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Biomedical subjects

M F Marmor

Publications and source records attributed to M F Marmor.

At least 55 records · Page 3Linked to original sources
PubMed1994

Retinal adhesiveness in the monkey.

PURPOSE: To determine factors that influence retinal adhesion in the primate and compare these with previous data from the rabbit. METHODS: Retinal adhesiveness was studied in monkey eyes immediately after enucleation. The retina was peeled manually from the retinal pigment epithelium, and the amount of pigment that remained adherent to the retina was used as an index of adhesiveness. RESULTS: The rate of post mortem failure of retinal adhesiveness in the monkey was less than in the rabbit under similar conditions. However, as in the rabbit, adhesiveness was sensitive to temperature, pH, and the concentrations of calcium and magnesium, and subretinal injections of neuraminidase weakened adhesion beyond the injection sites. CONCLUSIONS: Mechanisms of retinal adhesion are similar in primates and rabbits.

Adhesiveness↗
PubMed1993

Mannitol, dextromethorphan, and catalase minimize ischemic damage to retinal pigment epithelium and retina.

We studied the recovery of retinal pigment epithelium and retinal function after 80 minutes of pressure-induced ischemia in rabbits. Just before restoring circulation, we gave intravenous mannitol (an osmotic agent and free-radical scavenger), dextromethorphan (an N-methyl-D-aspartate receptor antagonist), or catalase (an antioxidant enzyme). Mannitol has not previously been shown to be protective for retinal or retinal pigment epithelial ischemia. At 24 hours after reperfusion, the electroretinogram b-wave was reduced to 37% of preischemic amplitude in untreated eyes, but it recovered to 67% to 80% after treatment with all three agents. The c-wave was replaced by a negative slow PIII response in control eyes and in seven of 12 catalase-treated eyes, but it recovered by 58% to 82% in the remaining catalase-treated eyes and all the mannitol- and dextromethorphan-treated eyes. Histologic examination confirmed that retinal pigment epithelium as well as retina had been damaged by the ischemia. The effects of mannitol seem of special interest, since the drug has a dual mechanism of action and is clinically available.

Animals↗
PubMed1993

Standard for clinical electro-oculography. International Society for Clinical Electrophysiology of Vision.

The electro-oculogram is a widely used electrophysiological test, but recording techniques vary among different laboratories. This standard, approved by the International Society for Clinical Electrophysiology of Vision (ISCEV), describes simple technical procedures that will allow reproducible and comparable electro-oculograms to be recorded under a few defined conditions. The document is intended to improve the comparability of electro-oculographic data obtained throughout the world by guiding both clinicians and manufacturers, and the ISCEV recommends that future published reports indicate whether the recording technique meets the international standard.

Austria↗
PubMed1993

Negative-type electroretinogram from cisplatin toxicity.

A 68-year-old woman with ovarian cancer suffered a loss of visual acuity and color perception after inadvertent overdosage with the antineoplastic agent cisplatin. Her acuity returned to normal but a tritan color defect persisted more than a year later. Her electroretinogram was stable between 7 weeks and 15 months after cisplatin administration, with a negative-type scotopic response, but also reduced cone b waves and a loss of some scotopic oscillatory potentials. With light stimuli between 10 and 100 ms in duration, the photopic on-responses were markedly reduced while the off-responses were normal or close to it. This case suggests that cisplatin may selectively injure on-pathways in the retina and indicates the need to expand the list of disorders that may cause a negative-type electroretinogram.

Aged↗
PubMed1993

Effects of hemicholinium-3, a photoreceptor and pigment epithelial toxin, on retinal adhesiveness and subretinal fluid absorption.

Retinal adhesiveness and subretinal fluid absorption was studied in Dutch rabbit eyes given intravitreal injections of hemicholinium-3 (HC-3) which causes loss of photoreceptor outer segments and retinal pigment epithelial (RPE) damage. After HC-3 administration, some areas of the fundus showed pigmentary changes and others appeared normal. Small, non-rhegmatogenous retinal detachments were made in both areas. Within 2-5 days after HC-3 injection, only in the areas of visible damage, subretinal fluid spread laterally to make very flat retinal detachments, and the fluid absorbed very quickly. At later intervals, absorption was slower than normal, presumably because of scarring and RPE metabolic damage. HC-3 provides an experimental technique for transiently weakening retinal adhesiveness in vivo but its use as a model must account for the effects of both outer segment and RPE damage.

Animals↗
PubMed1993

Standard for clinical electro-oculography. International Society for Clinical Electrophysiology of Vision.

The electro-oculogram is a widely used electrophysiologic test, but recording techniques vary among different laboratories. This Standard, approved by the International Society for Clinical Electrophysiology of Vision (ISCEV), describes simple technical procedures that will allow reproducible and comparable electro-oculograms to be recorded under a few defined conditions. The document is intended to improve the comparability of electro-oculogram data obtained throughout the world by guiding both clinicians and manufacturers, and ISCEV recommends that future published reports indicate whether the recording technique meets the international Standard.

Calibration↗
PubMed1993

Retinal pigment epithelium adhesion to Bruch's membrane is weakened by hemicholinium-3 and sodium iodate.

We have studied the effects of hemicholinium-3 (HC-3), an outer segment and retinal pigment epithelium (RPE) toxin and sodium iodate, an RPE toxin, on retinal and RPE adhesion in rabbits. During the first 3 days after intravitreal HC-3, the force required to peel retina from RPE fell to 50% of normal, and large patches of RPE separated from Bruch's membrane and adhered to the peeled retina. The same phenomena were observed during the first 100 min after intravenous sodium iodate. Beyond 3 days after HC-3, and 100 min after sodium iodate, the peeling force became even weaker, but separation occurred at the subretinal space or by fragmentation of RPE cells. Acute RPE toxicity probably accounts for the initial weakening of the bond between RPE and Bruch's membrane.

Animals↗
PubMed1993

Irregular retinal and RPE damage after pressure-induced ischemia in the rabbit.

PURPOSE: Pressure-induced ocular ischemia is a frequent model for the investigation of the mechanisms and therapy of retinal ischemic damage. It is important to know whether the tissue damage in such experiments is uniform or irregular. METHODS: We reviewed histologic features of Dutch rabbit eyes after 60-80 min of pressure-induced ischemia. The eyes were enucleated 4 hr, 1 day, or 1 wk after circulation was restored, at which times the electroretinogram b-wave was moderately reduced. RESULTS: Light microscopy showed an irregular distribution of damage involving all retinal layers and retinal pigment epithelium. Some regions of damage (or preservation) were several millimeters wide; others were as small as a few cell widths. Correlation with electroretinogram reduction in individual eyes was difficult. CONCLUSIONS: These results show that pressure-induced ischemic damage in the rabbit, sufficient to reduce the electroretinogram, has a patchy and irregular effect on retina and retinal pigment epithelium. Erroneous judgments may be made about ischemic damage, or therapeutic intervention, if only small or selected regions of retina are examined histologically.

Animals↗
PubMed1993

Protection of rabbit retina from ischemic injury by superoxide dismutase and catalase.

PURPOSE: To provide evidence that free radical damage is a component of postischemic retinal injury; to determine whether antioxidant enzymes, superoxide dismutase (SOD) and catalase, can protect the retina from ischemic injury. METHODS: Total retinal ischemia for 60 or 75 min was produced in Dutch rabbits by raising intraocular pressure. Retinal recovery was monitored with the electroretinogram. Enzymes were administered as an intravenous bolus dose 2-3 min before restoration of circulation. RESULTS: In eyes subjected to 60 min ischemia, the amplitude of the a-wave 4 hours after reperfusion averaged 114.9% of baseline value in control rabbits and 126.5% in SOD-treated animals. The b-wave amplitude at this time was 79.3% and 106.8% in control rabbits and SOD-treated rabbits, respectively. After an ischemic insult of 75 min, at 4 hours the a-wave amplitude was 89.2% of baseline in control eyes, 108.8% in SOD-treated eyes, 159.6% in eyes that received a combination of SOD and catalase, and 149.8% in catalase-treated eyes. The amplitude of the b-wave was reduced to 47.8% in control eyes and 44.8% in SOD-treated eyes, but recovered to 92.3% in rabbits that received the combination therapy and 98.8% in animals that received catalase alone. CONCLUSIONS: These findings suggest that free radical generation is involved in ischemic tissue damage. The fact that antioxidant enzymes can be protective has implications for the treatment of acute ischemic diseases of the retina.

Animals↗
PubMed1993

Oxygen dependency of retinal adhesion.

PURPOSE: Normal retina is firmly attached to the retinal pigment epithelium, but the force of this adhesion drops precipitously within the first 2-3 min after enucleation. The purpose was to study metabolic factors that might be relevant to this postmortem failure of adhesion. METHODS: Dutch rabbit retina was manually peeled from the retinal pigment epithelium on strips of enucleated eyecup within a 37 degrees C bath. Retinal adhesiveness was measured by observing the amount of retinal pigment epithelium that remained adherent to the retina. RESULTS: Autologous whole blood in place of salt solution retarded the decrease in adhesiveness. A solution of hemoglobin alone was similarly effective, whereas methemoglobin solution failed to help the persistence of retinal adhesion. Bubbling oxygen into the salt solution and circulating it to avoid oxygen depletion at the tissue boundary also proved effective at sustaining retinal adhesiveness. Eyes made ischemic in vivo for 5 min or longer, by elevating intraocular pressure, showed virtually no retinal adhesion when enucleated immediately thereafter. However, eyes made ischemic for 10 min, but allowed to regain circulation for 5 min before enucleation, showed a return of retinal adhesiveness to 80% of normal. CONCLUSIONS: Oxidative metabolism is critical to the maintenance of retinal adhesiveness, and the effects of oxygen deprivation on adhesion are reversible within a certain time period.

Adhesiveness↗
PubMed1992

Induction of serous retinal detachment in rabbit eyes by pigment epithelial and choriocapillary injury.

Serous retinal detachments have been produced experimentally by occluding the choroidal circulation. We sought a more realistic model by adjusting rose bengal photosensitization to injure the retinal pigment epithelium and choriocapillaris in rabbits without causing vascular occlusion. We accomplished this by either using low doses of rose bengal or cooling the animal to reduce ocular temperature by 4 degrees C. Detachments typically appeared within 1 day after light exposure, centered over the area of light damage. Fluorescein angiography showed no capillary occlusion, but there was leakage of dye from areas of light damage. Light microscopy of light-damaged areas showed swelling or disruption of retinal pigment epithelial cells but a patent choriocapillaris. These data suggest that a combination of retinal pigment epithelial and choriocapillary damage may be necessary for serous detachment to occur.

Animals↗
PubMed1992

Studies on the stability of the clinical electro-oculogram.

The electro-oculogram is variable as a clinical test, but the recording technique has not been standardized, and differences in the protocols for adaptation and stimulation among laboratories may contribute to the variability. To analyze some of these factors, we performed more than 100 electro-oculograms on a single subject under different conditions. Both the Arden ratio and the ratio of light peak amplitude to a stable dark-adapted baseline were independent of pupillary dilation but linearly related to retinal illumination measured in trolands. Between 3.0 and 4.0 log trolands, the values began to level off, but they were difficult to interpret because of subject discomfort above 3.5 log trolands. The Arden ratios were influenced by preadaptation light levels and were roughly 20% higher above 90 cd/m2 than below 45 cd/m2. There was a circadian rhythm in dark trough, baseline and light peak values, but the composite Arden ratio and light peak/baseline ratio showed little circadian effect. The light peak/baseline ratios were slightly more stable than the Arden ratios; the variability (defined as [standard deviation x 100]/mean) was 6.6% and 12.5%, respectively. Our results suggest that stimulus intensities for clinical electro-oculographic testing should be between 3.0 and 3.5 log trolands; pupil dilation is optional. This translates into light levels of 141-447 cd/m2 for a 3-mm pupil and 20-63 cd/m2 for an 8-mm pupil. The reduction in variability and independence from preadaptation achieved by using the light peak/baseline ratio instead of the Arden ratio must be weighed against the time required to achieve a stable dark baseline.

Adult↗
PubMed1992

Recovery of retinal adhesion after enzymatic perturbation of the interphotoreceptor matrix.

Previous investigations established that focal subretinal injections of neuraminidase, chondroitinase, and hyaluronidase in the rabbit lead to a diffuse loss of retinal adhesiveness beyond the site of injection. This loss of adhesiveness, measured by peeling of the retina immediately after enucleation, correlates with changes in the interphotoreceptor matrix (IPM), as monitored by lectin histochemistry. In this study, rabbits were evaluated during recovery of retinal adhesiveness after subretinal injections of neuraminidase and chondroitinase. Adhesion recovered steadily 5-20 days after chondroitinase injection. After administration of neuraminidase, adhesion remained low for approximately 14 days but recovered to normal by 20 days. The recovery of adhesiveness correlated closely with reestablishment of the normal distribution of peanut agglutinin-binding glycoconjugates in the IPM, one group of molecules thought to participate in retinal adhesion. Electroretinography and light microscopy showed no abnormalities in the retina or retinal pigment epithelium after recovery. These results suggest that IPM glycoconjugates participate in maintaining retinal adhesion.

Animals↗
PubMed1992

Retinal adhesive force in living rabbit, cat, and monkey eyes. Normative data and enhancement by mannitol and acetazolamide.

Small retinal detachments (blebs) were made in living eyes by injecting balanced salt solution into the subretinal space with a micropipette. A second micropipette, inserted into the same bleb, measured subretinal pressure using a resistance servonulling system. The adhesive force was calculated from the pressure difference across the retina according to Laplace's law. The retinal adhesive force in rabbit, cat, and monkey eyes averaged 1.0, 1.8, and 1.4 x 10(2) dyne/cm, respectively. In rabbit eyes, 2 hr after intravenous administration of 15 mg/kg acetazolamide, the retinal adhesive force was increased to 133%. In monkeys, this dose of acetazolamide increased retinal adhesion to 144% of control values. Mannitol (2 g/kg) increased retinal adhesion in the monkey to 153% of control values 90 min after intravenous injection (compared with an increase of 145% in previous experiments in the rabbit). Because both mannitol and acetazolamide enhance retinal adhesiveness in living primate eyes, it seems likely that they will have a similar effect in humans that they may be clinically useful.

Acetazolamide↗
PubMed1992

Effects on retinal adhesive force in vivo of metabolically active agents in the subretinal space.

The in vivo effects on the retinal adhesive force of injecting metabolically active agents into the subretinal space of rabbits were studied. Small retinal detachments (blebs) were made in living Dutch rabbit eyes by injecting experimental solutions into the subretinal space with a micropipette. A second micropipette, inserted into the same bleb, measured fluid pressure using a resistance servonulling system. The adhesive force was calculated according to Laplace's law. Blebs containing dibutyryl cyclic adenosine monophosphate, furosemide, and amiloride showed retinal adhesiveness to be decreased to 69%, 86%, and 81% of control values, respectively. Dibutyryl cyclic guanosine monophosphate and acetazolamide had no significant effect. Ouabain increased retinal adhesiveness to 119% of normal. The nonspecific metabolic toxin, dinitrophenol, reduced adhesiveness to an unmeasurable level. For some agents, the rate at which subretinal fluid was absorbed also was measured. Furosemide and amiloride in the subretinal space caused slight slowing of subretinal fluid absorption; acetazolamide had no effect. These data support the concept that metabolic factors contribute to retinal adhesion in vivo.

Adhesiveness↗