title: [Primary open angle glaucoma. Morphological bases for the understanding of the pathogenesis and effects of antiglaucomatic substances].
abstract: The pathogenesis of glaucomatic illnesses is poorly understood. An increase in ocular pressure can be caused by an increase in the secretion of aqueous humour or a reduction in its outflow. In the elderly, outflow is reduced while at the same time less aqueous humour is produced. This balance is easily disturbed, so that age represents a risk factor for glaucoma in addition to increased ocular pressure. Therapeutic possibilities involve, on the one hand, reducing the secretion of aqueous humour, for example using, beta blockers, carbonic anhydrase inhibitors and clonidine. On the other hand, aqueous humour outflow can also be influenced by drugs. Conventional outflow is increased by the administration of miotics. The uveoscleral outflow can be increased by prostaglandin derivates. Drugs which only influence trabecular outflow are not yet available. Future therapeutic possibilities involve new aspects of the pathophysiology, e.c. the use of growth factors, free radical scavenging enzymes and choroidal blood flow.
authors.affiliation: Institut für Anatomie, Lehrstuhl II, Universität Erlangen-Nürnberg, 91054, Erlangen, Germany. anat2.gl@anatomie2.med.uni-erlangen.de
authors.forename: E
authors.initials: E
authors.lastname: Lütjen-Drecoll
authors.forename: F E
authors.initials: FE
authors.lastname: Kruse
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000627:therapeutic use; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000367:Age Factors; D001082:Aqueous Humor / Q000378:metabolism; D002257:Carbonic Anhydrase Inhibitors / Q000627:therapeutic use; D002829:Choroid / Q000098:blood supply / Q000473:pathology; D002924:Ciliary Body / Q000648:ultrastructure; D003000:Clonidine / Q000627:therapeutic use; D005123:Eye / Q000098:blood supply / Q000473:pathology; D005544:Forecasting; D005902:Glaucoma, Open-Angle / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007150:Immunohistochemistry; D007429:Intraocular Pressure; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D008916:Miotics / Q000627:therapeutic use; D009882:Ophthalmic Nerve / Q000473:pathology; D010277:Parasympathomimetics / Q000627:therapeutic use; D011453:Prostaglandins / Q000627:therapeutic use; D012307:Risk Factors
chemical_list: D000316:Adrenergic alpha-Agonists; D000319:Adrenergic beta-Antagonists; D002257:Carbonic Anhydrase Inhibitors; D008916:Miotics; D010277:Parasympathomimetics; D011453:Prostaglandins; D003000:Clonidine