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Biomedical subjects

M F Marmor

Publications and source records attributed to M F Marmor.

At least 73 records · Page 4Linked to original sources
PubMed1992

Lowering the calcium concentration in the subretinal space in vivo loosens retinal adhesion.

Retinal adhesiveness in vitro is reduced by lowering the external calcium (Ca2+) concentration. The effects of lowering subretinal Ca2+ concentration in living rabbit eyes was investigated by making experimental retinal detachments (blebs) filled with Ca(2+)-free disodium edetate solution. Unlike blebs made with Hanks' solution, these low-Ca2+ blebs enlarged progressively after they were formed, and they were surrounded by a wide whitish halo. This halo region had weak adhesion (shown by the rapid spread of fluorescein solution into the halo and by the measurement of local adhesiveness after enucleation). The retinal pigment epithelial microvilli in the halo appeared stretched toward the center of the blebs as if there had been retinal traction or movement. Measurements of retinal adhesiveness in vivo showed it to be decreased to about 30% of normal by use of this solution.

Adhesiveness↗
PubMed1991

Systemic mannitol increases retinal adhesiveness measured in vitro.

Pigmented rabbits were given mannitol intravenously, and at various times thereafter blood osmolality was measured and eyes were enucleated to measure retinal adhesiveness to the retinal pigment epithelium. Both blood osmolality and retinal adhesion increased in proportion to the dose of mannitol. We found a measurable increase in retinal adhesion as early as 10 minutes and as late as 4 hours after mannitol injection. We suspect that mannitol dehydrates the subretinal space and thereby enhances the adhesive properties of the interphotoreceptor matrix or tightens the interdigitation between photoreceptors and pigment epithelial cells. Our data suggest that mannitol could have clinical application in the management of retinal detachments.

Animals↗
PubMed1991

Systemic mannitol increases the retinal adhesive force in vivo.

The effect of systemic mannitol administration on retinal adhesive force in the rabbit was investigated in vivo. The retinal adhesive force, 1 hour after intravenous mannitol injection (2.5 g/kg), was 45% greater than that in control eyes. When adhesiveness had been weakened by injecting Ca(2+)-free edetic acid (EDTA) solution into the subretinal space, intravenous mannitol still enhanced adhesion. Mannitol administration seems to be effective in enhancing retinal adhesion, even under the conditions where it has been weakened by other mechanisms.

Adhesiveness↗
PubMed1991

Clinical electrophysiology of the retinal pigment epithelium.

There is no ideal electrophysiological test for retinal pigment epithelial (RPE) function. The light-induced responses (EOG, c-wave, fast oscillation) that require photoreception are not pure RPE signals, and even the widely-used EOG has not been associated with any specific physiological disturbance of the RPE or retina. The discovery of non-photic RPE responses (hyperosmolarity, acetazolamide and bicarbonate) has enhanced the possibility of finding tissue-specific RPE tests, but these responses have yet to be correlated with specific RPE functional activity or pathology. We may face a dilemma in our search for RPE tests, insofar as electrophysiology measures membrane changes, but RPE membrane activity is related only indirectly to many functions of the RPE cell. These concerns notwithstanding, RPE electrophysiology can be a valuable clinical tool if one accounts for the physiological limitations and assets of the procedures.

Electrooculography↗
PubMed1991

Combined photic and nonphotic electro-oculographic responses in the clinical evaluation of the retinal pigment epithelium.

In an attempt to simplify the recording technique in electrophysiologic evaluation of the retinal pigment epithelium, we combined the electro-oculographic light rise, hyperosmolarity and acetazolamide responses in a single recording session. Recordings were performed in six normal subjects and in seven patients with diabetic retinopathy or retinitis pigmentosa. In the patients with background diabetic retinopathy, the hyperosmolarity responses were slightly reduced, while the acetazolamide response and the light rise was normal. In the patients with proliferative diabetic retinopathy, the hyperosmolarity response and light rise were remarkably reduced, while the acetazolamide response was normal. In the patients with retinitis pigmentosa, the hyperosmolarity response and light rise were decreased, while the acetazolamide response was normal. Despite a small study population, we concluded that the clinical results from our combined recording protocol were essentially the same as those reported for each response separately. Because this recording technique simplifies electrophysiologic evaluation of the retinal pigment epithelium, it may help clarify the mechanisms or localization of retinochoroidal and pigment epithelial diseases.

Adolescent↗
PubMed1991

Experimental studies on the accumulation of subretinal fluid.

In an attempt to develop a rabbit model for serous detachment, we damaged the pigment epithelium with low-intensity laser burns, lowered intraocular pressure and administered dibutyryl adenosine 3',5'-cyclic phosphate (cAMP), to inhibit pigment epithelial water transport. We produced only small areas of edema or very low detachment that persisted for a few days at best. These experiments suggest that it is remarkably difficult to make fluid stay in the subretinal space, and more stringent conditions will be needed to mimic the size and persistence of clinical serous detachments.

Animals↗
PubMed1991

Recovery of retinal pigment epithelial function after ischemia in the rabbit.

Survival of the rabbit retinal pigment epithelium (RPE) after ischemia was studied. The ischemia was induced by elevating intraocular pressure; retinal and RPE function were monitored by electrophysiologic recordings. The b-wave recovered to control amplitude in 1-4 hr after 30-60 min of ischemia, but it never recovered more than about 50% amplitude after 90 min of ischemia. The c-wave recovered after 30 min of ischemia but was replaced by a negative response after 60-90 min of ischemia. The RPE hyperosmolarity response was normal after 60 min of ischemia, but it was severely depressed after 90 min of ischemia. The RPE response to acetazolamide (cornea positive in the rabbit) was lost after both 60 and 90 min of ischemia. These results suggest that different components of RPE function have different tolerances to ischemia and is consistent with evidence that the RPE electrophysiologic responses differ in mechanism and response to disease.

Acetazolamide↗
PubMed1990

Diagnostic clinical findings of a new syndrome with night blindness, maculopathy, and enhanced S cone sensitivity.

We studied eight patients who had night blindness, maculopathy (often cystoid), degenerative changes in the region of the vascular arcades, relatively mild visual field loss, and an unusual but characteristic electroretinogram. The dark-adapted electroretinogram showed no response to low-intensity stimuli that normally activate the rods, but large, slow responses to high-intensity stimuli. These large, slow waveforms persisted without change under light adaptation, and showed a striking mismatch to photopically balanced short and long wavelength stimuli (with sensitivity much greater to short than long wave-lengths). Since there is evidence from other studies that the electroretinogram and psychophysical responses represent hypersensitivity of short wavelength-sensitive (S or blue) cones, we propose that this disorder be called the enhanced S cone syndrome. There can be different degrees of severity in this syndrome, and progression appears to be slow.

Adolescent↗
PubMed1990

L-cystein protects the pigment epithelium from acute sodium iodate toxicity.

Intravenous sodium iodate damages the retinal pigment epithelium, causing immediate loss of the electroretinogram c-wave and eventual pigmentary retinopathy. L-cystein, an agent that enhances the c-wave, has been reported to prevent the late development of pigmentary degeneration. We found in rabbits that L-cystein given 30 min before, or simultaneously with (but not 30 min after) sodium iodate also blocks the loss of the c-wave. This result occurred at doses of L-cystein lower than those needed to produce enhancement of the c-wave, suggesting that these two actions of L-cystein may be independent. The iodate-blocking action of L-cystein may depend on chemical interaction.

Animals↗
PubMed1990

Long-term follow-up of the physiologic abnormalities and fundus changes in fundus albipunctatus.

Fundus albipunctatus (FA) is considered to be a congenital stationary night-blinding disorder, but there has been no electrophysiologic or photographic documentation of long stability or change. This documentation is presented for two cases followed for 13 to 14 years. The physiologic (functional) deficits appeared to be stable, in support of the concept that FA is not a progressive dystrophy. However, the fundus lesions evolved in appearance from flecks in childhood to relatively permanent punctate dots that increase in number over the years.

Adult↗
PubMed1990

Control of subretinal fluid: experimental and clinical studies.

Experimental work shows that subretinal fluid is removed both by active transport across the retinal pigment epithelium (RPE) and by passive hydrostatic and oncotic forces that work most effectively when the RPE barrier has been damaged. The retina will stay attached whether or not the RPE is intact--but retinal function requires the RPE barrier and thus active transport is the primary mechanism of subretinal fluid control. RPE fluid transport is normally limited by the retina (which resists water flow from the vitreous) but can be quite powerful when a reservoir of subretinal fluid is present. Clinical serous detachments are unlikely to form solely as a result of small RPE defects or leaks, since the active and passive transport systems for removing subretinal fluid are both so strong. It is suggested that the primary pathology in most serous retinopathy is a diffuse metabolic or vascular abnormality of RPE fluid transport, and that RPE defects or leaks are necessary but only secondary components of the disease. Several hypotheses for removing subretinal fluid therapeutically are considered in terms of their physiology. The subretinal space between the photoreceptors and the retinal pigment epithelium (RPE) is the remnant of the embryonic optic vesicle. In the developed eye the subretinal space is of minimal size, but no tissue junctions form across it and it can re-open under pathological conditions of retinal detachment. In a sense, the title of this paper is misleading since normally there should be no subretinal fluid to control. However, ocular mechanisms are necessary to prevent an accumulation of fluid, and to remove it under conditions of stress or disease.

Animals↗
PubMed1990

Is thioridazine retinopathy progressive? Relationship of pigmentary changes to visual function.

Thioridazine toxicity has been described as a 'progressive chorioretinopathy', but this designation can be misleading. During the first year after thioridazine exposure retinal pigmentation evolves from a granular to a patchy or nummular appearance. However, visual function and the electroretinogram typically improve during this period. Some cases may show chorioretinal atrophy and functional loss many years later, but there is little evidence for ongoing drug-related progression. Late atrophy may represent degeneration of cells that were injured subclinically at the time of initial drug exposure. Although thioridazine toxicity produces an evolving pigmentary disturbance, functional changes must be monitored independently of fundus appearance.

Atrophy↗
PubMed1990

Retinal adhesiveness is weakened by enzymatic modification of the interphotoreceptor matrix in vivo.

The role of interphotoreceptor matrix (IPM) constituents in mediating adhesion between the retina and retinal pigment epithelium (RPE) was investigated by injecting specific enzymes into rabbit eyes either intravitreally or subretinally. Retinal adhesiveness was measured by peeling the retina from the pigment epithelium 1-3 days later and observing the amount of adherent pigment. Effects of enzymes on the IPM were monitored by observation of peanut agglutinin (PNA) binding to cone matrix sheaths; retinal and RPE toxicity was excluded by electroretinography and histology. Three enzymes that degrade glycosaminoglycans or saccharides known to be constituents of the IPM (chondroitinase ABC, neuraminidase, and testicular hyaluronidase) both weakened adhesion and altered PNA binding, although the effects on the cone matrix sheaths were different for each enzyme. An enzyme specific for hyaluronic acid (Streptomyces-derived hyaluronidase), which has not been identified as a major IPM constituent, had no effect on either adhesion or PNA binding. The authors conclude that IPM-associated glycoconjugates participate in retinal adhesion, although their precise composition, interaction with IPM components, and relationship to other mechanisms of adhesion remain to be determined.

Adhesiveness↗
PubMed1990

Blindness following blepharoplasty: two case reports, and a discussion of management.

We present two cases of unilateral permanent visual loss following four-eyelid blepharoplasty. Clinical and radiographic evidence suggested orbital hemorrhage was the cause of visual loss in both cases. In particular, electrophysiologic tests indicated that optic nerve dysfunction, and not retinal ischemia, was responsible for loss of vision. Timely orbital decompression is the cornerstone of managing these dramatic cases.

Blindness↗
PubMed1990

SWS (blue) cone hypersensitivity in a newly identified retinal degeneration.

Photoreceptor-mediated mechanisms were studied in patients with a recently identified retinopathy typified by night blindness, cystoid maculopathy, and similar scotopic and photopic electroretinograms (ERGs). Dark-adapted spectral sensitivity functions were only partly explained as composites of rod and cone curves shifted to lower sensitivities; there was unusually high sensitivity from 400-460 nm. A rod mechanism, reduced in sensitivity by at least 3 log units, was detectable with dark adaptometry. No measurable rhodopsin was found with fundus reflectometry. Light-adapted spectral sensitivities were subnormal for wavelengths greater than 500 nm but supernormal from 420-460 nm. On a yellow adapting field, the supernormal spectrum approximated that of the short-wavelength-sensitive (SWS) cone system. With spectral ERGs, two mechanisms were demonstrated. Dark- and light-adapted ERGs to green, orange-yellow, and red stimuli had similar waveforms and coincident intensity-response functions on a photopic intensity axis. ERGs to blue and blue-green stimuli were similar, and intensity-response functions coincided on a SWS cone intensity axis. Patients varied in the degree to which rod and midspectral cone function were decreased and SWS cone function was increased.

Adolescent↗
PubMed1990

Dark adaptation in locally detached retina.

Nonrhegmatogenous retinal detachments were formed in the eyes of Dutch rabbits by subretinal injection of Hanks' balanced salt solution. The electroretinogram (ERG) was recorded locally from the acutely detached retina, and simultaneously from the surrounding attached retina (vitreal ERG [VERG]), before and after exposure to diffuse intense irradiation. Light adaptation elevated b-wave threshold for both the local ERG (LERG) and VERG by about 3 log units; thresholds for both responses recovered fully within 60-90 min after the irradiation. The normal time course of dark adaptation of the LERG suggests the occurrence of substantial rhodopsin regeneration in the rod photoreceptors of nonrhegmatogenously detached retina. These results differ from reports that visual pigment regeneration is slow in central serous chorioretinopathy, possibly because our detachments were studied within hours of formation, whereas some photoreceptor degeneration may be present in older clinical detachments.

Animals↗