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    • Basic and Clinical Science Course - Excerpt
  • 2020–2021 BCSC Basic and Clinical Science Course™

    Go to Academy Store Learn more and Purchase.

    2 Fundamentals and Principles of Ophthalmology

    Part V: Ocular Pharmacology

    Chapter 16: Ocular Pharmacotherapeutics*

    Adrenergic Drugs

    Several ophthalmic medications affect the activity of adrenergic receptors (also called adrenoceptors) in synapses of the peripheral nervous system. These receptors are found in

    • the cell membranes of the iris dilator muscle, the superior palpebral smooth muscle of Müller, the ciliary epithelium and processes, the trabecular meshwork, and the smooth muscle of ocular blood vessels (supplied by postganglionic autonomic fibers from the superior cervical ganglion)

    • the presynaptic terminals of some sympathetic and parasympathetic nerves, where the receptors have feedback-inhibitory actions

    Although adrenergic receptors were originally defined by their response to epinephrine (adrenaline), the transmitter of most sympathetic postganglionic fibers is actually norepinephrine. Adrenergic receptors are subclassified into 5 categories—α1, α2, β1, β2, and β3—on the basis of their profile of responses to natural and synthetic catecholamines (Fig 16-4). α1-Receptors generally mediate smooth muscle contraction, whereas α2-receptors mediate feedback inhibition of presynaptic sympathetic (and sometimes parasympathetic) nerve terminals. β1-Receptors are found predominantly in the heart, where they mediate stimulatory effects; β2-receptors mediate relaxation of smooth muscle in most blood vessels and in the bronchi, whereas β3-receptors are found on fat cells mediating lipolysis.

    Table 16-6 Cholinergic Antagonists

    Figure 16-4 A, Major effects mediated by α-and β-adrenoceptors. B, Actions of propranolol and β1-blockers.

    (Reproduced with permission from Mycek MJ, Harvey RA, Champe PC, eds. Pharmacology. 2nd ed. Lippincott’s Illustrated Reviews. Philadelphia: Lippincott-Raven; 1997:60, 75.)

    Adrenergic drugs may be direct-acting agonists, indirect-acting agonists, or antagonists at one or more of the 5 types of receptors. Systemic absorption of ocular adrenergic drugs is frequently sufficient to cause systemic effects, which are manifested in the cardiovascular system, the bronchial airways, and the brain.

    α-Adrenergic Drugs

    Direct-acting α1-adrenergic agonists

    The primary clinical use of direct-acting α1-adrenergic agonists, such as phenylephrine, is stimulation of the iris dilator muscle to produce mydriasis. Because the parasympathetically innervated iris sphincter muscle is much stronger than the dilator muscle, the dilation achieved with phenylephrine alone is largely overcome by the pupillary light reflex during ophthalmoscopy. Co-administration of a cycloplegic drug allows sustained dilatation.

    Systemic absorption of phenylephrine may elevate systemic blood pressure. This effect is clinically significant if the patient is an infant or has an abnormally increased sensitivity to α-agonists, which occurs with orthostatic hypotension and in association with the use of drugs that accentuate adrenergic effects (eg, reserpine, tricyclic antidepressants, cocaine, monoamine oxidase [MAO] inhibitors—discussed later). Even with lower doses of phenylephrine (2.5%), infants may exhibit a transient rise in blood pressure because the dose received in an eyedrop is high for their weight.

    Phenylephrine, 10%, should be used cautiously, particularly in pledget application and in patients with vasculopathic risk factors. A 10% solution contains 5 mg of drug per drop, and ocular medications passing through the canalicular system are available for systemic absorption through the vascular nasal mucosa (see Chapter 15). In contrast, the typical systemic dose of phenylephrine for hypotension is 50–100 µg given all at once. The ophthalmic use of phenylephrine, 10%, has been associated with stroke, myocardial infarction, and cardiac arrest. Vascular baroreceptors are particularly sensitive to phenylephrine. An increase in blood pressure after topical application may therefore cause a significant drop in pulse rate that can be particularly dangerous in an individual with vasculopathy who is already taking a β-blocking medication for systemic effect.

    Intracameral use of phenylephrine to maintain dilatation during cataract surgery has recently been evaluated. The compound Omidria (phenylephrine 1%/ketorolac 0.3%) is added to the irrigating solution and has been approved by the FDA to prevent miosis during cataract surgery and prevent postoperative pain. One study recently demonstrated the efficacy of this compound for management of intraoperative floppy iris syndrome (IFIS) in patients taking tamsulosin.

    • Hovanesian JA, Sheppard JD, Trattler WB, et al. Intracameral phenylephrine and ketorolac during cataract surgery to maintain intraoperative mydriasis and reduce postoperative ocular pain: integrated results from 2 pivotal phase 3 studies. J Cataract Refract Surg. 2015;41(10):2060–2068.

    • Silverstein SM, Rana VK, Stephens R, et al. Effect of phenylephrine 1.0%-ketorolac 0.3% injection on tamsulosin-associated intraoperative floppy-iris syndrome. J Cataract Refract Surg. 2018;44(9):1103–1108.

    α2-Adrenergic agonists

    Apraclonidine hydrochloride (para-aminoclonidine) is a selective α2-adrenergic agonist and a clonidine derivative that prevents release of norepinephrine at nerve terminals (Tables 16-7, 16-8). It decreases aqueous production as well as episcleral venous pressure and improves trabecular outflow. However, its true ocular hypotensive mechanism is not fully understood. When administered preoperatively and postoperatively, the drug effectively diminishes the acute increase in IOP that follows argon laser iridotomy, argon or selective laser trabeculoplasty, Nd:YAG laser capsulotomy, and cataract extraction (see BCSC Section 10, Glaucoma, for additional information on apraclonidine). Apraclonidine hydrochloride may be effective for the short-term reduction of IOP, but the development of topical sensitivity and tachyphylaxis often limits its long-term use.

    Ligand binding to α2-receptors in other systems mediates inhibition of the enzyme adenylate cyclase. adenylate cyclase is present in the ciliary epithelium and is thought to have a role in aqueous production.

    Table 16-7 Adrenergic Agonists

    Table 16-8 Mode of Action of Antiglaucoma Drugs That Act Through Receptors

    Apraclonidine can also be used to diagnose Horner syndrome, characterized by denervation hypersensitivity of the α1-receptors in the iris. Under normal conditions, as a weak α1-adrenergic agonist, apraclonidine has no effect on pupil dilation; however, in cases of Horner syndrome, instillation of the drug results in dilation of the affected pupil (see BCSC Section 5, Neuro-Ophthalmology, for additional information on the role of apraclonidine in the diagnosis of Horner syndrome).

    Brimonidine tartrate is another selective α2-adrenergic agonist. Compared with apraclonidine, brimonidine tartrate is more α2 selective, is more lipophilic, and causes less tachyphylaxis during long-term use. The rate of reactions, such as follicular conjunctivitis and contact blepharodermatitis, is also lower (less than 15% for brimonidine but up to 40% for apraclonidine). Cross-sensitivity to brimonidine in patients with known hypersensitivity to apraclonidine is minimal.

    Brimonidine’s mechanism in lowering IOP is thought to involve both decreased aqueous production and increased uveoscleral outflow. As with β-blockers, a central mechanism of brimonidine, 0.2%, may account for some IOP reduction: A 1-week trial of treatment in a single eye caused a statistically significant reduction of 1.2 mm Hg in the fellow eye.

    The peak IOP reduction with brimonidine is approximately 26%. At peak (2 hours postdose), its IOP reduction is comparable to that of a nonselective β-blocker and superior to that of the selective β-blocker betaxolol; however, at trough (12 hours postdose), the reduction is only 14%–15%, which makes brimonidine at trough less effective than the nonselective β-blockers but comparable to betaxolol.

    As shown in animal models of optic nerve and retinal injuries, brimonidine may have neuroprotective properties that are independent of IOP reduction. The proposed mechanism of neuroprotection is upregulation of a neurotrophin, basic fibroblast growth factor, and cellular regulatory genes.

    In addition to brimonidine, 0.2%, preserved with benzalkonium chloride, a 0.15% solution preserved with polyquaternium-1 and 0.15% and 0.1% solutions preserved with sodium chlorite are available. Brimonidine tartrate, 0.15%, is comparable to brimonidine, 0.2%, when given 3 times daily.

    Ophthalmologists should exercise caution when using apraclonidine or brimonidine in patients taking MAO inhibitors or tricyclic antidepressants and in patients with severe cardiovascular disease. Use of these drugs concomitantly with β-blockers (ophthalmic and systemic), antihypertensives, and cardiac glycosides also requires prudence.

    Though effective for rapid lowering of IOP in angle-closure glaucoma, these drugs may also induce vasoconstriction that can prolong iris sphincter ischemia and reduce the efficacy of concurrent miotics. Apraclonidine has a much greater affinity for α1-receptors than does brimonidine and is therefore more likely to produce vasoconstriction in the eye. Brimonidine does not induce vasoconstriction in the posterior segment or the optic nerve.

    Because brimonidine is more lipophilic than apraclonidine, its penetration of the blood–brain barrier is presumably higher. Central nervous system (CNS) adverse effects include fatigue and drowsiness.

    CLINICAL PEARL

    Severe systemic toxicity, with hypotension, hypothermia, and bradycardia, has been reported in infants treated with topical ocular brimonidine. As a result, this drug is contraindicated in infants and should be used with caution in young children.

    Indirect-acting adrenergic agonists

    Indirect-acting adrenergic agonists (cocaine, 4% or 10%, and hydroxyamphetamine, 1%, currently available only through compounding pharmacies) are used to test for and localize defects in sympathetic innervation to the iris dilator muscle. Normally, pupil response fibers originating in the hypothalamus pass down the spinal cord to synapse with cells in the intermediolateral columns. In turn, preganglionic fibers exit the cord through the anterior spinal roots in the upper thorax to synapse in the superior cervical ganglion in the neck. Finally, postganglionic adrenergic fibers terminate in a neuroeffector junction with the iris dilator muscle. The norepinephrine released is inactivated primarily by reuptake into secretory granules in the nerve terminal (Fig 16-5). Approximately 70% of released norepinephrine is recaptured (see the discussion of Horner syndrome in BCSC Section 5, Neuro-Ophthalmology).

    Antagonists

    Thymoxamine hydrochloride (moxisylyte), an α1-adrenergic blocking agent, acts by competitively inhibiting norepinephrine at the receptor site. Thymoxamine inhibits α-adrenergic receptors of the dilator muscle of the iris and causes pupil constriction; however, it has no significant effect on ciliary muscle contraction and therefore does not induce substantial changes in anterior chamber depth, facility of outflow, IOP, or accommodation in POAG. In patients with an increase in IOP secondary to primary angle closure, thymoxamine may widen the peripheral angle and reduce IOP. Thymoxamine is useful in differentiating angle-closure glaucoma from POAG with narrow angles and in reversing the pupil dilation caused by phenylephrine. This drug is not commercially available in the United States, although it has been widely used in Europe for years.

    Dapiprazole hydrochloride (no longer available in the United States) is an α-adrenergic blocking agent that reverses, in 30 minutes, the mydriasis produced by phenylephrine and tropicamide but not by cycloplegics. It affects the dilator muscle but not ciliary muscle contraction (anterior chamber depth, facility of outflow, or accommodation).

    Excerpted from BCSC 2020-2021 series: Section 2 - Fundamentals and Principles of Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.

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