Publications by authors named "Paulson O"

During prolonged starvation, brain energy requirements are covered in part by the metabolism of ketone bodies. It is unknown whether short-term starvation of a few days' duration may lead to reduced brain glucose metabolism due to the change toward ketone body consumption. In the present study we measured the cerebral metabolism of glucose and ketone bodies in nine healthy volunteers before and after 3.

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Background: The 21-aminosteroids are a series of compounds designed to inhibit lipid peroxidation in the cell, and, as such, may have cerebral protective effects. The current study was performed to evaluate the effect of a 21-aminosteroid, tirilazad mesylate (U74006F), on cerebral blood flow, metabolism, and carbon dioxide reactivity.

Methods: Using a double-blind study design, eight volunteers received tirilazad mesylate, and eight others received only vehicle.

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Indomethacin is known to attenuate quite markedly the increase in CBF during hypercapnia. Hypercapnia is, in all likelihood, mediated by the acid shift at the level of the smooth muscle cells of the cerebral arterioles. We therefore investigated the effect of indomethacin on the CBF increase caused by acetazolamide (Az), a drug that induces brain extracellular acidosis, which triggers its effect on CBF.

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We repeatedly measured blood-brain barrier passage of phenylalanine, leucine, glucose and GABA in nine patients with hepatic encephalopathy using the intravenous double-indicator technique. Controls were four patients without liver disease and two of the patients who had recovered completely from their hepatic encephalopathy. The corrected cerebral venous output curves were fitted by use of a three-compartment model with four parameters.

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Cranial CT and high resolution measurements of regional cerebral blood flow (rCBF) with brain dedicated single photon emission computer tomography (SPECT) and [99mTc]-d,l-hexamethylpropyleneamine oxime ([99mTc]-d,l-HMPAO) were performed before and after shunt operation in 14 consecutive patients with dementia and normal pressure hydrocephalus (NPH). When compared with a control group of 14 age matched healthy volunteers, the group of NPH patients was characterised by an enlarged subcortical low-flow region, significantly reduced rCBF and enhanced side-to-side asymmetry of rCBF in the central white matter, and enhanced side-to-side asymmetry in the inferior and mid-temporal cortex. Global CBF was normal.

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Objective: To investigate the effect of the new angiotensin converting enzyme inhibitor ceranapril (1 mg/kg) on the cerebral blood flow (CBF) autoregulation in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).

Design: Sixteen WKY rats and 16 SHR were given ceranapril 1 mg/ml intravenously and compared with two untreated control groups (n = 16). The rats were furthermore divided into subgroups of eight to study the upper and lower limits of autoregulation separately.

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The possible role of nitric oxide (NO) on vibrissa-stimulated increase of regional cerebral cerebral blood flow (rCBF) and cerebral metabolic rate of glucose (rCMRglu) was investigated in conscious Wistar rats by using an inhibitor of NO synthase, NG-nitro-L-arginine (NOLAG) at a concentration of 30 mg/kg. In vivo autoradiography distribution with 14C-iodoantipyrine and 14C-deoxyglucose in two separate series showed CBF of 174% of control and CMRglu of 196% of control in the primary sensory cortex opposite the stimulated side in saline treated control animals. Similar increases were found in NOLAG-treated animals.

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Article Synopsis
  • Four patients with thalamic infarcts exhibited severe neuropsychological deficits, with imaging revealing reduced blood flow and glucose metabolism in various brain regions.
  • All patients demonstrated significant impairments in memory, verbal fluency, abstract reasoning, and showed distinct personality changes and insights.
  • The findings suggest that thalamic infarcts can disrupt broader brain functions, leading to extensive and varied cognitive and behavioral issues.
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Regional cerebral blood flow (rCBF) was studied in 18 patients with Huntington's disease (HD) and 19 age- and sex-matched controls with high resolution single photon emission computerised tomography (SPECT), using Tc-99m-HMPAO. Significant reductions in tracer uptake were found in the caudate and lentiform nuclei (20 and 8%) and in the cerebral cortex, especially in the frontal and parietal areas (11-13%). No significant reductions were found in the thalamus, mesial temporal cortex, and occipital cortex.

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The importance of nitric oxide (NO) for CBF variations associated with arterial carbon dioxide changes was investigated in halothane-anesthetized rats by using an inhibitor of nitric oxide synthase, NG-nitro-L-arginine (NOLAG). CBF was measured by intracarotid injection of 133Xe. In normocapnia, intracarotid infusion of 1.

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CBF was measured in 15 patients on chronic hemodialytic treatment. CBF was measured with xenon-133 inhalation using single photon emission tomography. In addition, computerized tomography (CT) and a neurological examination were done prior to hemodialysis.

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Hereditary essential myoclonus is a disease in which segmental myoclonus is the sole clinical abnormality and whose cause is unknown. It is characterized by an early onset, a benign course, an autosomal dominant pattern of inheritance, the absence of any other neurologic dysfunction, and normal results of auxiliary tests. Cerebral blood flow studies of a father and son with this disease showed a cortical blood flow reduction contralateral to the myoclonus symptoms.

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The effect of the anti-hypertensive agent ketanserin on the cerebral blood flow (CBF) and the cerebrovascular CO2 reactivity was examined in 10 healthy volunteers. Ketanserin was administered as an intravenous bolus of 10 mg followed by an infusion of 6 mg/h. Before administration CBF was measured by single photon emission computerized tomography (SPECT) of inhaled 133Xenon.

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Capillary circulation in the brain.

Cerebrovasc Brain Metab Rev

November 1992

A close relationship exists between the local capillary density in different brain structures and their local blood flow and metabolism. Capillary density appears to have developed depending on local functional demands. Investigation of single capillary perfusion has shown that all capillaries are perfused with plasma in the brain at any time point.

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A review is given of the normal regulation of cerebral blood flow (CBF) and its pathophysiology in hypertension and stroke. In otherwise healthy hypertensive patients, the absolute level of CBF is the same as in normal subjects. CBF autoregulation, however, is shifted towards higher pressure, thus impairing the tolerance to hypotension.

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Background And Purpose: The aim of the study was to selectively examine the effects of converting enzyme inhibition on the large brain arteries by using concomitant inhibition of carbonic anhydrase to cause severe dilatation of mainly parenchymal resistance vessels.

Methods: Cerebral blood flow was measured using the xenon-133 injection technique in three groups of Wistar rats either during carbonic anhydrase inhibition with acetazolamide (treatment A, n = 8), during carbonic anhydrase inhibition followed by converting enzyme inhibition with captopril 40 minutes later (treatment B, n = 10), or during carbonic anhydrase inhibition preceded by converting enzyme inhibition 20 minutes earlier (treatment C, n = 7).

Results: After treatment A, cerebral blood flow rose rapidly and stabilized within 20 minutes at an average of 220 ml/100 g.

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Blood-brain barrier permeability to L-lactate was studied in 18 patients with the double indicator technique. Venous outflow curves were obtained during normo- and hypercapnia and were analyzed by means of a model that takes tracer backflux and capillary heterogeneity of transit times into account. The average unidirectional extraction of L-lactate was 15%; the transport from the blood to the brain (PS1) was 0.

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The incidence of myasthenia gravis (MG) was found to be constant in calendar time. The mean annual incidence rate was 4.4 per million population.

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Single photon emission computed tomography (SPECT) with 99mTc-d,l-hexamethylpropyleneamine oxime (99mTc-d,l-HMPAO) was used to determine global and regional CBF in 53 healthy subjects aged 21-83 years. For the whole group, global CBF normalized to the cerebellum was 86.4% +/- 8.

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The regional density of perfused cerebral capillaries (rDPC) and regional cerebral blood flow (rCBF) were measured in 12 selected brain regions in rats after 3 and 20 weeks of streptozotocin-induced diabetes and in control groups. After 3 weeks of diabetes, both rCBF and rDPC were unchanged in the diabetic group compared to the control group. A diabetes duration of 20 weeks causing bilateral cataracts induced a significant (p less than 0.

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Inhibition of angiotensin-converting enzyme (ACE) shifts the limits of cerebral blood flow autoregulation toward lower blood pressure values. This effect seems to be mediated by blocking the formation of angiotensin II on the luminal side of the larger cerebral resistance vessels. Baseline cerebral blood flow (the flow within the autoregulatory limits) is not changed by acute or chronic ACE inhibition.

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The effect of a clinically relevant dose of ketanserin (10 mg as a bolus followed by an infusion of 6 mg/h) on cerebral blood flow (CBF) and CBF autoregulation was examined in 12 healthy volunteers. Changes in CBF were estimated by the cerebral arteriovenous-oxygen saturation difference method, while mean arterial blood pressure (MABP) was increased by norepinephrine and decreased by ganglionic blockade (trimethaphan camphosulphonate) combined with lower body negative pressure one hour after the infusion of ketanserin. During ketanserin infusion, MABP fell insignificantly by 2.

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The present study was undertaken in 8 healthy volunteers to examine the effect of a clinically relevant dose of nimodipine (NIM) (15 and 30 microgram/kg/h) on CBF, its CO2 reactivity, and CMRO2. Mean arterial blood pressure (MABP) was measured intra-arterially. Regional CBF was measured by SPECT of inhaled Xenon-133.

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