in smokers (p = 0.049 between groups, ANOVA). A similar response pattern was seen for fundus pulsation amplitude, which increased notably after carbogen breathing in non-smokers but not in smokers (p<0.001 between groups, ANOVA). Optic nerve head blood flow and retinal vessel diameters were reduced in both groups to a comparable degree during carbogen breathing. CONCLUSION: The study indicated abnormal choroidal vascular reactivity in chronic smokers. These early haemodynamic changes may be related to the increased risk to smokers of developing ocular vascular diseases. The specific mechanisms underlying abnormal choroidal vascular reactivity in chronic smokers remain to be characterised.

Adult↗
PubMed1975

Segmental nature of the choroidal vasculature.

The various in vivo studies on posterior ciliary arteries and choroidal vasculature reported piecemeal by the author over the past few years have now been collated. A coherent picture of the vasculature emerges which is of considerable clinical significance. The observations show that the posterior ciliary arteries and their branches right down to the terminal choroidal arterioles, the choriocapillaris, and the vortex veins have a segmental distribution in the choroid, and that the posterior ciliary arteries and choroidal arteries function as end-arteries. No special mascular artery supplying the submacular choroid has been found. The posterior ciliary arteries have only supply the choroid but are also the main source of blood supply to the anterior part of the optic nerve, and have an important role in the blood supply of the retina. The clinical significance of this segmental distribution of the uveal vasculature is discussed.

Animals↗
PubMed2000

Clinicopathological correlation in exudative age related macular degeneration: histological differentiation between classic and occult choroidal neovascularisation.

AIMS: To analyse the histopathology of classic and occult choroidal neovascular membrane surgical specimens in age related macular degeneration. METHODS: 35 membranes, from a consecutive series of surgically removed choroidal neovascular membranes in age related macular degeneration, were classified as classic or occult following the guidelines of the Macular Photocoagulation Study. Membranes with classic as well as occult components were considered as mixed membranes. The membranes were serially sectioned and stained with haematoxylin and eosin, Masson trichrome, periodic acid-Schiff, and phosphotungstic acid haematoxylin stain. The correlation has been made in a masked fashion. RESULTS: 31 membranes (19 classic, 10 occult, and two mixed membranes) could be analysed histologically. 18 classic choroidal neovascular membranes had a major subretinal fibrovascular component and 10 of these had an additional, minor fibrovascular component under the retinal pigment epithelium. The 10 occult membranes contained a fibrovascular component under the retinal pigment epithelium and the two mixed membranes contained fibrovascular tissue on both sides of the retinal pigment epithelium. Fibrin and remains of outer segments tended to occur at the lateral edges of classic membranes and to cover the inner surface of occult membranes. CONCLUSION: Classic choroidal neovascularisation in age related macular degeneration is predominantly composed of subretinal fibrovascular tissue while occult choroidal neovascularisation is composed of fibrovascular tissue at the choroidal side of the retinal pigment epithelium.

Aged↗
PubMed2001

Preretinal neovascularisation associated with choroidal melanoma.

BACKGROUND: The rare occurrence of iris neovascularisation and choroidal (subretinal) neovascularisation in patients with choroidal melanoma has been reported. However, the occurrence of preretinal neovascularisation (NVE) fed from the retinal circulation in eyes with choroidal melanoma is far less frequently reported. METHODS: Three case reports of choroidal melanoma with the very rare finding of overlying NVE. RESULTS: The three patients had choroidal melanomas, localised serous retinal detachment, and NVE. Two cases showed definite retinal capillary non-perfusion, and one of these two cases demonstrated retinal telangiectasis. One patient's melanoma responded quickly to iodine-125 plaque radiotherapy; however, the retinal neovascularisation persisted and caused vitreous haemorrhage. Localised scatter photocoagulation was successful in causing the complete regression of the neovascularisation. The other two patients had their eyes enucleated (one with planned pre-enucleation external beam radiotherapy). Demonstration of preretinal vessels in one of the cases was possible in histological sections. CONCLUSION: Preretinal neovascularisation may occur as a complication of choroidal melanoma. Possible aetiologies include the release of tumour angiogenic factors, inflammation, chronic retinal detachment with secondary retinal ischaemia, retinal vascular occlusion secondary to retinal vessel invasion by the tumour, or following radiation therapy. Optimal management of the neovascularisation is not known at this time. Supplemental localised scatter photocoagulation may be of benefit in some cases.

Adult↗
PubMed2003

Choroidal vascular remodelling in central serous chorioretinopathy after indocyanine green guided photodynamic therapy with verteporfin: a novel treatment at the primary disease level.

AIMS: To evaluate the changes in the choroidal vasculature in central serous chorioretinopathy (CSC) after photodynamic therapy (PDT) with verteporfin and to assess its potential role as a treatment option. METHODS: A prospective, non-comparative, interventional study was performed in eyes with persistent CSC or chronic CSC that had fluorescein leakage at the fovea. All eyes received one single session of PDT with verteporfin (6 mg/m2 body surface area) followed by application of 50 J/cm2 laser at 689 nm. The laser spot size was guided by findings in ICG-A. RESULTS: Six eyes from six patients with a mean follow up of 12.7 months were analysed. Narrowing of the original dilated choroidal vessels and decrease in extravascular leakage could be demonstrated in all (100%) PDT treated eyes. 3 months after PDT, the mean diameter of the dilated choroidal vessel reduced from 546 microm to 371 microm (p=0.028). Five (83%) patients had improvement in visual symptoms and best corrected visual acuity. Fluorescence leakage stopped at the 1 month follow up in five eyes (83%) and at 3 months in all six eyes (100%). One eye developed choroidal neovascularisation at 3 month follow up. There was no other serious ocular or systemic complication. CONCLUSIONS: PDT is successful in stopping the fluorescein leakage in all six patients without recurrence of CSC. The ICG-A findings of choroidal vascular remodelling and decreased choroidal permeability after PDT are encouraging. As the sample size is small and the mean follow up period is short, further trials of PDT with verteporfin for CSC are required to address the optimal parameters in ensuring longer term safety and efficacy outcome.

Adult↗
PubMed2003

The effects of dorzolamide on choroidal and retinal perfusion in non-exudative age related macular degeneration.

AIM: To comprehensively evaluate the effects of dorzolamide on the choroidal and retinal circulation in patients with age related macular degeneration (AMD). METHODS: In this randomised, double masked, parallel study, 36 non-exudative AMD patients were randomised in a 2 to 1 fashion to placebo versus topical dorzolamide and underwent assessment of their choroidal and retinal circulation. Scanning laser ophthalmoscope indocyanine green angiograms (ICGA) were analysed by a new area dilution analysis technique. Four areas in the perifoveal region and two areas in the temporal peripapillary region were evaluated by plotting intensity of fluorescence of each area over time. The means of the choroidal filling times and the heterogeneity of the filling times were assessed. Scanning laser ophthalmoscope fluorescein angiography (FA) was evaluated for retinal arteriovenous passage (AVP) times by plotting intensity of fluorescence of retinal vessels over time. Assessment was performed at baseline and at 4 months. RESULTS: Compared to placebo, AMD patients treated with dorzolamide showed a significantly increased rapidity of choroidal filling in the superior and inferior peripapillary regions (p=0.007, p=0.02, respectively). No significant difference in choroidal filling times was found in any of the perifoveal areas (p=0.9). Also, on FA assessment, treatment with dorzolamide showed no statistical differences in AVP times (p=0.19). CONCLUSIONS: Dorzolamide may increase peripapillary choroidal perfusion in non-exudative AMD patients. Further studies are merited.

Aged↗
PubMed1984

Choroidal detachment and ocular hypotony: CT evaluation.

The computed tomographic (CT) findings in 20 patients with hemorrhagic choroidal detachment, serous choroidal detachment, and/or ocular hypotony are described. Hemorrhagic choroidal detachment appeared as an area of high attenuation that was usually localized, uniformly hyperdense, and not position-dependent (i.e., there was no shift with changing patient position). Serous choroidal detachment appeared as a convex, thick line of increased density within the vitreous cavity. Inflammatory choroidal detachment produces a diffuse intrauveal and suprachoroidal accumulation of high-density, position-dependent fluid, and uveoscleral thickening and enhancement, which in cross section resembles a ring. On CT ocular hypotony produces a characteristic uveoscleral infolding. CT has proved valuable in localizing and differentiating serous or hemorrhagic choroidal detachment and uveoscleral infolding.

Adolescent↗
PubMed1988

Choroidal hematoma and effusion: evaluation with MR imaging.

To evaluate the usefulness of magnetic resonance (MR) imagining in the evaluation of choroidal pathologic conditions, the authors studied 15 patients with either choroidal hematoma or choroidal effusion with a 1.5-T MR imager. These two lesions were reliably distinguished from each other on the basis of MR findings. Choroidal hematomas appeared as lenticular-shaped masses in the wall of the eyeball, and signal intensity depended on the age of the hematoma. Choroidal effusions appeared as crescentic or ring-shaped areas of increased signal on both T1- and T2-weighted images in an anatomic distribution corresponding to the choroidal and suprachoroidal spaces.

Adult↗
PubMed2003

A SCL4A10 gene product maps selectively to the basolateral plasma membrane of choroid plexus epithelial cells.

The choroid plexus epithelium of the brain ventricular system produces the majority of the cerebrospinal fluid and thereby defines the ionic composition of the interstitial fluid in the brain. The transepithelial movement of Na+ and water in the choroid plexus depend on a yet-unidentified basolateral stilbene-sensitive Na+-HCO3- uptake protein. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed the expression in the choroid plexus of SLC4A10 mRNA, which encodes a stilbene-sensitive Na+-HCO3- transporter. Anti-COOH-terminal antibodies were developed to determine the specific expression and localization of this Na+-HCO3- transport protein. Immunoblotting demonstrated antibody binding to a 180-kDa protein band from mouse and rat brain preparations enriched with choroid plexus. The immunoreactive band migrated as a 140-kDa protein after N-deglycosylation, consistent with the predicted molecular size of the SLC4A10 gene product. Bright-field immunohistochemistry and immunoelectron microscopy demonstrated strong labeling confined to the basolateral plasma membrane domain of the choroid plexus epithelium. Furthermore, the stilbene-insensitive Na+-HCO3- cotransporter, NBCn1, was also localized to the basolateral plasma membrane domain of the choroid plexus epithelium. Hence, we propose that the SLC4A10 gene product and NBCn1 both function as basolateral HCO3- entry pathways and that the SLC4A10 gene product may be responsible for the stilbene-sensitive Na+-HCO3- uptake that is essential for cerebrospinal fluid production.

Animals↗
PubMed2005

Na+-dependent HCO3- uptake into the rat choroid plexus epithelium is partially DIDS sensitive.

Several studies suggest the involvement of Na+ and HCO3- transport in the formation of cerebrospinal fluid. Two Na+-dependent HCO3- transporters were recently localized to the epithelial cells of the rat choroid plexus (NBCn1 and NCBE), and the mRNA for a third protein was also detected (NBCe2) (Praetorius J, Nejsum LN, and Nielsen S. Am J Physiol Cell Physiol 286: C601-C610, 2004). Our goal was to immunolocalize the NBCe2 to the choroid plexus by immunohistochemistry and immunogold electronmicroscopy and to functionally characterize the bicarbonate transport in the isolated rat choroid plexus by measurements of intracellular pH (pHi) using a dual-excitation wavelength pH-sensitive dye (BCECF). Both antisera derived from COOH-terminal and NH2-terminal NBCe2 peptides localized NBCe2 to the brush-border membrane domain of choroid plexus epithelial cells. Steady-state pHi in choroidal cells increased from 7.03 +/- 0.02 to 7.38 +/- 0.02 (n=41) after addition of CO2/HCO3- into the bath solution. This increase was Na+ dependent and inhibited by the Cl- and HCO3- transport inhibitor DIDS (200 muM). This suggests the presence of Na+-dependent, partially DIDS-sensitive HCO3- uptake. The pHi recovery after acid loading revealed an initial Na+ and HCO3- -dependent net base flux of 0.828 +/- 0.116 mM/s (n = 8). The initial flux in the presence of CO2/HCO3- was unaffected by DIDS. Our data support the existence of both DIDS-sensitive and -insensitive Na+- and HCO3- -dependent base loader uptake into the rat choroid plexus epithelial cells. This is consistent with the localization of the three base transporters NBCn1, Na+-driven Cl- bicarbonate exchanger, and NBCe2 in this tissue.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1989

Effect of leukotriene D4 on blood flow to cerebrum and choroid plexus.

The purpose of this study was to examine effects of leukotriene D4 on blood flow to the cerebrum and choroid plexus. Blood flow was measured with microspheres in anesthetized rabbits. Under control conditions, blood flow to the cerebrum was 37 +/- 4 ml. min-1.100 g-1 (mean +/- SE) and blood flow to the choroid plexus was 428 +/- 52 ml.min-1.100 g-1. Intra-atrial infusion of leukotriene D4 at 0.1 and 1.0 microgram.kg-1.min-1 did not alter blood flow to the brain or choroid plexus, but produced a 49 +/- 3% and 69 +/- 5% decrease in blood flow to the bowel. We also examined effects of intracerebroventricular administration of leukotriene D4. Intraventricular injection of 1.0 microgram of leukotriene D4 did not affect blood flow to the cerebrum or choroid plexus. In contrast, intraventricular injection of 1.0 microgram of angiotensin II produced a 42 +/- 4% decrease in blood flow to the choroid plexus. In summary, neither intravascular nor intraventricular administration of leukotriene D4 affects blood flow to the brain or choroid plexus.

Angiotensin II↗
PubMed1991

Stimulation of area postrema decreases blood flow to choroid plexus.

The goal of this study was to examine effects of stimulation of the area postrema on blood flow to choroid plexus and brain. In chloralose-anesthetized dogs, the area postrema was stimulated electrically, and arterial pressure and blood gases were maintained at control levels. We measured blood flow to brain and choroid plexus of the fourth and lateral ventricles with microspheres. Stimulation of the area postrema at 10 +/- 2 microA (means +/- SE), which was the threshold for changes in arterial pressure and heart rate, decreased blood flow to choroid plexus of the fourth and lateral ventricles by 41 +/- 11 and 51 +/- 6%, respectively (from 349 +/- 38 and 503 +/- 46 ml.min-1.100 g-1, respectively). Stimulation at high amplitudes (67 +/- 5 microA) produced only slightly greater decreases in blood flow to choroid plexus. In contrast, cerebral blood flow did not change during stimulation of the area postrema. After blockade of autonomic ganglia with intravenous chlorisondamine, stimulation of the area postrema had minimal effects on blood flow to choroid plexus. The results indicate that stimulation of the area postrema decreases blood flow to choroid plexus, probably by an autonomic mechanism. We speculate that the area postrema may play a role in regulation of volume in the central nervous system by modulating production of cerebrospinal fluid.

Animals↗
PubMed2005

Effect of histamine and cimetidine on retinal and choroidal blood flow in humans.

Intravenous administration of histamine causes an increase in choroidal blood flow and retinal vessel diameter in healthy subjects. The mechanism underlying this effect remains to be elucidated. In the present study, we hypothesized that H2 receptor blockade alters hemodynamic effects of histamine in the choroid and retina. Eighteen healthy male nonsmoking volunteers were included in this randomized, double-masked, placebo-controlled two-way crossover study. Histamine (0.32 microg.kg(-1).min(-1) over 30 min) was infused intravenously in the absence (NaCl as placebo) or presence of the H2 blocker cimetidine (2.3 mg/min over 50 min). Ocular hemodynamic parameters, blood pressure, and intraocular pressure were measured before drug administration, after infusion of cimetidine or placebo, and after coinfusion of histamine. Subfoveal choroidal blood flow and fundus pulsation amplitude were measured with laser-Doppler flowmetry and laser interferometry, respectively. Retinal arterial and venous diameters were measured with a retinal vessel analyzer. Retinal blood velocity was assessed with bidirectional laser-Doppler velocimetry. Histamine increased subfoveal choroidal blood flow (+14 +/- 15%, P < 0.001), fundus pulsation amplitude (+11 +/- 5%, P < 0.001), retinal venous diameter (+3.0 +/- 3.6%, P = 0.002), and retinal arterial diameter (+2.8 +/- 4.2%, P < 0.01) but did not change retinal blood velocity. The H2 antagonist cimetidine had no significant effect on ocular hemodynamic parameters. In addition, cimetidine did not modify effects of histamine on choroidal blood flow, fundus pulsation amplitude, retinal venous diameter, and retinal arterial diameter compared with placebo. The present data confirm that histamine increases choroidal blood flow and retinal vessel diameters in healthy subjects. This ocular vasodilator effect of histamine is, however, not altered by administration of an H2 blocker. Whether the increase in blood flow is mediated via H1 receptors or other hitherto unidentified mechanisms remains to be elucidated.

Adult↗
PubMed1990

Thyroxine transport from blood to brain via transthyretin synthesis in choroid plexus.

The transport of thyroxine from the bloodstream to the brain and the synthesis and secretion of transthyretin (formerly called prealbumin) were studied in rats and in sheep choroid plexus perfused in vitro. Rat choroid plexus contained 4.4 micrograms and rat liver 0.39 micrograms transthyretin mRNA per gram wet tissue. The specific radioactivity of transthyretin isolated from cerebrospinal fluid of rats 60 min after intravenous injection of [14C]leucine was greater than 50 times that of transthyretin from serum. After adding [14C]leucine to the perfusion medium of an in vitro perfused sheep choroid plexus, highly radioactive transthyretin was isolated from freshly secreted cerebrospinal fluid collected from the exposed choroid plexus surface. Secretion of newly synthesized transthyretin into the perfusion medium could not be demonstrated. After intravenous injection of [125I]-thyroxine into rats, a maximum in the curve of radioactivity in tissue plotted against time after injection was observed first for choroid plexus, thereafter for cerebrospinal fluid, and still later for cortex and striatum. Based on the obtained data, a hypothesis is derived for the mechanism of the transport of thyroid hormones from the bloodstream to the brain involving transthyretin synthesized in choroid plexus and secreted into the cerebrospinal fluid.

Animals↗
PubMed1992

Strong conservation of the expression of cystatin C gene in choroid plexus.

The expression of the cystatin C gene was studied by Northern analysis of RNA isolated from the choroid plexus, other brain tissues, and liver from 11 mammalian and 4 avian species. The probe used for hybridization was cystatin C cDNA isolated previously from a rat choroid plexus cDNA library. Strong conservation of the expression of the cystatin C gene in choroid plexus was suggested by the observation of substantial levels of cystatin C mRNA in choroid plexus RNA from all mammalian and avian species studied. In contrast, levels of cystatin C mRNA in total liver RNA varied widely for mammalian as well as for avian species. It was concluded that the synthesis of cystatin C in choroid plexus has probably been conserved since the stage of the stem reptiles, the common ancestors of mammals and birds. The cystatin C gene was also found to be expressed early in ontogeny, as indicated by the observation of similar cystatin C mRNA levels in choroid plexus RNA from newly hatched and adult chickens.

Animals↗
PubMed2000

Regional regulation of choroidal blood flow by autonomic innervation in the rat.

Regional influences of parasympathetic and sympathetic innervation on choroidal blood flow were investigated in anesthetized rats. Parasympathetic pterygopalatine neurons were activated by electrically stimulating the superior salivatory nucleus, whereas sympathetic neurons were activated by cervical sympathetic trunk stimulation and uveal blood flow was measured by laser Doppler flowmetry. Parasympathetic stimulation increased flux in the anterior choroid and nasal vortex veins but not in the posterior choroid. Vasodilation was blocked completely by the neuronal nitric oxide synthase inhibitor 1-(2-trifluoromethylphenyl)imidazole but was unaffected by atropine. Sympathetic stimulation decreased flux in all regions, and this was blocked by prazosin. Parasympathetic stimulation did not affect vasoconstrictor responses to sympathetic stimulation in the posterior choroid but attenuated the decrease in blood flow through the anterior choroid and vortex veins via a nitrergic mechanism. We conclude that sympathetic alpha-noradrenergic vasoconstriction occurs throughout the choroid, whereas parasympathetic nitrergic vasodilation plays a selective role in modulating blood flow in anterior tissues of the eye.

Adrenergic alpha-Antagonists↗