Cerebral blood flow and end-tidal PCO2 during prolonged acetazolamide treatment in humans

Friberg, Lars; Kastrup, Jens; Rizzi, D; Jensen, Johannes Rude; Lassen, Niels A.

doi:10.1152/ajpheart.1990.258.4.h954

Cited by 22 publications

(19 citation statements)

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“…There is evidence that CAIs may cause extracellular acidosis. 35 It is worth noting that an increase in arterial pCO 2 -a stimulus M12 M18 M24 M30 M36 M42 M48 M54 M60 an effect on the vascular smooth muscle cells alone or on these cells in interplay with other cellular elements in the surrounding tissue. However, this response depended on the type of the CAI.…”

Section: Discussionmentioning

confidence: 99%

A Comparison of the Long-Term Effects of Dorzolamide 2% and Brinzolamide 1%, Each Added to Timolol 0.5%, on Retrobulbar Hemodynamics and Intraocular Pressure in Open-Angle Glaucoma Patients

Martínez

Sánchez-Salorio²

2009

Journal of Ocular Pharmacology and Therapeutics

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Purpose: To compare the effect on the retrobulbar hemodynamics and intraocular pressure (IOP) of dorzolamide 2% and brinzolamide 1%, each added to timolol 0.5% in patients with primary open-angle glaucoma (POAG). Methods: 146 POAG patients were prospectively randomized to receive either dorzolamide 2% or brinzolamide 1% BID, each added to timolol 0.5%, during a 60-month evaluator-masked study. At baseline and every 6 months for 60 months, we measured the retrobulbar hemodynamic parameters in the ophthalmic artery (OA), central retinal artery (CRA), and short posterior ciliary arteries (SPCA) using color Doppler imaging (CDI), intraocular pressure (IOP), and blood pressure measurements. Results: Dorzolamide signifi cantly increased the end-diastolic velocity (EDV) in the OA in 1.22 cm/s, 95% confi dence interval (95% CI) 0.90-1.56 cm/s, P < 0.001 and reduced the resistivity index (RI) in the OA in 0.04 units, 95% CI 0.03-0.05, P < 0.001. None of the retrobulbar parameters changed signifi cantly on therapy with brinzolamide when the results were analyzed at month 60. Both dorzolamide and brinzolamide signifi cantly decreased IOP (-4.3, 95% CI -4.5 to -4.2 mmHg and -4.3, 95% CI -4.4 to -4.2 mmHg, respectively). Dorzolamide significantly reduced the RI in the OA from 0.74 (0.02) to 0.70 (0.02), CRA from 0.66 (0.02) to 0.62 (0.02), and SPCA from 0.66 (0.02) to 0.62 (0.02), P < 0.001, respectively. Conclusions: Our results suggest augmented retrobulbar blood fl ow after 5 years of treatment with dorzolamide but not with brinzolamide, each added to timolol, in POAG patients.

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Section: Discussionmentioning

confidence: 99%

A Comparison of the Long-Term Effects of Dorzolamide 2% and Brinzolamide 1%, Each Added to Timolol 0.5%, on Retrobulbar Hemodynamics and Intraocular Pressure in Open-Angle Glaucoma Patients

Martínez

Sánchez-Salorio²

2009

Journal of Ocular Pharmacology and Therapeutics

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“…(1983) reported a 50% decrease of the maximum at 95 min after administering AZ. Two days after administration of AZ, no CBF change could be detected (Friberg et al. , 1990).…”

Section: Dose Dependency and Kinetics Of Actionmentioning

confidence: 90%

“…, 1987). A significant increase in the CBF was detected in humans after administering 1000 mg of AZ, both orally and intravenously (Friberg et al. , 1990).…”

Section: Dose Dependency and Kinetics Of Actionmentioning

confidence: 99%

Acetazolamide as a vasodilatory stimulus in cerebrovascular diseases and in conditions affecting the cerebral vasculature

Settakis¹,

Molnár

Kerényi³

et al. 2003

Euro J of Neurology

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Pathologic processes affecting the brain vessels may damage cerebral vasodilatory capacity. Early detection of cerebral dysfunction plays an important role in the prevention of cerebrovascular diseases. In recent decades acetazolamide (AZ) has frequently been used for this purpose. In the present work the mechanism of action and the previous studies are reviewed. The authors conclude that AZ tests are useful in cerebrovascular research. Further investigations are recommended to prove how impaired reserve capacity and reactivity influence the stroke risk in patients and whether these tests may indicate therapeutic interventions.

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“…However, there is evidence that carbonic anhydrase inhibitors may cause extracellular acidosis. 22 It is worth noting that an increase in arterial PCO 2 , a stimulus that produces extracellular acidosis, also strongly increases choroidal [23][24][25][26][27] and cerebral 1,3,5,18,19,27 blood flow. Moreover, the response to hypercapnia is considerably smaller in the OA.…”

Section: Discussionmentioning

confidence: 99%

Effects of Acetazolamide on Choroidal Blood Flow

Dallinger

Bobr

Findl

et al. 1998

Stroke

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Background and Purpose-The acetazolamide provocation test is commonly used to study cerebrovascular vasomotor reactivity. On the basis of the effect of a carbonic anhydrase inhibitor in the central nervous system, we hypothesized that acetazolamide may also increase blood flow in the human choroid. Methods-In a placebo-controlled, randomized, double-blind, three-way crossover design, acetazolamide (500 mg or 1000 mg IV) or placebo was administered to nine healthy subjects. The effect of acetazolamide was studied at 15-minute intervals for 90 minutes. Pulsatile choroidal blood flow was assessed with laser interferometric measurement of fundus pulsation. In addition, mean blood flow velocity and resistive index in the ophthalmic artery were measured with Doppler sonography. In a second study in six healthy subjects, we assessed the effect of acetazolamide (1000 mg IV) on intraocular pressure. Results-Acetazolamide increased fundus pulsation amplitude in a dose-dependent manner (1000 mg: ϩ33%; 500 mg: ϩ20%; PϽ0.001, ANOVA). The effect of acetazolamide on MFV (1000 mg: ϩ18%; 500 mg: ϩ8%; Pϭ0.003, ANOVA) and RI (1000 mg: Ϫ4%; 500 mg: Ϫ2%; Pϭ0.006, ANOVA) was less pronounced but also significant. Acetazolamide did not induce any changes in systemic hemodynamic parameters but significantly decreased intraocular pressure (1000 mg: Ϫ37%; PϽ0.0001). Conclusions-The present data show for the first time that intravenously administered acetazolamide increases choroidal blood flow in humans. This phenomenon therefore indicates that the acetazolamide provocation test may qualify as a tool to investigate ocular vasomotor reactivity in a variety of ocular diseases. Moreover, the increase in choroidal blood flow after carbonic anhydrase inhibition can be expected to contribute to the therapeutic efficacy of carbonic anhydrase inhibitors in glaucoma. (Stroke. 1998;29:997-1001.)

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Cerebral blood flow and end-tidal PCO2 during prolonged acetazolamide treatment in humans

Cited by 22 publications

References 0 publications

A Comparison of the Long-Term Effects of Dorzolamide 2% and Brinzolamide 1%, Each Added to Timolol 0.5%, on Retrobulbar Hemodynamics and Intraocular Pressure in Open-Angle Glaucoma Patients

A Comparison of the Long-Term Effects of Dorzolamide 2% and Brinzolamide 1%, Each Added to Timolol 0.5%, on Retrobulbar Hemodynamics and Intraocular Pressure in Open-Angle Glaucoma Patients

Acetazolamide as a vasodilatory stimulus in cerebrovascular diseases and in conditions affecting the cerebral vasculature

Effects of Acetazolamide on Choroidal Blood Flow

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