Glaucoma is one of the most common causes of blindness in the industrialized nations. For a long time glaucoma has been defined as a disease in which high intraocular pressure (IOP) leads to irreversible optic disc damage and subsequent visual field loss. However, recent investigations show that IOP is not the only factor that is involved in the glaucomatous process leading to retinal ganglion cell death. The role of vascular factors in the pathogenesis of glaucoma has recently received much attention based on animal experiments and epidemiological studies. The main focus of glaucoma is still directed towards a decrease in IOP. There is, however, also considerable interest whether antiglaucoma drugs influence ocular perfusion. Although measurement of ocular blood flow is still difficult, a number of innovative techniques have been realized which cover different aspects of ocular perfusion. In the present study Xalacom® (latanoprost/timolol) and the fixed combination of Combigan® (brimonidine/timolol) will be compared with respect to their IOP lowering efficacy as well as their ocular hemodynamic effects.

Inclusion Criteria:

• Men and women over 18 years
• Unilateral or bilateral primary open angle glaucoma, ocular hypertension, exfoliation glaucoma, pigmentary glaucoma with IOP between 22 -35mmHg
• At least 3 reliable visual field testings
• 4 weeks for ß adrenergic receptor antagonists and prostaglandin analogues, 2 weeks for adrenergic agonists, and 5 days for cholinergic agonists and carbonic anhydrase inhibitors

Exclusion Criteria:

• History of acute angle closure
• Closed or barely open anterior chamber angle
• Mean deviation of visual field testing > 10
• Intraocular surgery or argon laser trabeculoplasty within the last six months
• Ocular inflammation or infection within the last three months
• Contact lenses
• Patients with bradycardia (heart rate < 50 beats/min)
• Second and third degree heart block
• Asthma
• COPD
• Congestive heart failure
• Severe renal impairment (creatinine clearance < 1.8 L/h)
• History of hypersensitivity to one of the study drugs or drugs with similar chemical structure
• Topical or systematically/oral therapy with steroids
• History of non-IOP responder to beta-blockers, alpha-2 adrenergic or prostaglandin analogues
• Pregnancy