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Autonomic Drugs in the Treatment of Canine and Feline Glaucoma – Part I: Medications That Lower Intraocular Pressure by Increasing the Outflow of Aqueous Humour

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Autonomic Drugs in the Treatment of Canine and Feline Glaucoma – Part I: Medications That Lower Intraocular Pressure by Increasing the Outflow of Aqueous Humour Polish Journal of Veterinary Sciences Vol. 17, No. 4 (2014), 741–752 DOI 10.2478/pjvs-2014-0110 Review Autonomic drugs in the treatment of canine and feline glaucoma – Part I: Medications that lower intraocular pressure by increasing the outflow of aqueous humour T. Maślanka Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Warmia and Mazury, Oczapowskiego 13, 10-718 Olsztyn, Poland Abstract One characteristic of the most common types of glaucoma is increased intraocular pressure (IOP), which has a damaging effect on optic nerve axons, leading to progressive loss of retinal ganglion cells. Therefore, ocular hypotensive drugs are the mainstay of pharmacological therapy for glaucoma. This review article, which is the first part of a two-part series, is dedicated to autonomic drugs which lower IOP by increasing the outflow of aqueous humour. These agents are subdivided into two groups: (a) drugs that lower IOP by increasing the trabecular outflow and the uveoscleral outflow (i.e. nonselective adrenergic agonists), and (b) medications that lower IOP by opening of the drainage angle and by increasing the conventional outflow via the trabecular outflow (i.e. parasym- pathomimetics). This paper summarizes the current state of knowledge on the mechanism of action of these drugs and their effect on IOP in dogs and cats. Moreover, it discusses possible undesirable side effects of these medications and presents the current ideas about their role and position in the medical management of glaucoma in small animals. Key words: glaucoma, IOP, adrenergic agonists, parasympathomimetics, dogs, cats Introduction therefore widely considered a neurodegenerative disease (McLellan and Miller 2011). The „Glaucoma” is not a single entity. It refers to pathophysiological process of glaucomatous optic a group of ocular disorders; as these disorders have neuropathy is not fully understood, but it is likely to diverse features, perhaps „the glaucomas” as a plural be a multifactorial event. An increase in intraocular would be better (Casson et al. 2012). In all species, pressure (IOP) is the principal risk factor for glau- this group of disorders is unified in their final com- coma, and the primary goal of treatment is to reduce mon pathway of characteristic optic nerve and retinal IOP to values that will halt the death of retinal gan- pathology resulting in the loss of vision. Glaucoma is glion cells (Smith et al. 2010). Pathologic elevation of Correspondence to: T. Maślanka, e-mail: [email protected], tel.: +48 89 523 37 58 Unauthenticated Download Date | 3/31/15 6:15 PM 742 where along itsof course the from aqueous theIOP humour is posterior the (AH) consequence chamber of flow obstruction or or misdirection outflow any- administration. Fig. 1. Proposed classification of drugs used clinically to reduce IOP according to their way of action, target site and route of Ocular Agents that increase Agents that reduce hypotensive aqueous humor outflow: aqueous humor production agents via the uveoscleral via the trabecular via opening pathway pathway of the drainage angle Download Date|3/31/15 6:15PM Parasympathomimetics b Selective Prostaglandin Nonselective Osmotic Carbonic -adrenergic Selective Unauthenticated a F a analogues agents antagonists a 2-adrenergic 2 adrenergic s anhydrase 2-adrenergic agonists agonists inhibitors agonists nous plexus (Grahn andtrabecular Peiffer meshwork 2007). (TM), Elevated IOP through and into the the pupil scleral into ve- the ciliary cleft, across the – brimonidine – latanoprost – epinephrine Direct-acting: – dorzolamide – timolol – apraclonidine – travoprost – dipivefrin – pilocarpine – brinzolamide – levobunolol – brimonidine Topical agents – bimatoprost – carbachol – metipranolol – tafluprost Indirect-acting: – carteolol – demecarium – betaxolol – echothiophate iodide – isofluorophate Systemic agents – mannitol – acetazolamide – urea – methazolamid – glycerol – dichlorphenamide – isosorbide T. Maślanka Autonomic drugs in the treatment of canine and feline glaucoma – Part I... 743 Narrow/closed-angle glaucoma Primary angle closure glaucoma Secondary angle closure glaucoma (PACG) (SACG) Secondary closed-angle Secondary closed-angle glaucoma with an anterior glaucoma with a posterior pulling mechanism pushing mechanism With pupill block Without pupill block Congenital failure Abnormalities in the – Epithelial downgrowth – Posterior synechiae to lens – Cysts of the iris and in the development conformation of the into anterior chamber (iris bombe), vitreous, or IOL ciliary body of the pectinate eye's anterior segment – Fibrovascular – Lens-induced (intumescent – Forward vitreous ligament (shallow anterior proliferation over angle cataract, subluxation of lens) shift after lens (goniodysgenesis) chamber, plateau iris – Inflammatory induced – Miotic-induced extraction configuration and (peripheral anterior – Vitreous herniation with – Intraocular tumors increased lens synechiae) aphakia/displaced lens thickness) – Inflammatory membranes – Ciliary body-vitreous-lens – Pigment proliferation in block (aqueous humor the angle with obstruction misdirection) Open-angle glaucoma Primary open-angle glaucoma Secondary open-angle glaucoma (POAG) (SOAG) Pretrabecular form Trabecular form Posttrabecular form „Clogging’’ of TM with: Alterations of TM Disturbances in TM Anterior luxated lens – Erythrocytes and fibrin / – Scarring and/or – Episcleral vein glycosaminoglycan and may block the aqueous Hemorrhagic glaucoma sclerosis obstructions glycoprotein synthesis humor's access to the – Pigment particles / – Edema – Scleral outlet and degradation (?) outflow pathways of Pigmentary glaucoma (trabeculitis) channel the drainage angle – Inflammatory cellular obstructions debris and fibrin (without – Angular aqueous developing synechiae) / plexus obstructions Inflammatory glaucoma – Neoplastic cells Fig. 2. Proposed classification of glaucoma in small animals. almost invariably is the result of impaired AH outflow system (Brooks et al. 1997) and aberrations in immun- (Miller 2008). Separately or in addition to IOP, other ity (Schwartz 2003)] can contribute to death of retinal factors [such as dysfunction of ocular blood-flow regu- ganglion cells (Greller et al. 2008). lation with local ischemia-hypoxia (Flammer and Or- The ultimate goal of glaucoma therapy is to delay gul 1998), excessive stimulation of the glutamatergic or stop or sometimes reverse the glaucomatous Unauthenticated Download Date | 3/31/15 6:15 PM 744 T. Maślanka changes to the optic nerve and ganglion cell layer discussed drugs, the paper also contains basic infor- caused by raised IOP. Current pharmacological mation about AH dynamics and the classification of treatment of glaucoma focuses on indirect protection veterinary glaucomas (Fig. 2). of the optic nerve, i.e. through IOP lowering. There are two ways to lower IOP: surgical and pharmacol- ogical treatment. Pharmacological treatment means Aqueous humor dynamics topical and/or systemic application of ocular hypo- tensive drugs. There are two principal ways to reduce AH is formed in the ciliary processes from arter- IOP pharmacologically: by lowering AH formation ial blood. Three mechanisms are involved in its for- and by increasing AH outflow. Although some ocular mation: diffusion, ultrafiltration and active secretion. hypotensivedrugsarelikelytodepressIOPbyaffect- The first two processes are passive and do not entail ing both AH formation and outflow, based on the active cellular participation. Active secretion is dominant way of action they are divided into: (a) thought to be the major contributor to AH forma- those that reduce AH production [i.e. carbonic an- tion, responsible for approximately 80% to 90% of hydrase inhibitors (CAIs), β-adrenergic antagonists, the total AH formation (Goel et al. 2010). After en- and selective α2-adrenergic agonists], (b) those that tering the anterior chamber via the pupil, the AH is increase AH outflow [i.e. nonselective adrenergic drainedbytwodifferentpathways,bothlocatedin agonists, parasympathomimetics, and prostaglandin the iridocorneal angle (also known as drainage or F2α analogues (PGAs)], and (c) those that dehyd- filtration angle): ratate the intraocular space via osmotic gradient (al- – The trabecular outflow (also known as con- though these agents also enhance the outflow of AH ventional outflow) is the drainage of AH sequen- and most probably reduce AH formation, they are tially through the ciliary cleft, the trabecular mesh- traditionally distinguished as a separate group). Fur- work, Schlemm’s canal, collector channels, episcleral ther classification of ocular hypotensive drugs relies veins, anterior ciliary veins and into the systemic cir- on their target site (e.g. selective α2-adrenergic agon- culation (Nilsson 1997). This pathway has been de- ists), the way in which they increase the AH outflow termined to be „pressure-dependent”; elevations in and the route of administration (Fig. 1). IOP cause a large difference in pressure between the It is worth mentioning that literature data anterior chamber and the episcleral vasculature, indicate large inter-species differences in the clinical leading to a proportional increase in outflow through efficacy of topical ocular hypotensive drugs in the TM (Barrie et al. 1985). The trabecular pathway therapy of human, canine and feline glaucomas. The represents the main outflow route in the mammalian major reasons are most probably species- and eye. breed-related differences in (a)
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