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At least 19 recordsLinked to original sources

Effects of the substance P antagonist [D-Arg1,D-Pro2,D-Trp7,9,Leu11]SP on miosis caused by echothiophate iodide or pilocarpine hydrochloride.

The anticholinesterase agent echothiophate iodide (EI) and the cholinergic agent pilocarpine hydrochloride (pilocarpine), drugs commonly used in glaucoma therapy, cause miosis in rabbits as well as in man. In rabbits the miotic effect decreases after a few days of treatment, a phenomenon possibly due to a drug-induced decrease in the number of muscarinic receptors. However, the muscarinic pupillary contraction caused by stimulation of the retina with light is intact. In this investigation the miosis caused by the doses of EI was found to be very resistant to muscarinic or nerve blockade but inhibited by the substance P (SP) analog [D-Arg1,D-Pro2,D-Trp7,9, Leu11]SP, which seems to be a SP/SPLI blocker in the rabbit pupillary sphincter. Miosis caused by pilocarpine was partly inhibited by muscarinic blockade and partly by the SP blocker. In eyes treated with EI topically twice daily for three weeks, SP or the red pepper extract capsaicin, a releaser of SP-like immunoreactivity (SPLI), had less miotic effect than in control eyes. Capsaicin caused more pronounced miosis in eyes treated with topical pilocarpine for three weeks than in controls. The radioimmunoassay technique did not reveal a significant change in the amount of SPLI in the retinas or iris-ciliary bodies from EI-treated eyes as compared with the controls. It is concluded that, besides cholinergic miosis, EI causes non-muscarinic miosis, probably by release of SP or a related substance and that pilocarpine may have similar effects.

Animals↗

Effect of topically applied demecarium bromide and echothiophate iodide on intraocular pressure and pupil size in beagles with normotensive eyes and beagles with inherited glaucoma.

Topically applied demecarium bromide (0.125 and 0.25%) and echothiophate iodide (0.125 and 0.25%) solutions were evaluated in Beagles with normotensive eyes and Beagles with inherited glaucoma. In single-dose studies, the effects of intraocular pressure (IOP) and pupil size (PS) were measured in eyes before drug treatment and in drug- and nondrug-treated eyes. Both concentrations of the 2 drugs induced long-term miosis and decrease in IOP in normotensive eyes of Beagles and of eyes of Beagles with inherited glaucoma. Demecarium bromide (0.125 and 0.5%) decreased IOP for 49 and 55 hours, respectively. Echothiophate iodide (0.125 and 0.5%) reduced IOP for 25 and 53 hours, respectively. The miosis associated with both concentrations of the 2 drugs generally paralleled the decreases in IOP.

Administration, Topical↗

Possible non-muscarinic miotic action of echothiophate iodide in humans.

The proposed non-muscarinic pupillary action of echothiophate iodide (EI) was investigated in humans. In 10 healthy volunteers the variations of the pupillary area, induced by EI eye drops, were evaluated by using an electronic pupillometer. When instilled alone, as well as after homatropine, EI caused pupillary constriction. The reduction of the homatropine-induced mydriasis by EI was not accompanied by any increase in the almost abolished pupillary response to light, thus excluding that an enhancement of the parasympathetic activity contributes to pupillary constriction. These findings suggest a non-muscarinic component in the EI-induced miosis, the nature of which remains to be elucidated.

Adolescent↗

Echothiophate iodide for flat anterior chamber following cataract extraction.

Three cases are presented of late flat anterior chambers which were cured by echothiophate iodide treatment. Two of the cases required repeated instillations to achieve permanent restoration of normal chamber depth. We now recommend that echothiophate treatment be considered in cases of late flat anterior chamber unresponsive to standard medical treatment.

Aged↗

Cystoid macular edema associated with topical echothiophate iodide.

We report the case of a patient with visual loss and cystoid macular edema that was associated with the topical use of echothiophate iodide. After cessation of the drops, the cystoid macular edema nearly disappeared, and vision returned to normal.

Administration, Topical↗

Electroconvulsive therapy and the chronic use of pseudocholinesterase-inhibitor (echothiophate iodide) eye drops for glaucoma. A case report.

A case is presented in which a patient who required treatment with electroconvulsive therapy had a history of being treated with pseudocholinesterase-inhibitor eye drops (echothiophate iodide) for glaucoma. As treatment with this antiglaucoma agent contraindicated the use of succinylcholine for a minimum of 10-14 days, the short-acting nondepolarizing agent atracurium was employed instead. The anesthetic management of this patient is described as a guide for clinicians facing similar clinical situations.

Aged↗

Cycloplegic refraction after echothiophate iodide.

Retinoscopy under cycloplegia using cyclopentolate (Cyclogyl) hydrochloride was performed on 18 patients (36 eyes) with partial or complete accommodative esodeviation, during and after treatment with echothiophate (Phospholine) iodide. Measurements were clinically comparable on both occasions, regardless of concentration of echothiophate, duration of administration, or interval from discontinuance until refraction. It appears to be unnecessary to discontinue echothiophate iodide in order to obtain reliable cycloplegic retinoscopic measurements.

Accommodation, Ocular↗

Serum cholinesterase, serum lipase, and serum amylase levels during long-term echothiophate iodide therapy.

Previous studies have found increased pancreatic intraductal pressures in dogs and the development of acute pancreatitis in humans after cholinergic stimulation. However, we did not find abnormally high levels of serum lipase or serum amylase in 44 patients with glaucoma using therapeutic doses of echothiophate iodide for intraocular pressure control on a long-term basis.

Amylases↗