title: Acetazolamide and CO2: acute effects on cerebral and retrobulbar hemodynamics.
abstract: OBJECTIVE
  Acetazolamide and CO2 are cerebral vasodilators whose specific effects in various brain regions have not been carefully defined. We investigated the effects of these agents in both larger cerebral and smaller, retrobulbar arteries, to compare their general cerebral vasodilatory influence with their specific ocular vascular effects.
  
  
  METHODS
  Twelve young adults with healthy eyes were studied under normocapnic and hypercapnic (6% CO2, 94% O2 tanked gas) conditions after receiving either placebo or 1,000 mg acetazolamide (3 h before study). Color Doppler imaging was used to measure peak systolic and end-diastolic velocities (PSV and EDV) in the internal carotid, middle cerebral, ophthalmic, and central retinal arteries under each condition.
  
  
  RESULTS
  Acetazolamide and CO2 each lowered intraocular pressure; combining the agents provided no additive ocular hypotensive effect. Hypercapnia or acetazolamide per se failed to alter PSV, EDV, or the derived resistance index [RI; (PSV-EDV)/PSV] in the internal carotid or in either orbital artery. However, when hypercapnia was superimposed upon acetazolamide, the resistance index fell in the internal carotid and central retinal arteries (each p < 0.05). In contrast, the middle cerebral artery was responsive to either vasodilator and to their combination: PSV and EDV rose, and RI fell with each experimental treatment.
  
  
  CONCLUSIONS
  In the brain, the middle cerebral artery exhibits substantial dependence of flow velocity on the vasodilators CO2 and acetazolamide. In contrast, the ophthalmic and central retinal arteries appear less responsive. Nonetheless, the combination of carbonic anhydrase inhibition (acetazolamide) with CO2 augmentation did lower vascular resistance distal to the central retinal artery, suggesting that this mechanism vasodilates critical ocular tissues.
authors.affiliation: Department of Ophthalmology, Indiana University, Indianapolis, USA.
authors.forename: A
authors.initials: A
authors.lastname: Harris
authors.forename: S
authors.initials: S
authors.lastname: Tippke
authors.forename: C
authors.initials: C
authors.lastname: Sievers
authors.forename: G
authors.initials: G
authors.lastname: Picht
authors.forename: W
authors.initials: W
authors.lastname: Lieb
authors.forename: B
authors.initials: B
authors.lastname: Martin
mesh_terms: D000086:Acetazolamide / Q000494:pharmacology*; D000328:Adult; D002245:Carbon Dioxide / Q000494:pharmacology*; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology*; D002536:Cerebral Arteries / Q000000981:diagnostic imaging / Q000187:drug effects / Q000502:physiology*; D004338:Drug Combinations; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology; D007429:Intraocular Pressure / Q000187:drug effects; D009880:Ophthalmic Artery / Q000000981:diagnostic imaging / Q000187:drug effects / Q000502:physiology*; D012016:Reference Values; D012161:Retinal Artery / Q000000981:diagnostic imaging / Q000187:drug effects / Q000502:physiology*; D018615:Ultrasonography, Doppler, Color; D014664:Vasodilation
chemical_list: D002257:Carbonic Anhydrase Inhibitors; D004338:Drug Combinations; D002245:Carbon Dioxide; D000086:Acetazolamide