Miotics
Miosis
Arecoline
Reflex, Pupillary
Sarin
Pilocarpine
Parasympathomimetics
Quinuclidines
Iris
Ophthalmic Solutions
Glaucoma
Cholinesterase Inhibitors
Interaction of amylin with calcitonin gene-related peptide receptors in the microvasculature of the hamster cheek pouch in vivo. (1/81)
1. This study used intravital microscopy to investigate the receptors stimulated by amylin which shares around 50% sequence homology with the vasodilator calcitonin gene-related peptide (CGRP) in the hamster cheek pouch microvasculature in vivo. 2. Receptor agonists dilated arterioles (diameters 20-40 microm). The -log of the concentrations (+/- s.e.mean; n = 8) causing 50% increase in arteriole diameter were: human betaCGRP (10.8 +/- 0.3), human alphaCGRP (10.8 +/- 0.4), rat alphaCGRP (10.4 +/- 0.3). Rat amylin and the CGRP2 receptor selective agonist [Cys(ACM2,7]-human alphaCGRP were 100 fold less potent (estimates were 8.5 +/- 0.4 and 8.2 +/- 0.3 respectively). 3. The GCRP1 receptor antagonist, CGRP8-37 (300 nmol kg(-1); i.v.) reversibly inhibited the increase in diameter evoked by human alphaCGRP (0.3 nM) from 178 +/- 22% to 59 +/- 12% (n = 8; P < 0.05) and by rat amylin (100 nM) from 138 +/- 23% to 68 +/- 24% (n = 6; P < 0.05). CGRP8-37 did not inhibit vasodilation evoked by substance P (10 nM; n = 4: P > 0.05). 4. The amylin receptor antagonist, amylin8-37 (300 nmol kg(-1); i.v.) did not significantly inhibit the increase in diameter evoked by human alphaCGRP (0.3 nM) which was 112 +/- 26% in the absence, and 90 +/- 29% in the presence of antagonist (n = 4; P < 0.05); nor that evoked by rat amylin (100 nM) which was 146 +/- 23% in the absence and 144 +/- 32% in the presence of antagonist (n = 4; P > 0.05). 5. The agonist profile for vasodilatation and the inhibition of this dilatation by CGRP8-37, although not the amylin8-37 indicates that amylin causes vasodilatation through interaction with CGRP1 receptors in the hamster cheek pouch. (+info)Topical therapies for glaucoma: what family physicians need to know. (2/81)
Medication classes historically used in the management of glaucoma include beta blockers, miotics, sympathomimetics and carbonic anhydrase inhibitors. Because topically applied medications are more site specific, they are preferred in the treatment of glaucoma. Compared with oral medications, topical agents are associated with a decreased incidence of systemic side effects. With topical administration, conjunctival and localized skin allergic reactions are relatively common, whereas severe reactions, including death, are rare. Recently introduced topical agents for glaucoma therapy include dorzolamide and brinzolamide, the first topical carbonic anhydrase inhibitors; brimonidine and apraclonidine, more ocular-specific alpha agonists; and latanoprost, a prostaglandin analog, which is a new class of glaucoma medication. Latanoprost has the unique side effect of increasing iris pigmentation. Like their predecessors, the newer agents lower intraocular pressure by a statistically significant degree. Preservation of visual field, the more substantial patient-oriented end point, continues to be studied. (+info)Pilocarpine induces an increase in the anterior chamber angular width in eyes with narrow angles. (3/81)
AIM: To determine the mechanical effects of pilocarpine on the trabecular-iris angle opening in eyes with narrow angles, compared with its effects on healthy control subjects with wide angles. METHODS: A narrow angle was defined as 25 degrees or less of trabecular-iris angle on ultrasound biomicroscopic examination. The change in anterior chamber depth (ACD), trabecular-iris angle (TIA), angle opening distance (AOD, distance between trabecular meshwork and iris) measured at 250 microm and 500 microm from the scleral spur (AOD250 and AOD500), and iris thickness was determined in 30 eyes of 30 patients (13 men and 17 women, between 63 and 82 years (mean 70.4 years)) with narrow angles and in 30 sex and age matched control subjects with wide angles before and 1 hour after the instillation of 2% pilocarpine hydrochloride by ultrasound biomicroscopy. RESULTS: In all eyes with narrow angles, pilocarpine increased the TIA, AOD250, and AOD500; these changes increased significantly and linearly as the corresponding pretreatment values decreased (r = 0.807, p = 0.0001; r = 0.787, p = 0.0001; r = 0.852, p = 0.0001). Of 30 eyes with wide angles, 23 eyes whose ACD was 2670 microm and more showed a decrease in the TIA, AOD250, and AOD500; the changes in TIA, AOD250, and AOD500 also significantly correlated with the corresponding pretreatment values (r = 0.913, p = 0.0001; r = 0.882, p = 0.0001; r = 0.895, p = 0.0001). Pilocarpine induced a smaller decrease in ACD in eyes with narrow angles than in those with wide angles (p = 0.0001). There was a linear correlation between the increase in ACD change and the decrease in pretreatment ACD in eyes with narrow angles and those with wide angles (r = 0.781, p = 0.0003; r = 0.798, p = 0.0001). CONCLUSIONS: The finding that pilocarpine increases angular width in patients with narrow angles indicates that this agent is useful for treating patients with narrow angles and angle closure glaucoma. The prediction of the pilocarpine induced change in the angle may assist ophthalmologists in treating such patients. (+info)The effect of miotics on the intraocular pressure of conscious owl monkeys. (4/81)
The intraocular pressure of conscious, unsedated owl monkeys (Aotus trivirgatus) was measured with an applanation tonometer. Untreated eyes of the conscious animals were found to have higher values than those reported for owl monkeys anesthetized with pentobarbitone. Locally applied pilocarpine, carbachol, and oxotremorine gave concentration-related reduction in pressure, oxotremorine being the most potent and having longer duration of effect than the other compounds. Slight reductions were also observed with aceclidine and R. S. 86. These results are discussed in relation to the effects of miotics in man. (+info)Adrenomedullin receptor antagonism by calcitonin gene-related peptide(8-37) inhibits carotid artery neointimal hyperplasia after balloon injury. (5/81)
Intimal injury by angioplasty results in a series of changes, including smooth muscle cell hyperplasia, that lead to vascular restenosis. Adrenomedullin, a potent vasodilator peptide, has natriuretic effects, and its plasma concentration is elevated in cardiovascular diseases. Adrenomedullin is secreted by endothelial and vascular smooth muscle cells, but its role in neointimal hyperplasia after balloon injury has not been previously described. We investigated the role of endogenous adrenomedullin in neointimal hyperplasia using an in vivo rat model of postinjury vascular restenosis. In the injured rats, bromodeoxyuridine-labeled nuclei in the media of untreated common carotid arteries were increased 2 days after injury, which were suppressed by in vivo treatment with the adrenomedullin receptor antagonist calcitonin gene-related peptide (CGRP)(8-37). Inhibition of neointimal hyperplasia by CGRP(8-37) was distinct at 7 and 14 days, whereas CGRP(1-37) had no effect. The expression of adrenomedullin in the media of both untreated and treated common carotid arteries was elevated at 2 days and further enhanced in hyperplastic intima of untreated common carotid arteries at 7 days. Our findings suggest a novel role for endogenous adrenomedullin in balloon injury-induced restenosis and indicate that CGRP(8-37) may be useful for the prevention of vascular restenosis. (+info)An autocrine or a paracrine role of adrenomedullin in modulating cardiac fibroblast growth. (6/81)
OBJECTIVE: The aim of the present study was to determine the role of adrenomedullin (AM) in cardiac fibroblasts. METHODS: The production and secretion of AM were examined in cultured neonatal rat cardiac fibroblasts, and the effects of AM on proliferation and protein synthesis of these cells were assessed by [3H]thymidine and [3H]phenylalanine incorporation, respectively. RESULTS: Cultured cardiac fibroblasts secreted AM into the medium time-dependently at a rate of 20.3 +/- 3.0 fmol/5 x 10(4) cells/48 h, mean +/- S.D. Northern blot analysis showed expression of preproAM mRNA of 1.6 kb in these cells. In addition, 10(-6) mol/l of angiotensin II (Ang II) and endothelin-1 (ET-1) significantly increased the AM secretion by 55 and 48%, respectively. Synthetic AM significantly reduced 10(-6) mol/l Ang II- or 10(-7) mol/l ET-1-stimulated [3H]thymidine and [3H]phenylalanine incorporation in a dose-dependent manner, and these effects were attenuated by a calcitonin gene-related peptide (CGRP) type 1 receptor antagonist, CGRP(8-37). Synthetic AM also had a dose-dependent stimulatory effect on cAMP accumulation in these cells, which was significantly attenuated by CGRP(8-37). A cAMP analogue, 8-bromo-cAMP, mimicked the AM effects, inhibiting the Ang II-stimulated [3H]thymidine and [3H]phenylalanine incorporation. Blockage of the effect of endogenous AM by anti-AM monoclonal antibody not only significantly reduced the basal level of intracellular cAMP, but also enhanced the [3H]thymidine and [3H]phenylalanine incorporation into the cells. CONCLUSIONS: Cultured neonatal rat cardiac fibroblasts produce and secrete AM, and the secreted AM may inhibit proliferation and protein synthesis of these cells. AM may exert these inhibitory effects partly by elevating intracellular cAMP. It is suggested that AM has an important role in modulating the growth of cardiac fibroblasts in an autocrine or a paracrine manner. (+info)Comparison of the intraocular pressure lowering effect of latanoprost and a fixed combination of timolol-pilocarpine eye drops in patients insufficiently controlled with beta adrenergic antagonists. French Latanoprost Study Group, and the Swedish Latanoprost Study Group. (7/81)
AIMS: To compare the effect on intraocular pressure (IOP) of latanoprost monotherapy and timolol-pilocarpine in patients with glaucoma or ocular hypertension with inadequately controlled IOP on topical beta adrenergic antagonists. METHODS: This was a multicentre, randomised, observer masked, 6 week study performed in France and Sweden. 23 centres enrolled 237 patients with glaucoma or ocular hypertension and an IOP of at least 22 mm Hg on treatment with topical beta adrenergic antagonists, alone or in combination. After a 21 day run in period on timolol 0.5% twice daily, patients were randomised either to latanoprost 0.005% once daily or to a fixed combination of timolol-pilocarpine twice daily. Changes in mean diurnal IOP from the baseline to the 6 week visit were determined with an analysis of covariance. RESULTS: Mean diurnal IOP was statistically significantly decreased from baseline in both groups (p<0.001). Switching to latanoprost treatment reduced mean diurnal IOP by 5.4 (SEM 0.3) mm Hg (ANCOVA -22%) and switching to timolol-pilocarpine treatment reduced mean diurnal IOP by 4.9 (0.4) mm Hg (-20%). Blurred vision, decreased visual acuity, decreased twilight vision, and headache were statistically significantly more frequent in the timolol-pilocarpine group. CONCLUSIONS: Latanoprost monotherapy was at least as effective as fixed combination timolol-pilocarpine twice daily treatment in reducing mean diurnal IOP in patients not adequately controlled on topical beta adrenergic antagonists. Latanoprost was better tolerated than timolol-pilocarpine regarding side effects. These results indicate that a switch to latanoprost monotherapy can be attempted before combination therapy is initiated. (+info)Effect of cataract extraction and posterior chamber lens implantation on outflow facility and its response to pilocarpine in Korean subjects. (8/81)
AIM: To investigate the effect of the lens on outflow facility in Korean patients with cataracts. METHODS: Intraocular pressure was measured by Goldmann applanation tonometry in 42 patients with cataracts and outflow facility was determined by tonography preoperatively, before and after instillation of pilocarpine. All patients received clear corneal phacoemulsification and silicone foldable intraocular lens implantation within the capsular bag by one surgeon. Two months after surgery, slit lamp examination and gonioscopy were performed and intraocular pressure and outflow facility were again determined. Statistical analysis was carried out using the Student's paired t test. RESULTS: There were no anterior chamber reactions and no visible trabecular meshwork damage 2 months after surgery. Intraocular pressure 2 months after lens extraction decreased by a mean of 2.4 (SE 0.4) mm Hg (p<0.001) compared with the preoperative value; postoperative outflow facility with and without pilocarpine increased by 0.080 (0.019) microl/min/mm Hg (p<0.001) and 0.045 (0.014) microl/min/mm Hg (p<0.001), respectively, at 2 months compared with preoperative values. The facility response to pilocarpine after lens extraction, relative to the baseline value and preoperative response, increased by 10.7 (7.1)% which was not statistically significant (p>0.1). CONCLUSION: Lens extraction causes a reduction in intraocular pressure and an increase in outflow facility in Korean subjects. Pilocarpine causes an increase in outflow facility which persists after cataract extraction and posterior chamber lens implantation. (+info)Miotics, also known as parasympathomimetics or cholinergic agents, are a class of medications that stimulate the parasympathetic nervous system. They work by activating muscarinic receptors, which are found in various organs throughout the body, including the eye. In the eye, miotics cause contraction of the circular muscle of the iris, resulting in pupillary constriction (miosis). This action can help to reduce intraocular pressure in patients with glaucoma.
Miotics may also have other effects on the eye, such as accommodation (focusing) and decreasing the production of aqueous humor. Some examples of miotics include pilocarpine, carbachol, and ecothiopate. It's important to note that the use of miotics can have side effects, including blurred vision, headache, and brow ache.
Miosis is the medical term for the constriction or narrowing of the pupil of the eye. It's a normal response to close up viewing, as well as a reaction to certain drugs like opioids and pilocarpine. Conversely, dilation of the pupils is called mydriasis. Miosis can be also a symptom of certain medical conditions such as Horner's syndrome or third cranial nerve palsy.
A pupil, in medical terms, refers to the circular opening in the center of the iris (the colored part of the eye) that allows light to enter and reach the retina. The size of the pupil can change involuntarily in response to light intensity and emotional state, as well as voluntarily through certain eye exercises or with the use of eye drops. Pupillary reactions are important in clinical examinations as they can provide valuable information about the nervous system's functioning, particularly the brainstem and cranial nerves II and III.
Arecoline is a parasympathomimetic alkaloid that is the primary active component found in the areca nut, which is chewed for its psychoactive effects in various parts of the world. It can cause stimulation of the nervous system and has been associated with several health risks, including oral cancer and cardiovascular disease.
The medical definition of Arecoline is:
A parasympathomimetic alkaloid found in the areca nut, which is chewed for its psychoactive effects. It stimulates the nervous system and has been associated with several health risks, including oral cancer and cardiovascular disease. The chemical formula for Arecoline is C7H9NO2.
A pupillary reflex is a type of reflex that involves the constriction or dilation of the pupils in response to changes in light or near vision. It is mediated by the optic and oculomotor nerves. The pupillary reflex helps regulate the amount of light that enters the eye, improving visual acuity and protecting the retina from excessive light exposure.
In a clinical setting, the pupillary reflex is often assessed as part of a neurological examination. A normal pupillary reflex consists of both direct and consensual responses. The direct response occurs when light is shone into one eye and the pupil of that same eye constricts. The consensual response occurs when light is shone into one eye, causing the pupil of the other eye to also constrict.
Abnormalities in the pupillary reflex can indicate various neurological conditions, such as brainstem injuries or diseases affecting the optic or oculomotor nerves.
Sarin is a potent and deadly nerve agent, a type of organic compound called a phosphoro-organic fluid. It is a colorless, odorless, and tasteless liquid, which is also known as GB. Sarin is a human-made chemical warfare agent that is considered a weapon of mass destruction and is banned under the Chemical Weapons Convention of 1993.
Sarin works by inhibiting the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the body. This leads to an overaccumulation of acetylcholine at the neuromuscular junctions and synapses, causing uncontrolled muscle contractions, paralysis, respiratory failure, and ultimately death if not treated promptly.
Exposure to Sarin can occur through inhalation, skin contact, or ingestion. Symptoms of exposure include runny nose, tightness in the chest, difficulty breathing, nausea, vomiting, diarrhea, blurred vision, and confusion. Immediate medical attention is required for anyone exposed to Sarin, as antidotes such as atropine and pralidoxime can be administered to counteract its effects.
Mydriatics are medications that cause mydriasis, which is the dilation of the pupil. These drugs work by blocking the action of the muscarinic receptors in the iris, leading to relaxation of the circular muscle and constriction of the radial muscle, resulting in pupil dilation. Mydriatics are often used in eye examinations to facilitate examination of the interior structures of the eye. Commonly used mydriatic agents include tropicamide, phenylephrine, and cyclopentolate. It is important to note that mydriatics can have side effects such as blurred vision, photophobia, and accommodation difficulties, so patients should be advised accordingly.
Pilocarpine is a cholinergic agonist, which means it stimulates the parasympathetic nervous system by binding to muscarinic receptors. It is primarily used in the treatment of dry mouth (xerostomia) caused by radiation therapy or Sjögren's syndrome, as well as in the management of glaucoma due to its ability to construct the pupils and reduce intraocular pressure. Pilocarpine can also be used to treat certain cardiovascular conditions and chronic bronchitis. It is available in various forms, including tablets, ophthalmic solutions, and topical gels.
Parasympathomimetics are substances or drugs that mimic the actions of the parasympathetic nervous system. The parasympathetic nervous system is one of the two branches of the autonomic nervous system, which regulates involuntary physiological functions. It is responsible for the "rest and digest" response, and its neurotransmitter is acetylcholine.
Parasympathomimetic drugs work by either directly stimulating muscarinic receptors or increasing the availability of acetylcholine in the synaptic cleft. These drugs can have various effects on different organs, depending on the specific receptors they target. Some common effects include decreasing heart rate and contractility, reducing respiratory rate, constricting pupils, increasing glandular secretions (such as saliva and sweat), stimulating digestion, and promoting urination and defecation.
Examples of parasympathomimetic drugs include pilocarpine, which is used to treat dry mouth and glaucoma; bethanechol, which is used to treat urinary retention and neurogenic bladder; and neostigmine, which is used to treat myasthenia gravis and reverse the effects of non-depolarizing muscle relaxants.
Quinuclidines are a class of organic compounds that contain a unique cage-like structure consisting of a tetrahydrofuran ring fused to a piperidine ring. The name "quinuclidine" is derived from the Latin word "quinque," meaning five, and "clidis," meaning key or bar, which refers to the five-membered ring system that forms the core of these compounds.
Quinuclidines have a variety of biological activities and are used in pharmaceuticals as well as agrochemicals. Some quinuclidine derivatives have been found to exhibit anti-inflammatory, antiviral, and anticancer properties. They can also act as inhibitors of various enzymes and receptors, making them useful tools for studying biological systems and developing new drugs.
It is worth noting that quinuclidines are not typically used in medical diagnosis or treatment, but rather serve as building blocks for the development of new pharmaceutical compounds.
In medical terms, the iris refers to the colored portion of the eye that surrounds the pupil. It is a circular structure composed of thin, contractile muscle fibers (radial and circumferential) arranged in a regular pattern. These muscles are controlled by the autonomic nervous system and can adjust the size of the pupil in response to changes in light intensity or emotional arousal. By constricting or dilating the iris, the amount of light entering the eye can be regulated, which helps maintain optimal visual acuity under various lighting conditions.
The color of the iris is determined by the concentration and distribution of melanin pigments within the iris stroma. The iris also contains blood vessels, nerves, and connective tissue that support its structure and function. Anatomically, the iris is continuous with the ciliary body and the choroid, forming part of the uveal tract in the eye.
Ophthalmic solutions are sterile, single-use or multi-dose preparations in a liquid form that are intended for topical administration to the eye. These solutions can contain various types of medications, such as antibiotics, anti-inflammatory agents, antihistamines, or lubricants, which are used to treat or prevent ocular diseases and conditions.
The pH and osmolarity of ophthalmic solutions are carefully controlled to match the physiological environment of the eye and minimize any potential discomfort or irritation. The solutions may be packaged in various forms, including drops, sprays, or irrigations, depending on the intended use and administration route.
It is important to follow the instructions for use provided by a healthcare professional when administering ophthalmic solutions, as improper use can lead to eye injury or reduced effectiveness of the medication.
Intraocular pressure (IOP) is the fluid pressure within the eye, specifically within the anterior chamber, which is the space between the cornea and the iris. It is measured in millimeters of mercury (mmHg). The aqueous humor, a clear fluid that fills the anterior chamber, is constantly produced and drained, maintaining a balance that determines the IOP. Normal IOP ranges from 10-21 mmHg, with average values around 15-16 mmHg. Elevated IOP is a key risk factor for glaucoma, a group of eye conditions that can lead to optic nerve damage and vision loss if not treated promptly and effectively. Regular monitoring of IOP is essential in diagnosing and managing glaucoma and other ocular health issues.
Glaucoma is a group of eye conditions that damage the optic nerve, often caused by an abnormally high pressure in the eye (intraocular pressure). This damage can lead to permanent vision loss or even blindness if left untreated. The most common type is open-angle glaucoma, which has no warning signs and progresses slowly. Angle-closure glaucoma, on the other hand, can cause sudden eye pain, redness, nausea, and vomiting, as well as rapid vision loss. Other less common types of glaucoma also exist. While there is no cure for glaucoma, early detection and treatment can help slow or prevent further vision loss.
Cholinesterase inhibitors are a class of drugs that work by blocking the action of cholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine in the body. By inhibiting this enzyme, the levels of acetylcholine in the brain increase, which can help to improve symptoms of cognitive decline and memory loss associated with conditions such as Alzheimer's disease and other forms of dementia.
Cholinesterase inhibitors are also used to treat other medical conditions, including myasthenia gravis, a neuromuscular disorder that causes muscle weakness, and glaucoma, a condition that affects the optic nerve and can lead to vision loss. Some examples of cholinesterase inhibitors include donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon).
It's important to note that while cholinesterase inhibitors can help to improve symptoms in some people with dementia, they do not cure the underlying condition or stop its progression. Side effects of these drugs may include nausea, vomiting, diarrhea, and increased salivation. In rare cases, they may also cause seizures, fainting, or cardiac arrhythmias.
Miotic - Ophtechnics Unlimited
Physostigmine
-
Cholinesterase Inhibitors, Miotics, ATC:S01EB05, ATC:V03AB19
Glaucoma Treatments: Eye Drops, Lasers, Surgery
Diagnostic Tests Pertaining to Ocular Medications in Animals - Pharmacology - Merck Veterinary Manual
Miotic & Aneshetic Solution - Carbachol Intraocular Solution Exporter from Gurgaon
Penetrating Keratoplasty and Glaucoma (PKPG): Practice Essentials, Epidemiology, Etiology
I'm Allergic to My Glaucoma Eye Drops. Is This Common? | glaucoma.org
Cataract - Wikipedia
Overview - HealthyWomen
Phospholine Iodide Dosage Guide - Drugs.com
Carteolol Hydrochloride Ophthalmic Solution USP, 1% (Bausch & Lomb), Drug Reference Encyclopedia
DailyMed - BENZTROPINE MESYLATE tablet
NCLEX Quiz: Take The Trivia Test On Eye Disorders And care! - ProProfs Quiz
Strabismus - StatPearls - NCBI Bookshelf
2020-2021 BCSC Basic and Clinical Science Course™
Side Effects Of Hydrocodone-acetaminophen | DrugAbuse.com
Buy Isopto Carpine Eye Drops - Best Prices Online | Canada Pharmacy
Tudorza Pressair (Aclidinium Bromide): Uses, Dosage, Side Effects, Interactions, Warning
News Releases
What is Presbyopia? Symptoms & Treatment | Warby Parker
Rex Parker Does the NYT Crossword Puzzle: August 2011