Brain Carbonic Acid Acidosis after Acetazolamide

Heuser, D.; Astrup, Jens; Lassen, Niels A.; Betz, E.

doi:10.1111/j.1748-1716.1975.tb05827.x

Cited by 76 publications

(27 citation statements)

References 14 publications

(5 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This occurs within 1 min in the erythrocyte (3) but is somewhat slower in the brain tissues because of the retarded passage of the drug across the blood-brain barrier (4). The effect upon CBF has been shown to agree well with the locally induced changes of pH in the extracellular fluid compartment and, possibly, the intracellular compartment (5,6). Some investigators looked for but could not demonstrate an additional hypoxic effect caused by inhibition of the Bohr effect in the microcirculation (7).…”

Section: Introductionmentioning

confidence: 50%

Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen.

Vorstrup¹,

Henriksen²,

Paulson³

1984

J. Clin. Invest.

282

146

View full text Add to dashboard Cite

Abstract. The aim of this study was to evaluate the effect of acetazolamide on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2). CBF, arterial and jugular venous partial 02 pressure, partial CO2 pressure, pH, and 02 saturation percentage were measured in six patients before and 3 and 20 minutes after intravenous administration of 1 g of acetazolamide. CBF was measured by the intracarotid '33xenon injection technique. In addition, changes in CBF were estimated from the arteriovenous oxygen content difference. CBF increased in all patients after acetazolamide, by 55 and 70% after 3 and 20 min, respectively. The CBF changes were of the same order whether calculated from the '33Xe clearance or from the arteriovenous oxygen differences (A -V)02. CMRO2, calculated from (A -V)02 differences and CBF, remained constant. Except for an increase in the venous oxygen saturation, the blood gases remained constant.Acetazolamide, in a dose sufficient to inhibit the erythrocyte carbonic anhydrase (EC 4.2.1.1), thus induced a rapid and marked increase in CBF, leaving CMRO2 unchanged. This effect of acetazolamide on CBF is probably explained by a decrease in brain pH rather than by brain tissue hypoxia due to inhibition of oxygen unloading in the brain capillaries.

show abstract

Section: Introductionmentioning

confidence: 50%

Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen.

Vorstrup¹,

Henriksen²,

Paulson³

1984

J. Clin. Invest.

282

146

View full text Add to dashboard Cite

show abstract

“…9 Acetazolamide inhibits carbonic anhydrase, an enzyme that catalyzes either the dissociation or the formation of carbonic acid, thus causing a marked cerebral acidosis. 10 This effect develops rather slowly, peaking after 10 minutes, and is a very strong vasodilatory stimulus. 11 Acetazolamide increases cerebral blood flow (CBF) usually to a greater extent than that induced by 5 minutes of 5% CO 2 inhalation.…”

Section: S Ince Publication Of the Results Of The Internationalmentioning

confidence: 99%

Evaluation of vasomotor reactivity by transcranial Doppler and acetazolamide test before and after extracranial-intracranial bypass in patients with internal carotid artery occlusion.

Karnik

Valentin

Ammerer

et al. 1992

Stroke

View full text Add to dashboard Cite

Background and Purpose:The aim of this trial was to evaluate the effectiveness of extracranialintracranial bypass with respect to vasomotor reactivity in patients with internal carotid artery occlusions and absent vasomotor reactivity, comparing them with a control group treated conservatively.Methods: To test vasomotor reactivity in 104 patients with unilateral occlusion of the internal carotid artery, we measured blood flow velocity in the middle cerebral artery by transcranial Doppler sonography both at rest and after injection of acetazolamide. Among the 39 patients who failed to show increased mean blood flow velocity after the acetazolamide test distal to an occluded internal carotid artery by 2:10%, 14 subjects subsequently underwent extracranial-intracranial bypass surgery (group A) and 14 age-and sex-matched subjects in whom no such procedure was done composed the control group (group B). Follow-up examinations were performed 3-6 months postoperatively and in the control group 3-6 months after initial examination.Results: Baseline values of the mean blood flow velocity at rest on the affected side were reduced in both groups compared with the contralateral healthy side (group A, 46.0±15.1 cm/sec; group B, 48.1 ±16.7 cm/sec) and revealed only a marginal increase after acetazolamide. The contralateral side showed a normal blood flow velocity at rest and an adequate response to acetazolamide in both groups. On the follow-up examination group A demonstrated a normalized vasodilatory capacity. Blood flow velocity increased significantly after acetazolamide from 41.9±13.1 cm/sec to 53.5±16.0 cm/sec (p<0.002). In group B, the compromised vasomotor reactivity remained unchanged.Conclusions: Our results demonstrate that transcranial Doppler sonography together with the acetazolamide test can identify subjects with reduced vasomotor reactivity distal to an occluded internal carotid artery, who may improve hemodynamically by an extracranial-intracranial bypass. (Stroke 1992^3:812-817) KEY WORDS • acetazolamide • cerebral revascularization • ultrasonics

show abstract

“…has been measured previously only by Heuser, Astrup, Lassen & Betz (1975) and Astrup, Heuser, Lassen, Nilsson, Norberg & Siesj6 (1976). Both groups recorded changes in pHe.c.f.…”

Section: Blood Supply Of the Medullamentioning

confidence: 99%