Mean carbon dioxide tension in the brain after carbonic anhydrase inhibition

Brzeziński, J; Kjällquist, Å.; Siesjö, Bo K.

doi:10.1113/jphysiol.1967.sp008120

Cited by 63 publications

(17 citation statements)

References 17 publications

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“…Also, an increased CO2 tension on the cerebral cortex (17) and an intracellular carbonic acidosis with a decrease of brain tissue lactate and pyruvate after acetazolamide administration correspond to the observations in tissue acidosis produced by hypercapnia (18). These results seem to indicate that the effect of acetazolamide on CBF is mediated via inhibition ofcarbonic anhydrase in the erythrocytes by impeding the removal of CO2 in the brain tissue by the blood stream.…”

Section: Discussionmentioning

confidence: 49%

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

Vorstrup¹,

Henriksen²,

Paulson³

1984

J. Clin. Invest.

283

146

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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.

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Section: Discussionmentioning

confidence: 49%

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

Vorstrup¹,

Henriksen²,

Paulson³

1984

J. Clin. Invest.

283

146

View full text Add to dashboard Cite

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“…Statistical correction of our CBF data for the Paco2 increase reduces the observed CBF increase from 29.2 to 15.4%. We may well be overestimating the effect of Paco2 in our data due to the difficulties in measuring Paco2 after the administration ofacetazolamide (14,15). When an arterial sample is drawn, there is a relative excess of HCO .…”

Section: Resultsmentioning

confidence: 79%

The Effect of Acetazolamide on Cerebral Blood Flow and Oxygen Utilization in the Rhesus Monkey

Laux¹,

Raichle²

1978

J. Clin. Invest.

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“…Brzezinski et al [ 12] reported that the partial CO2 pressure measured in brain tissue in creased after acetazolamide administration and Kjallquist et al [13] reported that brain tissue lactate and pyruvate decreased. Vorstrup et al [14] concluded that the increase in CBF was mediated via inhibition of car bonic anhydrase in the erythrocytes, imped ing removal by the blood of CO2 in the brain tissue.…”

Section: Introductionmentioning

confidence: 99%

Effect of Acetazolamide on Cerebral Blood Flow Velocity and CO<sub>2</sub> Elimination in Normotensive and Hypotensive Newborn Piglets

Thoresen

Whitelaw²

1990

Neonatology

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The objectives of this study were to measure the effect of acetazolamide on cerebral circulation, pulmonary elimination of CO₂ and cerebrovascular response to hypotension in newborn piglets. Eighteen anaesthetized newborn piglets were studied. A fontanelle was surgically created and the cerebral blood flow velocity (CBFV) in an intracranial artery measured by a computerized Doppler system. In 8 piglets, 30 ml/kg of blood was removed to produce hypotension before the administration of acetazolamide. Acetazolamide (50 mg/kg i.v.) given to normotensive piglets consistently produced a large increase in CBFV (median 45% by 5 min) with no change in mean arterial blood pressure or heart rate. The rise in CBFV was negatively correlated with the starting partial pressure of CO₂ in arterial blood. Within 1 min of administration of acetazolamide, the end-expiratory CO₂ pressure started to fall (mean fall 1.4 kPa), and the partial pressure of CO₂ in the arterial blood started to rise (mean rise 2.0 kPa), despite the controlled ventilation being unchanged. Acetazolamide had no effect on CBFV in the hypotensive piglet. It seems likely that acetazolamide produces cerebral vasodilatation by inhibiting the elimination of CO₂ In hypotension, there is maximal cerebral vasodilatation, and acetazolamide cannot increase CBFV further. The interference of acetazolamide with CO₂ elimination could seriously limit its use in the treatment of hydrocephalus in preterm infants.

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Mean carbon dioxide tension in the brain after carbonic anhydrase inhibition

Cited by 63 publications

References 17 publications

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

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

The Effect of Acetazolamide on Cerebral Blood Flow and Oxygen Utilization in the Rhesus Monkey

Effect of Acetazolamide on Cerebral Blood Flow Velocity and CO<sub>2</sub> Elimination in Normotensive and Hypotensive Newborn Piglets

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