Retinal light exposure and cystoid macular edema.
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Biomedical subjects
Publications and source records attributed to B Becker.
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Prazosin hydrochloride, a systemic antihypertensive agent, lowers intraocular pressure when applied topically to normal rabbit eyes. A 0.01% solution of topically administered prazosin did not alter out-flow facility, episcleral venous pressure, systemic blood pressure, or ocular blood flow. Tonography suggested a 27% decrease in the rate of aqueous humor formation two hours following topical administration. Posterior chamber aqueous ascorbate levels were increased following topical administration of prazosin, which also suggested a decreased entry rate of water into the eye. The effect of prazosin on IOP was prevented by systemic pretreatment with phentolamine mesylate, an alpha-adrenergic blocking agent, but not by propranolol hydrochloride or atropine sulfate. This was consistent with the known action of prazosin as a postsynaptic alpha-adrenergic blocking agent.
A prospective collaborative study was conducted in five centers during a 13-year period to identify factors that influence the development of visual-field defects (GVFDs) of open angle glaucoma. In 5,000 subjects, GVFDs developed in only 1.7% of eyes. Statistical analysis of 26 factors at first examination identified five that were significantly related to the development of GVFDs--outflow facility, age, applanation pressure, cup-disc ratio, and pressure change after water drinking. Their absolute initial value, and not its change with time, was the important predictor. Multivariate analysis showed their collective predictive power to be undesirably poor, indicating that other factors must play an important role in the development of GVFDs. Mortality-table analysis indicated that during a period of five years, 98.54% of eyes with initial pressure less than 20 mm Hg continued to be free from GVFDs as compared with 93.34% of those with pressure of 20 mm Hg or greater.
The dwarf tapeworm, Hymenolepis nana, was studied by means of scanning and transmission electron microscopy after in vitro exposure to 1, 10, and 100 micrograms/ml of the anthelmintic praziquantel (Droncit) for 5, 15, 30, and 60 min. The resulting vacuolization of the tegument was exclusively confined to the neck region of the tapeworms and was already observed after treatment for 5 min with 1 microgram/ml. This vacuolization finally led to the disruption of the syncytial layer in the apical region of the tegument. The tegumental microtriches and the surface coat remained unaffected. Proglottids of the middle or posterior regions of the worms never showed destruction.
The fine structure of the tegument of three trematode species, Schistosoma mansoni, Dicrocoelium dendriticum, and Fasciola hepatica, was studied by means of light scanning (SEM) and transmission electron microscopy (TEM) after in vitro exposure to 0, 1, 10, and 100 micrograms/ml of the anthelmintic praziquantel for 5, 15, 30, and 60 min. In S. mansoni and D. dendriticum the resulting vacuolization of the tegument was confined to numerous small areas scattered all over the surface of the parasites and this finally led to the disruption of the apical tegumental layer. No changes were found in the tegument of F. hepatica after treatment with praziquantel.
We performed filtration surgery with a unidirectional, pressure-sensitive valve implant in 40 eyes with neovascular glaucoma. The device consisted of an open Supramid tube (outside diameter 0.58 mm, inside diameter 0.38 mm) sealed to a Silastic tube with a slit valve. The Supramid tube was inserted at the corneoscleral limbus 1 to 4 mm into the anterior chamber and the Silastic portion was located under a lamellar scleral flap. Twenty-seven of 40 eyes (68%) had a postoperative IOP less than or equal to 24 mm Hg with a mean follow-up of 13.8 months. Ten of these 27 eyes required postoperative medical therapy to achieve this level of IOP control. The glaucoma valve implant failed to return IOP to normal in 13 of the 40 eyes (32%), 11 of these as a consequence of scarring of the external bleb.
The stereoscopic photographs of 102 patients with increased intraocular pressure (IOP) and normal visual fields were graded for cup:disk ratio. All patients were followed up for a five-year period, during which time 27 patients developed glaucomatous visual field loss and 75 patients did not. The patients who subsequently developed glaucomatous visual field loss had significantly larger cup:disk ratios than did the patients who did not develop glaucomatous visual field loss. Patients with a mean IOP greater than or equal to 28 mm Hg and a vertical contour cup:disk ratio greater than or equal to 0.6 had a 100% incidence of the development of glaucomatous visual field loss as compared to a 2% incidence in those with a mean IOP less than 28 mm Hg and a vertical cup:disk ratio less than 0.6. Disk:cup asymmetry and progressive increase in the area of the disk occupied by the cup was more common in the group that developed glaucomatous visual field loss.
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H1-blocking antihistamines were administered topically to rabbits to determine their effects on intraocular pressure. Chlorcyclizine which is in the piperazine class of H1-inhibitors was found to elevate intraocular pressure. This effect was prevented by the systemic administration of indomethacin and is probably a prostaglandin induced change. Of the other agents tested, antazoline which is in the ethylenediamine class, was the only drug found to lower intraocular pressure. The antazoline-induced lowering of intraocular pressure was associated with no changes in outflow facility, episcleral venous pressure, systemic blood pressure, or ocular blood flow. Tonographic and aqueous humor ascorbate humor ascorbate data suggested a decreased (41% and 33% respectively) rate of aqueous flow as the mechanism for the decrease in intraocular pressure. The systemic administration of the alpha-adrenergic blocker phentolamine prevented the decrease in intraocular pressure but systemically administered blockers of cholinergic (atropine) or beta-adrenergic (propranolol) activity had no effect.
Pro-drugs are agents that require biotransformation prior to exhibiting pharmacologic activity. Dipivefrin (dipivalyl epinephrine or DPE) is an epinephrine pro-drug produced by the addition of two pivalic acid groups to the parent compound. This creates a more lipophilic molecule which penetrates the cornea more readily than epinephrine. Enzymes in ocular tissues convert dipivefrin into its active form, epinephrine. In concentrations approximately one-tenth that of epinephrine, topically applied dipivefrin therefore produces: (1) similar intra-ocular concentrations of epinephrine; (2) similar reductions in intra-ocular pressure (IOP); (3) similar degrees of mydriasis; and (4) fewer extraocular and systemic side effects. For reasons that are discussed, dipivefrin should probably not be used in conjunction with anticholinesterases. Dipivefrin offers the same risk of cystoid macular oedema as does epinephrine. Dipivefrin is a safe, effective, and well-tolerated alternative to epinephrine in the treatment of elevated IOP. It is particularly useful for patients who cannot tolerate epinephrine.
Topical administration of 0.5% vanadate lowers intraocular pressure in monkey and rabbit eyes. This appears to be a consequence of a reduction in the rate of aqueous humor secretion, probably resulting from the inhibition of ciliary epithelium membrane. NaK ATPase. The ubiquitous vanadate and its interactions with catecholamines and ascorbate may play a role in regulating the sodium pump of the ciliary epithelium. Adrenergic blocking agents may also lower intraocular pressure by inhibiting the NaK ATPase of the ciliary epithelium.
In unanesthetized rabbits the topical application of vanadate lowered intraocular pressure. Tonographic outflow facility and episcleral venous pressure were unaltered by topical vanadate. As estimated from the tonographic data, aqueous humor flow was reduced by approximately 30%. Posterior chamber aqueous humor ascorbate increased in the eye receiving topical vanadate, and this was compatible with a decreased rate of aqueous humor flow. Topical vanadate did not alter anterior chamber aqueous humor protein or cyclic AMP. In five monkeys intraocular pressure was also significantly reduced by topical vanadate.
Halothane anesthesia decreased intraocular pressure (IOP) by approximately 4 mm Hg in both normal rabbits and monkeys. The administration of nitrous oxide or 100% oxygen had no effect on IOP. Although PO2 and PCO2 increased following halothane administration in rabbits, similar blood changes occurred without IOP reduction in control rabbits receiving 100% oxygen. Outflow facility in both species as measured by tonography remained unchanged by halothane administration. Aqueous humor flow as estimated by tonography decreased by about 39% in rabbits and 31% in monkeys. Posterior chamber aqueous humor ascorbate was significantly elevated 90 min after halothane administration in rabbits. The ratio of the aqueous humor flow coefficient to diffusion coefficient for ascorbate (kfa/kdpa) was reduced approximately 47% following the administration of halothane. Halothane did not alter the in vitro accumulation of 131I-hippuran or 86Rb by rabbit ciliary body--iris preparations.
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