Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was undertaken to determine whether the antiesterase activity of echothiophate iodide would prevent the conversion of dipivefrin to epinephrine. Dipivefrin was administered singly and in combination with echothiophate to 24 adult rabbits. Administration of dipivefrin lowered the intraocular pressure (IOP) 8 +/- 1 mm Hg (P less than .001). When echothiophate was given before and concomitant with dipivefrin, there was no further decrease in IOP compared with that produced by echothiophate alone (5 +/- 1 mm Hg). Addition of epinephrine to eyes receiving dipivefrin plus echothiophate resulted in a significant additional decrease in IOP of 4 +/- 1 mm Hg (P less than .001). When echothiophate was given after dipivefrin had lowered the IOP and both drugs were continued, the IOP rose to baseline levels. These results fit the theory that the esterase converting dipivefrin to epinephrine is inactivated by cholinesterase inhibitors. The clinical use of cholinesterase inhibitors and dipivefrin may be contraindicated.
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PMID:Dipivefrin and echothiophate: contraindications to combined use. 48 20

The intraocular projection of the cat pterygopalatine (sphenopalatine) ganglion was examined by using retrograde axoplasmic transport techniques in order to investigate the possibility of the involvement of the facial nerve in ocular parasympathetic innervation. Following an injection of horseradish peroxidase (HRP) or wheat germ agglutinin-HRP into the eye, retrogradely labeled cells were observed in the ipsilateral pterygopalatine ganglion, principally in the caudal part. By dissection of silver-impregnated, acetylcholinesterase- and cholinesterase-stained orbital preparations, it was determined that two different nerve pathways link the pterygopalatine ganglion and the eye. One took a retrograde course to join the retro-orbital plexus and then traveled forward accompanying the ciliary artery, the long ciliary nerve, the short ciliary nerve, and/or the optic nerve sheath. The other entered the orbit directly, fused with the ethmoidal nerve or the infratrochlear nerve in a retrograde fashion, and then turned forward along the long ciliary nerve to enter the eye. All these nerves arose from the caudal part of the ganglion. These results are discussed in relation to recent biochemical and histochemical data demonstrating the involvement of the facial nerve in the control of ocular blood flow and intraocular pressure.
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PMID:Intraocular projections from the pterygopalatine ganglion in the cat. 170 52

The adverse reactions seen following administration of neuromuscular blocking agents are mainly cardiovascular. Due to the lack of specificity for the nicotinic receptor at the neuromuscular junction, these agents may interact with receptors in autonomic ganglia and muscarinic receptors in the heart. Furthermore, muscle relaxants may have histamine-releasing properties. The cardiovascular effects vary with potency and specificity of the drug, depending mainly on the chemical structure. Pancuronium, fazadinium and especially gallamonium block cardiac muscarinic receptors, and tachycardia may be seen. Atracurium, metocurine and in particular d-tubocurarine have histamine-releasing properties and may cause flushing, hypotension and tachycardia. Vecuronium has no effect on the cardiovascular system. The effect of succinylcholine on heart rate differs between children, where bradycardia is seen, and adults in whom tachycardia may follow. However, bradycardia may occur in adults following a single dose. Succinylcholine increases plasma potassium, especially in patients with nerve damage, and arrhythmias may be observed. The neuromuscular adverse effects of succinylcholine, such as fasciculations and increased gastric and intraocular pressure, may be prevented by precurarisation. Many drugs interact with neuromuscular blocking agents and there is often a potentiation of the neuromuscular effect. This is of clinical importance in the case of antibiotics, inhalational anaesthetics, lithium and cyclosporin. Difficulty in reversing the block may occur with calcium channel blockers and polymyxin. However, some drugs, such as phenytoin, carbamazepine and lithium, may cause resistance to neuromuscular blocking agents. Furthermore, clinically important interactions exist between individual neuromuscular blocking drugs. Precurarisation with a non-depolarising drug prolongs the onset of succinylcholine, and conversely a prolonged effect of non-depolarising drugs is seen following succinylcholine. The effect of succinylcholine is markedly prolonged if the drug is administered during recovery from pancuronium blockade or following neostigmine for reversal. Succinylcholine is hydrolysed by plasma cholinesterase, and drugs which decrease the activity of this enzyme may produce a prolonged block, i.e. contraceptive pills, cyclophosphamide, echothiopate and organophosphate.
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PMID:Adverse reactions and interactions of the neuromuscular blocking drugs. 268 31

Two men were accidentally exposed to vapors of sarin, a cholinesterase inhibitor and extremely toxic nerve gas. Diagnosis was confirmed by depressed cholinesterase activity, and fixed extremely miotic pupils. No other signs or symptoms developed and neither man required treatment. Recovery to normal cholinesterase activity was gradual over a 90-day period. Pupillary reflexes were not detectable until 11 days after exposure; the miotic pupils dilated slowly over a 30-45 day-period. Eye pain and blurred vision did not occur; visual acuity and amplitude of accommodation were improved for several weeks. Other functions not affected significantly were intraocular pressure, visual fields, color vision, heterophorias, and vergences.
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PMID:Accidental exposure to sarin: vision effects. 397 1

The most conspicuous short-term effects of exposure to organophosphates are miotic pupils and a reduced visual field. Two men accidentally exposed to vapors of sarin, a cholinesterase inhibitor and extremely toxic nerve gas, showed these effects but no adverse effects on near- or far-visual acuities, oculomotor functions, intraocular pressure or color vision. However, reports of other accidental exposures to organophosphorus compounds suggest that there are visual and ocular changes, including myopia and decreased visual acuity.
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PMID:Vision and ocular changes following accidental exposure to organophosphates. 802 6

Exposure to anticholinesterase pesticides has been associated with the development of ocular toxicity in humans and animals, ranging from blurred vision to degeneration of the optic nerve. Based on the concern for human safety, the US Environmental Protection Agency has recently required additional studies for this class of compounds, focusing on biochemical, functional and histopathological evaluation of the ocular system. This study was designed to determine the effects on the eye of ethyl parathion, a highly toxic organophosphate, when administered orally to 30 beagle dogs (five of each sex per group) at doses of 2.4, 7.9 or 794 micrograms kg-1day-1 for 6 months. Control animals received corn oil. Routine ophthalmoscopic and slit lamp examinations, refraction and intraocular pressure determinations and electroretinograms were performed as functional assessments at various intervals over the study. Plasma and erythrocyte cholinesterase were determined at weeks 1, 6, 14, 20 and 26, while brain, retinal and ocular muscle cholinesterase were measured at week 26 only. Histopathological examination of the retina, optic nerve, ocular muscle and ciliary body was conducted at termination. Plasma and erythrocyte cholinesterase was markedly depressed at 7.9 and 794 micrograms kg-1day-1 as early as week 1. Retinal cholinesterase was decreased (37-55%) from control values in the 794 micrograms kg-1day-1 group only. Ocular muscle cholinesterase was comparable in treated and control groups at termination. No functional impairment of the eye was noted over the 6-month study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of ocular toxicity in dogs during 6 months' exposure to a potent organophosphate. 802 10

To investigate the pathogenesis of retina lesions caused by intraocular pressure elevation, activities and distribution of enzymes in retina including lactic dehydrogenase (LDH), succinate dehydrogenase (SDH), adenosinetriphosphatase (AT-Pase), acid phosphatase (ACP), cholinesterase (ChE), cytochrome oxidase (CCO), nucleotidase (5'-Nase) and glucose-6-phosphatase (G6Pase) were determined histochemically in 30 rabbits. It was found that 1) in the early stage of intraocular pressure elevation, the activities of LDH, SDH, ATPase, ACP, and ChE in retina were increased, while the activities of CCO, 5'-Nase decreased; 2) in the late stage of intraocular pressure elevation, the activities of all these enzymes but ACP, which showed a reduced activity, were close to the normal level; 3) in superoxide dismutase.(SOD-CCE) treated group, except the slight increase of LDH and G6Pase activities, the activities of the remaining enzymes were near to normal. Our results suggest that the various histochemical changes in retina induced by intraocular pressure elevation were compensatory in the early stage and were beneficial to the supply of energy needed in retinal tissue and cellular metabolism; while in the late stage, the lesion of retina cells developed due to decompensation. SOD-CCE could alleviate the retinal lesions caused by intraocular pressure elevation, and can be used as auxiliary drug for the treatment of intraocular pressure elevation.
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PMID:Enzymatic histochemistry of retina with experimental intraocular pressure elevation in rabbits. 873 48

Technical grade disulfoton (DiSyston) was fed to Beagle dogs (four animals per sex and treatment level) at nominal concentrations of 0, 0.5, 4 and 12 ppm for 1 year. The purpose of this study was to characterize the potential general and neurovisual toxicity according to routine Environmental Protection Agency (EPA) guideline requirements, and by use of ancillary ocular and neurologic tests established in this Laboratory. Ophthalmological tests included: ocular tissue cholinesterase and histopathology, electroretinography (ERG), tracking, refractivity, intraocular pressure and pachymetry (corneal thickness) measurements. Neurological examinations included; peripheral and cranial reflex tests, task performance tests, gait and behavioral observations, and rectal temperature measurements. Plasma, erythrocyte and corneal cholinesterase were significantly depressed at 4 and 12 ppm in both sexes. Brain cholinesterase was depressed at 4 and 12 ppm in females. Retinal cholinesterase was depressed at 4 ppm in females and at 12 ppm in males. Ciliary body cholinesterase was depressed at 12 ppm in both sexes. Despite these cholinergic effects, there were no ophthalmologic findings in measurements of ERG, tracking, refractivity, intraocular pressure or pachymetry. There were no clinical neurology findings related to compound administration. We conclude that 0.5 ppm was a no-observable effect level (NOEL), and effects were limited to cholinesterase changes that had no detectable physiologic impact. This study demonstrates that special mechanistic investigations incorporated within guideline studies, enhances scientific integrity and can minimize the need for dedicated organ system studies.
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PMID:Absence of neurovisual effects due to tissue and blood cholinesterase depression in a chronic disulfoton feeding study in dogs. 1040 62

For some time the medical treatment of glaucoma has consisted of topical beta-blockers, adrenergic agents, miotics and oral carbonic anhydrase inhibitors (CAIs). However, the therapeutic arsenal available for the medical treatment of glaucoma has recently extended with new classes of ocular hypotensive agents i.e. prostaglandins, local CAIs and alpha2-adrenergic agents. Beta-blockers are still the mainstay in glaucoma treatment and are first line drugs. However, even if they are applied once daily, as with timolol in gel forming solution and levobunolol, the possible cardiopulmonary adverse effects of beta-blockers remain a cause for concern. When monotherapy with beta-blockers is ineffective in reducing intraocular pressure (IOP) or is hampered by adverse effects, a change of monotherapy to prostaglandins, local CAIs, alpha2-adrenergic agonists (brimonidine) or to dipivalyl epinephrine is advised. Prostaglandins, local CAIs and alpha2-adrenergic agonists, such as brimonidine, may in time become first line drugs because they reduce IOP effectively and until now systemic adverse effects have rarely been reported with these agents. The development of a pro-drug of either a local CAI or an alpha2-adrenergic agonist with a sustained and continuous effect on IOP level, which could be applied once a day is suggested. Because of these new developments, miotics, i.e. pilocarpine and carbachol, are recommended as second or third line drugs. The cholinesterase inhibitors are considered third line drugs as better agents with fewer local and systemic adverse effects have become available. Oral CAIs may be used temporarily in patients with elevated IOPs e.g. postsurgery or post-laser, or continuously in patients with glaucoma resistant to other treatment. Combining ocular hypotensive drugs is indicated when the target pressure for an individual patient cannot be reached with monotherapy. Combination therapy of beta-blockers is additive with prostaglandins, topical CAIs and miotics. Prostaglandins such as latanoprost can be combined with beta-blockers, adrenergic agents, local CAIs and miotics. Combinations with brimonidine or local CAIs need further investigation. Treatment of glaucoma with the new ocular hypotensive agents, either in monotherapy or combination therapy, may provide lower IOPs and delay or postpone the need for surgery.
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PMID:Pharmacological therapy for glaucoma: a review. 1077 28

We have studied the effects of various angiotensin-converting enzyme (ACE) inhibitors on intraocular pressure (IOP) of rabbits with experimentally induced ocular hypertension and their mechanism of action. Acute ocular hypertension was induced by infusion of 5% glucose (15 ml/kg) through marginal ear vein, whereas chronic glaucoma was induced by injection of alpha-chymotrypsin into the posterior chamber of the eye. IOP was measured by tonometer. All ACE inhibitors were instilled topically in the eye in a sterile solution. The effect of ACE inhibitors also was studied on serum cholinesterase (true and pseudo) and the enzyme ACE in vitro. Enalaprilat, ramiprilat, and fosinopril produced a time-dependent decrease of IOP in both acute and chronic models of ocular hypertension in rabbits. The decrease in IOP was observed for >4 h, and the extent of decrease was comparable to that with both pilocarpine and betaxolol. Prodrugs enalapril and ramipril failed to produced any change in IOP. Losartan also produced a significant decrease in IOP in the chronic model of ocular hypertension in rabbits. All the three ACE inhibitors were found to inhibit ACE activity in aqueous humor. The enzyme cholinesterase was found to be inhibited by enalaprilat, ramiprilat, and fosinopril. However, atropine did not alter the IOP-lowering effect of enalaprilat in rabbits. Indomethacin pretreatment produced slight but significant inhibition of the IOP-lowering effect of enalaprilat in rabbits. Our data suggest that ACE inhibitors enalaprilat, ramiprilat, and fosinopril produce a significant ocular hypotensive effect in acute and chronic models of ocular hypertension in rabbits. Inhibition of ACE in aqueous humor, and in ocular tissues, resulting in reduced angiotensin II formation, could be one of the major mechanisms responsible for the IOP reduction by ACE inhibitors in rabbits.
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PMID:Oculohypotensive effect of angiotensin-converting enzyme inhibitors in acute and chronic models of glaucoma. 1094 57


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