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Pilocarpine
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Pilocarpine is a natural alkaloid extracted from plants of the genus Pilocarpus with cholinergic agonist activity. As a cholinergic parasympathomimetic agent, it predominantly binds to muscarinic receptors, thereby inducing exocrine gland secretion and stimulating smooth muscle in the bronchi, urinary tract, biliary tract, and intestinal tract. When applied topically to the eye, this agent stimulates the sphincter pupillae to contract, resulting in miosis. It also stimulates the ciliary muscle to contract, resulting in spasm of accommodation and may cause a transitory rise in intraocular pressure followed by a more persistent fall due to opening of the trabecular meshwork and an increase in the outflow of aqueous humor. Pilocarpine is indicated for the treatment of radiation-induced dry mouth (xerostomia) and symptoms of dry mouth in patients with Sjögren’s syndrome. It is also used as a miotic in the treatment of glaucoma. In pharmaceutical products, pilocarpine is employed as pilocarpine hydrochloride (CAS number 54-71-7, EC number 200-212-5, molecular formula C11H17CIN2O2) (1).
Peripheral Autonomic Neuropathies
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
The treatment of diabetic cystopathy includes use of an indwelling catheter for 10 days together with appropriate antibiotics. Thereafter, the patient should void every 3 h, aided by manual compression of the suprapubic area (Crede manoeuvre) and receive parasympathomimetic drugs. About 40% of patients respond to this therapy, at least temporarily, until urinary tract infection recurs. Transurethral surgery and bladder neck resection in those without obvious mechanical obstruction may also be useful. Initially, the parasympathomimetic drug can be given parenterally, for example, bethanechol twice weekly and may be continued orally in a dose of 40-50 mg every 6 or 8 h. Cholinergic treatment is withdrawn when residual volumes are less than 100 ml for at least a week (Ellenberg, 1980a).
Current and new pharmacotherapeutic approaches for glaucoma
Published in Expert Opinion on Pharmacotherapy, 2020
Wesam Shamseldin Shalaby, Vikram Shankar, Reza Razeghinejad, L. Jay Katz
Cholinergic agonists improve the outflow of aqueous humor via contraction of smooth muscles within the ciliary body and widening of the trabecular meshwork. Pilocarpine is the most widely used drug in this class, and has been shown to reduce IOP by 20–25% [12,14]. Laboratory studies of retinal neurons in rats suggest a neuroprotective effect of pilocarpine through upregulation of oxidant defense genes; however, no clinical studies support these findings in patients with glaucoma [20]. Historically, cholinergic agents were the first widely used treatments for glaucoma, but have fallen out of favor due to a myriad of local and systemic side effects [14]. Ocular side effects of parasympathomimetics include ciliary spasm, miosis, pseudomyopia, and an increased risk of retinal detachments and pupillary block. A wide array of systemic side effects such as intestinal cramps and bronchospasm have also been reported, commonly resulting in patient intolerance or medication discontinuation [14].
Brimonidine tartrate for the treatment of glaucoma
Published in Expert Opinion on Pharmacotherapy, 2019
Daniel J. Oh, Judy L. Chen, Thasarat S. Vajaranant, Mark S. Dikopf
As a consequence of alpha adrenergic activation in the iris, all generations of topical alpha agonists may alter pupil size. Earlier generations (e.g. apraclonidine) with higher alpha-1 activity led to pupillary mydriasis; however, brimonidine with high alpha-2 selectivity leads to dampening of pupillary mobility and miosis [33,34]. A number of pupillometry studies have demonstrated a moderate miotic effect of various concentrations of brimonidine, as well as an anti-mydriatic effect in scotopic conditions [35–37]. The authors believe that these effects may provide utility in primary angle closure (PAC) and pigmentary dispersion syndrome (PDS). In PAC, contact between the iris and crystalline lens leads to resistance of aqueous outflow from the posterior chamber, anteriorly bowing peripheral iris into the trabecular meshwork (TM). Laser or surgical treatments to relieve this iridolenticular contact are essential, as early relief of contact may prevent irreversible TM damage. When adjunctive medical therapy is employed, brimonidine may be preferable, as the induced miosis may pull peripheral iris from contacting the TM. While parasympathomimetic agents (e.g. pilocarpine) may also provide this benefit, significant ocular and systemic effects arise with parasympathomimetic use, especially in phakic individuals. In PDS, pupillary mobility and contact of the posterior iris and the crystalline lens and zonules leads to shedding of iris pigment. Liberated granules may cause short- or long-term dysfunction of the TM and IOP dysregulation[34]. The limitation of pupillary mobility and induced miosis by brimonidine may be preferable in preventing pigmentary release and lowering IOP, also in lieu of parasympathomimetic agents which have been reported to carry an increased risk of retinal detachment in this population[38].
Neostigmine and ketorolac as adjuvants to local anesthetic through peribulbar block in patients undergoing vitrectomy surgeries: A randomized controlled trial
Published in Egyptian Journal of Anaesthesia, 2022
Mayada K. Mohamad, Norhan A. Sherif, Rehab S. Khattab, Noha A. Osama, Iman S. Aboul Fetouh
Neostigmine is a parasympathomimetic drug that binds to the active side of the acetylcholine esterase enzyme, preventing it from hydrolyzing the acetylcholine molecule, increasing its level at peripheral muscarinic receptors present in peripheral nerve endings, activating cholinergic-mediated antinocieption, and thus prolonging postoperative analgesia. Neostigmine has been co-administered with local anesthetics and other adjuvants in obstetric surgeries [10].