title: Retrobulbar arterial hemodynamic effects of betaxolol and timolol in normal-tension glaucoma.
abstract: OBJECTIVE
  beta-Adrenergic blocking drugs lower intraocular pressure. The question of whether these drugs also alter, either directly or indirectly, orbital hemodynamics is potentially of great importance for patients with normal-tension glaucoma who may have some degree of reversible vasospasm.
  
  
  METHODS
  We compared the effect of selective (betaxolol) and nonselective (timolol) beta-adrenergic blocking drugs on flow velocities (as determined by color Doppler imaging) in orbital vessels in 13 patients with normal-tension glaucoma (mean age, 62 +/- 3 years; mean intraocular pressure, 15 +/- 2 mm Hg). A one-month drug treatment double-masked crossover design, with a three-week washout before each drug, was used.
  
  
  RESULTS
  Neither drug changed peak systolic velocity in any of the four vessels studied (ophthalmic, nasal and temporal posterior ciliary, and central retinal arteries). Additionally, timolol did not alter end-diastolic velocity or resistance index (defined as [peak systolic velocity minus end-diastolic velocity] divided by peak systolic velocity) in any of the vessels measured. In contrast, betaxolol tended to increase end-diastolic velocity and to decrease resistance index: the four-vessel average end-diastolic velocity increased 30% (P = .08), and the four-vessel average resistance index decreased significantly (P = .04). These reductions in resistance index occurred despite that betaxolol, in contrast to timolol, did not significantly decrease intraocular pressure.
  
  
  CONCLUSIONS
  These results suggest that, in patients with normal-tension glaucoma, selective beta-adrenergic blockade (betaxolol) may have ocular vasorelaxant effects independent of any influence on intraocular pressure, whereas nonselective blockade (timolol) lowers intraocular pressure without apparently altering orbital hemodynamics.
authors.affiliation: Department of Ophthalmology, Indiana University School of Medicine, Indianapolis 46202-5175, USA.
authors.forename: A
authors.initials: A
authors.lastname: Harris
authors.forename: G L
authors.initials: GL
authors.lastname: Spaeth
authors.forename: R C
authors.initials: RC
authors.lastname: Sergott
authors.forename: L J
authors.initials: LJ
authors.lastname: Katz
authors.forename: L B
authors.initials: LB
authors.lastname: Cantor
authors.forename: B J
authors.initials: BJ
authors.lastname: Martin
mesh_terms: D001158:Arteries / Q000000981:diagnostic imaging / Q000187:drug effects / Q000502:physiology; D015784:Betaxolol / Q000008:administration & dosage / Q000494:pharmacology*; D001783:Blood Flow Velocity; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005260:Female; D005901:Glaucoma / Q000188:drug therapy / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007429:Intraocular Pressure / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009883:Ophthalmic Solutions; D009915:Orbit / Q000098:blood supply* / Q000000981:diagnostic imaging / Q000187:drug effects; D011446:Prospective Studies; D013999:Timolol / Q000008:administration & dosage / Q000494:pharmacology*; D018615:Ultrasonography, Doppler, Color; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D009883:Ophthalmic Solutions; D013999:Timolol; D015784:Betaxolol