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Biomedical subjects

O B Paulson

Publications and source records attributed to O B Paulson.

At least 19 recordsLinked to original sources
PubMed1992

Cerebral blood flow deficits in hereditary essential myoclonus.

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. We postulate the cause to be a focal unilateral subcortical cerebral lesion, either in the basal ganglia or in the brain stem, with subsequent cortical deafferentation.

Adult↗
PubMed1992

The effect of ketanserin on cerebral blood flow and cerebrovascular CO2 reactivity in healthy volunteers.

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. Then arterial CO2 tension was subsequently decreased by voluntary hyperventilation and increased by breathing an air/CO2 mixture. The relative changes in CBF induced by the changes in arterial CO2 tension were estimated by the cerebral arterio-venous oxygen content difference method. One hour following the start of ketanserin infusion the SPECT measurement and CO2 manipulations were repeated. The CO2 reactivity (expressed as the slope of the regression line of the linear relation between CBF and PaCO2), was unchanged, i.e. 3.2%/0.1 kPa before ketanserin and 4.1%/0.1 kPa during ketanserin, respectively. Using regression lines from a semi-logarithmic plot the CO2 reactivity was also unchanged 3.4%/0.1 kPa and 3.5%/0.1 kPa, respectively. Ketanserin did not change CBF. The cerebral oxygen metabolism (CMRO2) was decreased 19% one hour after the start of infusion of ketanserin. In conclusion administration of ketanserin in a clinically relevant dose to healthy volunteers does not change the regional CBF not the cerebrovascular CO2 reactivity, but a decrease in CMRO2 was observed. However further studies are needed to clarify whether ketanserin in fact has a depressing effect on CMRO2 or whether the different results are caused by methodological errors or stochastic variation.

Adult↗
PubMed1992

Increased cerebral blood flow in anemic patients on long-term hemodialytic treatment.

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. Mean CBF was 66.2 +/- 17.3 (SD) ml 100 g-1 min-1, which was significantly higher (t-test, p less than 0.05) than for an age-matched control group (54.7 +/- 10.2 ml 100 g-1 min-1). However, the hematocrit for the patients was considerably lower, 0.30 +/- 0.07, as compared to 0.43 +/- 0.03 in the controls. A significant negative correlation was observed between CBF and the hematocrit (y = -1.79x + 120.7, r = -0.71, p less than 0.01). Calculating CBF from this equation in the dialyzed patients using a hematocrit of 0.43 yielded a mean CBF value of 43.7 ml 100 g-1 min-1, i.e., 20% below the expected. Two patients showed a focal CBF decrease. CT showed central or cortical atrophy in five patients, and two had small hypodense lesions. The neurological examination revealed slight to moderate dementia in seven cases. Although mean CBF was found to be increased by 21% as compared to the control group, an even higher CBF level would have been expected to outweigh the decreased oxygen carrying capacity of the blood. The findings suggest a lowered metabolic demand of the brain tissue, probably due to subtle brain damage.

Adult↗
PubMed1992

Effect of nitric oxide blockade by NG-nitro-L-arginine on cerebral blood flow response to changes in carbon dioxide tension.

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 1.5, or 7.5, or 30 mg/kg NOLAG induced a dose-dependent increase of arterial blood pressure and a decrease of normocapnic CBF from 85 +/- 10 to 78 +/- 6, 64 +/- 5, and 52 +/- 5 ml 100 g-1 min-1, respectively. This effect lasted for at least 2 h. Raising PaCO2 from a control level of 40 to 68 mm Hg increased CBF to 230 +/- 27 ml 100 g-1 min-1, corresponding to a percentage CBF response (CO2 reactivity) of 3.7 +/- 0.6%/mm Hg PaCO2 in saline-treated rats. NOLAG attenuated this reactivity by 32, 49, and 51% at the three-dose levels. Hypercapnia combined with angiotensin to raise blood pressure to the same level as the highest dose of NOLAG did not affect the CBF response to hypercapnia. L-Arginine significantly prevented the effect of NOLAG on normocapnic CBF as well as blood pressure and also abolished its inhibitory effect on hypercapnic CBF. D-Arginine had no such effect. Decreasing PaCO2 to 20 mm Hg reduced control CBF to 46 +/- 3 ml 100 g-1 min-1 with no further reduction after NOLAG. Furthermore, NOLAG did not change the percentage CBF response to an extracellular acidosis induced by acetazolamide (50 mg/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Regulation of cerebral blood flow in health and disease.

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. In most patients, this does not interfere with the beneficial effect of treatment, i.e., stroke prevention. Cerebral ischemia, however, may be provoked by overzealous pressure lowering in selected clinical settings: initial or intensified treatment of very severe hypertension, treatment of hypertension in the elderly, and treatment of hypertension in acute stroke. In the latter, a complicated sequence of brain ischemia and hyperemia makes antihypertensive intervention difficult in the early phase, when blood pressure is probably best allowed to decrease spontaneously.

Antihypertensive Agents↗
PubMed1992

Reduced regional cerebral blood flow in Huntington's disease studied by SPECT.

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. Fourteen patients had neuropsychological testing. Relationship between rCBF and cognitive function was tested by regression analysis. A linear relationship was found between test scores of Wisconsin Card Sorting Test, Picture Arrangement Test and blood flow in the caudate nucleus. Other tests of cognitive function (Block Design Test, Face and Word Recognition Test, Street Fragmented Pictures Test, and Similarities Test) correlated better with flow in the cortical regions believed to be involved in solving those particular tests. These findings indicate, that blood flow is reduced in both cortical and subcortical structures in symptomatic HD, and that both reductions in cortical and subcortical blood flow may be related to cognitive function in HD.

Adult↗
PubMed1992

Capillary circulation in the brain.

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. Theories of capillary cycling and capillary recruitment have been based on experimental artifacts. Indirect evidence exists for a heterogeneity of perfusion under normal conditions, especially with respect to erythrocyte flow. The capillary diffusion capacity depends on, among other things, the available capillary surface area, which would increase with recruitment of capillaries. In the case of capillary perfusion heterogeneity, the capillary diffusion capacity may also be increased by homogenization of the perfusion rate (slowly perfused capillaries becoming faster perfused). This could give a physiological impression of an "apparent" increase in the capillary surface area. It is recommended that the terms "capillary cycling" and "recruitment" should be used in conjunction with more specific explanations, like "recruitment of erythrocytes" and "recruitment of previously nonperfused capillaries".

Animals↗
PubMed1991

Epidemiology of myasthenia gravis in Denmark. A longitudinal and comprehensive population survey.

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. Age- and sex-specific incidence rates disclosed a bimodal appearance for both sexes, with a peak age at onset located in the early-onset group and another peak for late onset of MG. Early onset of MG appeared 10 years later for male individuals than for female individuals, whereas the peak for late onset of MG was located at the same age for both sexes. It is suggested that the separation between early onset and late onset of MG should be at the age of 50 years for both sexes, rather than at 35 to 40 years as accepted in most studies. The prevalence of MG has increased in time. On January 1, 1988, the point prevalence rate was 77 per million population (female subjects, 96, and male subjects, 57). This reflects an improvement in prognosis despite the fact that life expectancy was found to be significantly lower for MG patients than that of the sex- and age-matched population. The factors causing increased mortality were found to be operative throughout the duration of the disease. Maximum severity of disease was reached within 2 years from onset in 78% of the cases, and more than 50% of all MG-related deaths occurred during the same period. In the course of MG, 70% of all patients experience generalized muscular weakness, and 30% to 40% also suffer from respiratory problems.

Denmark↗
PubMed1991

Effect of ketanserin on cerebral blood flow autoregulation in healthy volunteers.

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 2.5 mmHg (6 to -2), while CBF rose insignificantly by 5 ml/100 g/min. Autoregulation was preserved in all volunteers. CO2-correction factors from 0 to 4.6% CBF/0.1 kPa were used. The lower limit of CBF autoregulation was 82 mmHg (80-86) with an SE of 3 mmHg (1-5) similar to a previous control group of healthy volunteers. Aside from a major decrease in MABP in one subject, no adverse side effects were observed. The present study shows that CBF autoregulation is maintained during ketanserin infusion.

Blood Flow Velocity↗
PubMed1991

The acute effect of nimodipine on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers.

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. During the CO2 reactivity tests changes in CBF were estimated by the arterio-venous-oxygen-difference method. Median CBF was 52 ml/100 g/min (48-53) with a normal regional distribution, and median baseline MABP was 96 mmHg (92-99). MABP was slightly reduced, by 8 mmHg (7-9), and 9 mmHg (4-11) after infusion of NIM for 2 and 4 hours, respectively. CBF, however, remained constant, although correction for changes in PaCO2, revealed a slight increase after 4 hours (p = 0.08). CMRO2 was 3.5 ml/100g/min (3.2-3.5) and was not changed by the infusion of NIM. At arterial CO2 tensions ranging from 4.0 to 6.5 Kpa the CO2 reactivity was 3.0% CBF/0.1 kPa (2.6-3.7) and decreased significantly to 2.6% CBF/0.1 kPa (1.8-3.2) after the infusion of NIM for 3 hours (p = 0.02). The median slope of the LnCBFsat/PaCO2 relationship was 1.5 at baseline compared to 1.3 after NIM (p less than 0.01). No side effects were observed. The present study shows a decreased CO2 of the cerebral vessels and a maintained coupling of CBF and CMRO2 during the infusion of nimodipine.

Adult↗
PubMed1991

Kinetic analysis of the human blood-brain barrier transport of lactate and its influence by hypercapnia.

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 0.081 ml g-1 min-1 and the transport from the brain to the blood (PS2) was on the same order of magnitude. In hypercapnia, arterial pH decreased from 7.39 to 7.26 and PS1 to L-lactate increased significantly by 110%. PS2 also increased although a statistically significant difference compared to the resting state was not reached. It is concluded that L-lactate is easily taken up by the human brain, and that the mechanism by which it crosses the blood-brain barrier is equilibrative. Furthermore, the brain permeability to lactate is enhanced by hypercapnia and the mechanism is believed to act through the decrease in pH.

Adult↗
PubMed1991

Regional density of perfused capillaries and cerebral blood flow in untreated short-term and long-term streptozotocin diabetes.

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 0.05) reduction in rCBF in two structures in the visual system compared to the control group (visual cortex: 105 versus 129 ml 100 g-1 min-1; lateral geniculate body: 106 versus 128 ml 100 g-1 min-1) and in the pontine reticular nucleus (82 versus 128 ml 100 g min-1), whereas rDPC remained unchanged. A highly significant correlation between rCBF and rDPC was found in both control groups (r = 0.8, p less than 0.005) whereas the correlation was more scattered in the diabetic groups (r = 0.6, p less than 0.05). The present results show that during chronic diabetes, a reduction of rCBF does not affect the number of perfused capillaries.

Animals↗
PubMed1991

99mTc-d,l-HMPAO and SPECT of the brain in normal aging.

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% +/- 8.4 (SD). The contribution of age, sex, and atrophy to variations in global CBF was studied using stepwise multiple regression analysis. There was a significant negative correlation of global CBF with subjective ratings of cortical atrophy, but not with ratings of ventricular size, Evans ratio, sex, or age. In a subgroup of 33 subjects, in whom volumetric measurements of atrophy were performed, cortical atrophy was the only significant determinant for global CBF, accounting for 27% of its variance. Mean global CBF as measured with the 133Xe inhalation technique and SPECT was 54 +/- 9 ml/100 g/min and did not correlate significantly with age. There was a preferential decline of CBF in the frontal cortex with advancing age. The side-to-side asymmetry of several regions of interest increased with age. A method was described for estimation of subcortical CBF, which decreased with advancing cortical atrophy. The relative area of the subcortical low-flow region increased with age. These results are useful in distinguishing the effects of age and simple atrophy from disease effects, when the 99mTc-d,l-HMPAO method is used.

Adult↗
PubMed1991

Role of the local renin-angiotensin system in the autoregulation of the cerebral circulation.

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. An interaction between the vascular reninangiotensin and the sympathetic nervous system is present. Activation of the latter inhibits the downwards shift of the upper limit of autoregulation following ACE inhibition.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Cerebrovascular effects of angiotensin converting enzyme inhibition involve large artery dilatation in rats.

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.min; flow remained stable until at least 60 minutes. After treatment B, cerebral blood flow increased by a further 17.4%, from an average of 219 ml/100 g.min to an average of 257 ml/100 g.min (p less than 0.01). After treatment C, cerebral blood flow stabilized at an average of 238 ml/100 g.min, with flow from 20 to 60 minutes always being higher (from 5% to 17%) than during carbonic anhydrase inhibition alone (p less than 0.02). Thus the additional inhibition of converting enzyme resulted in higher cerebral blood flow than during inhibition of carbonic anhydrase alone. CONCLUSIONS: These results suggest that converting enzyme inhibition reduced resistance of large brain arteries and support the hypothesis that there is some angiotensin II-induced tone in large cerebral arteries.

Acetazolamide↗
PubMed1990

Quantitation of blood-brain barrier defect by magnetic resonance imaging and gadolinium-DTPA in patients with multiple sclerosis and brain tumors.

In this study quantitation of the degree of deficiency of the blood-brain barrier (BBB) in patients with multiple sclerosis or brain tumors, by using MRI, is shown to be possible. As a measure of permeability of the BBB to Gadolinium-DTPA (Gd-DTPA) the flux per unit of distribution volume per unit of brain mass was used. This quantity was found by introducing the longitudinal relaxation rate (R1) as a measure of concentration of Gd-DTPA in the brain tissue in the mathematical model for the transcapillary transport over the BBB. High accordance between the observed data points and the model was found, and the results were comparable to results obtained from similar studies using positron emission tomography. The improved possibility of quantitating the defect of the BBB by MRI may give new information about pathogenesis or etiology, and leads to improved methods in monitoring the efficacy of treatments in intracranial diseases.

Blood-Brain Barrier↗
PubMed1990

Effect of acute and prolonged treatment with propranolol on cerebral blood flow and cerebral oxygen metabolism in healthy volunteers.

The effect of acute and long-term treatment with propranolol on cerebral blood flow (CBF) and the cerebral metabolic rate of oxygen (CMRO2) has been studied in 8 young healthy volunteers. CBF was measured by 133Xe-inhalation and single photon emission computer tomography, and CMRO2 was calculated from the arterio-venous oxygen difference and CBF. Studies were done before and 1 h after i.v. injection of 5 mg propranolol and after three weeks on oral propranolol 80 mg/d for 1 week and 160 mg/d for 2 weeks. Cerebrovascular CO2 reactivity in terms of the A-V oxygen difference was tested on all three occasions during hypercapnia and hyperventilation. CBF, CMRO2 and cerebrovascular CO2 reactivity remained stable both after acute and after 3 weeks of treatment with propranolol.

Administration, Oral↗