The Toxic Effects of Carbon Dioxide and Acetazolamide in Hepatic Encephalopathy *

Posner, Jerome B.; Plum, Fred

doi:10.1172/jci104140

Cited by 173 publications

(81 citation statements)

References 32 publications

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“…4). DISCUSSION Our data show that the intravenous administration of acetazolamide sufficient to acutely inhibit all circulat- 4 The effect of intravenous administration acetazolamide on CMRO2. The mean control CMRO2 was 4.16 ml/min per 100 g. FIGURE 5 The effect of hemolysis of the oxygen-15-labelecl blood used to measure the CMRO2 before (control) and after the intravenous administration of acetazolamide to rhesus monkeys.…”

Section: Resultsmentioning

confidence: 55%

“…Such an approach to the measurement of CBF makes the important assumption that CMRO2 remains constant (8). The evidence that the CMRO2 is unaffected by intravenous acetazolamide is based on a single report (4). We observed a significant decrease in CMRO2 minutes after intravenous acetazolamide.…”

Section: Introductionmentioning

confidence: 58%

“…We have reexamined the effect of acetazolamide on CBF and although we observed an increase, it was consistently less than the large increases in CBF others have reported (1)(2)(3)(4)(5)(6)(7). This apparent discrepancy prompted us to measure the effect of acetazolamide on the CMRO2 because the reported CBF changes after intravenous acetazolamide (Table I) are based, in large measure, on the use of the brain arteriovenous oxygen difference as an index of CBF.…”

Section: Introductionmentioning

confidence: 63%

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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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Section: Resultsmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 58%

Section: Introductionmentioning

confidence: 63%

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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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“…In humans, direct measturemiients of' the arterial andcl cerebral venous concentration differences for ammonia have failed to show a consistent pattern for brain ammonia metabolism. Although most data indicate that the brain extracts a small fraction of the ammonia present in arterial blood (25,26), other data show no extraction or ammonia production (27). The failure to demonstrate that ammonia enters the brain has been cited as a weakness in the hypothesis that hyperammonemia produces hepatic encephalopathy (2).…”

Section: * Includes Isotope In Tumormentioning

confidence: 99%

The dynamics of ammonia metabolism in man. Effects of liver disease and hyperammonemia.

Lockwood¹,

McDonald²,

Reiman³

et al. 1979

J. Clin. Invest.

375

201

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A B S T R A C T The cyclotron-produced radionuclide, 13N, was used to label ammonia and to study its metabolism in a group of 5 normal subjects and 17 patients with liver disease, including 5 with portacaval shunts and 11 with encephalopathy. Arterial ammonia levels were 52-264 ,AM. The rate of ammonia clearance from the vascular compartment (metabolism) was a linear function of its arterial concentration: Amol/min = 4.71 [NH3Ia + 3.76, r = +0.85, P < 0.005. Quantitative body scans showed that 7.4+±0.3% of the isotope was metabolized by the brain. The brain ammonia utilization rate, calculated from brain and blood activities, was a function of the arterial ammonia concentration: ,umol/ min per whole brain = 0.375 [NH3]a -3.6, r = +0.93, P < 0.005. Assuming that cerebral blood flow and brain weights were normal, 47 + 3% of the ammonia was extracted from arterial blood during a single pass through the normal brains. Ammonia uptake was greatest in gray matter. The ammonia utilization reaction(s) appears to take place in a compartment, perhaps in astrocytes, that includes <20% of all brain ammonia. In the 11 nonencephalopathic subjects the [NH3Ia was 100±8 ,uM and the brain ammonia utilization rate was 32±3 ,umol/min per whole brain; in the 11 encephalopathic subjects these were respectively elevated to 149±18 AM (P < 0.01), and 53 ± 7 ,umol/min per whole brain (P <0.01). In normal subjects, -50% of the arterial ammonia was metabolized by skeletal muscle. In patients with portal-systemic shunting, muscle may become the most important organ for ammonia detoxification.

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“…It was reported that the vasodilatation is mediated by inhibition of carbonic anhydrase, which is localized in the brain and circulating red blood cells (Posner and Plum, 1960;Maren, 1967Maren, , 1977. Acetazolamide induces a local extracellular acidosis in the brain that triggers an increase in CBF as CO 2 does (Wang et al , 1993).…”

mentioning

confidence: 99%

Acetazolamide Reactivity on ¹²³I-IMP Single Photon Emission Computed Tomography in Patients with Major Cerebral Artery Occlusive Disease: Correlation with Positron Emission Tomography Parameters

Hirano

Minematsu

Hasegawa

et al. 1994

J Cereb Blood Flow Metab

135

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Single photon emission computed tomography (SPECT) with acetazolamide challenge has increasingly been used for evaluating hemodynamic reserve in stroke patients. The accuracy of this test, however, has not been validated with positron emission tomography (PET). In 14 patients who had occlusive disease of the internal carotid artery or the trunk of the middle cerebral artery (MCA) with minimal or no infarction on computed tomography (CT) and magnetic resonance imaging (MRI), we compared acetazolamide reactivity on SPECT with N-isopropyl- p-[123I]-iodoamphetamine to hemodynamic parameters determined with gas inhalation labeled 15O steady-state PET studies. The asymmetry index (AI)—i.e., the percentage of the activity rate of the ischemic MCA territory versus the contralateral one, was determined by SPECT. Acetazolamide reactivity expressed as ΔAI, or change in AI after acetazolamide challenge, was significantly lower in seven patients than −8.4%, the lower limit of the 95% confidence interval for the normal reactivity. Values of ipsilateral CBF, cerebral blood volume (CBV)/CBF, and oxygen extraction fraction (OEF) and contralateral OEF were significantly different between patients with normal and reduced acetazolamide reactivity. Values of AAI were correlated with OEF ( r = −0.87; p < 0.001) and CBV/CBF ( r = −0.56; p < 0.05). All patients with OEF >0.52, the mean + 2 SD calculated from five normal volunteers, also had reduced acetazolamide reactivity, while the patients with normal OEF values had normal reactivity. The present study has demonstrated that SPECT studies with an acetazolamide challenge can detect the Stage II hemodynamic failure.

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The Toxic Effects of Carbon Dioxide and Acetazolamide in Hepatic Encephalopathy *

Cited by 173 publications

References 32 publications

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

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

The dynamics of ammonia metabolism in man. Effects of liver disease and hyperammonemia.

Acetazolamide Reactivity on ¹²³I-IMP Single Photon Emission Computed Tomography in Patients with Major Cerebral Artery Occlusive Disease: Correlation with Positron Emission Tomography Parameters

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The Toxic Effects of Carbon Dioxide and Acetazolamide in Hepatic Encephalopathy *

Cited by 173 publications

References 32 publications

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

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

The dynamics of ammonia metabolism in man. Effects of liver disease and hyperammonemia.

Acetazolamide Reactivity on 123I-IMP Single Photon Emission Computed Tomography in Patients with Major Cerebral Artery Occlusive Disease: Correlation with Positron Emission Tomography Parameters

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Acetazolamide Reactivity on ¹²³I-IMP Single Photon Emission Computed Tomography in Patients with Major Cerebral Artery Occlusive Disease: Correlation with Positron Emission Tomography Parameters