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Biomedical subjects

S Vorstrup

Publications and source records attributed to S Vorstrup.

At least 19 recordsLinked to original sources
PubMed1992

Focal reductions of cerebral blood flow in amyotrophic lateral sclerosis: a [99mTc]-d,l-HMPAO SPECT study.

We investigated regional cerebral blood flow (rCBF) using the [99mTc]-d,l-HMPAO technique with brain dedicated high resolution single photon emission computer tomography (SPECT) in 14 consecutive patients with amyotrophic lateral sclerosis (ALS), median age 62 years (45-77). Global CBF, expressed in % relative to the cerebellum, was significantly lower (P less than 0.05) in the ALS group (80.5 +/- 6.7%) than in the control group of 14 age-matched healthy volunteers (87.0 +/- 7.5%). Eight patients (57%) had abnormal rCBF distribution maps with reduced flow, primarily in the frontal lobes. Three of the 8 patients with abnormal rCBF had mild to moderate dementia and another one had mild aphasia. None of the patients with normal rCBF distribution maps had dementia. In the group of ALS patients as a whole rCBF was significantly reduced in the frontal cortex, the hippocampus, and the central white matter. We conclude that reduced rCBF, primarily in the frontal lobes, is a frequent finding in patients with ALS. The decreased rCBF may be associated with cognitive deficits and is most likely caused by neuronal degeneration and reduced metabolic needs.

Aged↗
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

CBF and transcranial Doppler sonography during vasodilatory stress tests in patients with common carotid artery occlusion.

Cerebral blood flow (CBF) and the cerebral vasoreactivity was measured in patients with cerebrovascular disease and longstanding occlusion of the common carotid artery (CCA). In addition, regional CBF was correlated with transcranial doppler (TCD) measurements at baseline and during 6% CO2 inhalation and after intravenous administration of 1 g of acetazolamide. Twelve patients with a mean age of 62 years (range 45 to 71 years) were included, and the data compared to age-matched healthy controls. CBF was measured by intravenous injection of xenon-133 and SPECT (Tomomatic 564). TCD of the middle cerebral artery (MCA) was done by EME TC-64B. A very low global CBF value of 28 +/- 5 (SD) ml 100 g-1 min-1 was found at baseline as compared to 55 +/- 5 ml 100 g-1 min-1 in the normal controls. During 6% CO2-inhalation and after acetazolamide administration, CBF increased by 58 +/- 24% and 51 +/- 21%, respectively, indicating substantial collateral supply. Correlative analysis of CBF in the MCA territory and TCD in the MCA showed statistical significance only for the pooled data, i.e. compiling the data obtained during baseline and the two vasodilatory tests, and then only for the mean and peak TCD velocity (e.g. r = 0.59, p less than 0.002, n = 35, mean velocity, right side). We conclude that TCD measurements do not predict regional CBF in patients with CCA occlusion. The study emphasizes that these two methods yield supplementary information, with TCD measurements providing information of the circle of Willis and CBF studies of the flow distribution.

Acetazolamide↗
PubMed1992

Mental stress and cognitive performance do not increase overall level of cerebral O2 uptake in humans.

We measured cerebral metabolic rate of oxygen (CMRO2), cerebral blood flow (CBF), and cerebral lactate output during rest, during the execution of mental arithmetic, and during mental stress induced by physical and psychological annoyance. Measurements were performed in healthy volunteers by use of the Kety-Schmidt technique with 133Xe as the inert gas. Electroencephalographic desynchronization and highly significant increases in plasma catecholamines and heart rate verified that the test measurements were performed during conditions differing distinctly from the resting state. In accordance with an earlier study (Sokoloff et al. J. Clin. Invest. 34: 1101-1108, 1985), a minimal and nonsignificant 1% reduction of global CMRO2 during mental arithmetic was observed, signifying that this form of mental activation was unassociated with any detectable increase in overall cerebral synaptic activity. Mental stress induced a slight but highly significant (P less than 0.002) 6% reduction in global CMRO2. This finding is in contrast to results from earlier investigations and contradicts the generally accepted notion of an association between mental arousal and a diffuse upregulation of cerebral synaptic activity. During mental arithmetic and mental stress, cerebral lactate output increased by 207 and 344%, respectively, but because of large individual variations in the measured responses, the elevations reached statistical significance only during mental arithmetic.

Adult↗
PubMed1991

Cerebral oxygen metabolism and cerebral blood flow in man during light sleep (stage 2).

We measured cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) during light sleep (stage 2) in 8 young healthy volunteers using the Kety-Schmidt technique with 133Xe as the inert gas. Measurements were performed during wakefulness and light sleep as verified by standard polysomnography. Unlike our previous study in man showing a highly significant 25% decrease in CMRO2 during deep sleep (stage 3-4) we found a modest but statistically significant decrease of 5% in CMRO2 during stage 2 sleep. Deep and light sleep are both characterized by an almost complete lack of mental activity. They differ in respect of arousal threshold as a stronger stimulus is required to awaken a subject from deep sleep as compared to light sleep. Our results suggest that during non-rapid eye movement sleep cerebral metabolism and thereby cerebral synaptic activity is correlated to cerebral readiness rather than to mental activity.

Adult↗
PubMed1991

Human regional cerebral blood flow during rapid-eye-movement sleep.

Owing to the coupling between CBF and neuronal activity, regional CBF is a reflection of neural activity in different brain regions. In this study we measured regional CBF during polysomnographically well-defined rapid-eye-movement (REM) sleep by the use of single photon emission computerized tomography and the new tracer 99mTc-dl-hexamethylpropyleneamine. Eleven healthy volunteers aged between 22 and 27 years were studied. CBF was measured on separate nights during REM sleep and during EEG-verified wakefulness. On awakening from REM sleep, all subjects reported visual dreams. During REM sleep CBF increased by 4% (p less than 0.01) in the associative visual area, while it decreased by 9% (p less than 0.01) in the inferior frontal cortex. The CBF increase in the associative visual area suggests that activation of cerebral structures processing complex visual material is correlated to visual dream experiences. On the other hand, the reduced involvement of the inferior frontal cortex observed during REM sleep might explain the poor temporal organization and bizarreness often experienced in dreams.

Adult↗
PubMed1991

Cerebral O2 metabolism and cerebral blood flow in humans during deep and rapid-eye-movement sleep.

It could be expected that the various stages of sleep were reflected in variation of the overall level of cerebral activity and thereby in the magnitude of cerebral metabolic rate of oxygen (CMRO2) and cerebral blood flow (CBF). The elusive nature of sleep imposes major methodological restrictions on examination of this question. We have now measured CBF and CMRO2 in young healthy volunteers using the Kety-Schmidt technique with 133Xe as the inert gas. Measurements were performed during wakefulness, deep sleep (stage 3/4), and rapid-eye-movement (REM) sleep as verified by standard polysomnography. Contrary to the only previous study in humans, which reported an insignificant 3% reduction in CMRO2 during sleep, we found a deep-sleep-associated statistically highly significant 25% decrease in CMRO2, a magnitude of depression according with studies of glucose uptake and reaching levels otherwise associated with light anesthesia. During REM sleep (dream sleep) CMRO2 was practically the same as in the awake state. Changes in CBF paralleled changes in CMRO2 during both deep and REM sleep.

Adult↗
PubMed1991

Cerebral blood flow and metabolism during sleep.

A review of the current literature regarding sleep-induced changes in cerebral blood flow (CBF) and cerebral metabolic rate (CMR) is presented. Early investigations have led to the notion that dreamless sleep was characterized by global values of CBF and CMR practically at the level of wakefulness, while rapid eye movement (REM) sleep (dream sleep) was a state characterized by a dramatically increased level of CBF and possibly also of CMR. However, recent investigations firmly contradict this notion. Investigations on CBF and CMR performed during non-REM sleep, taking the effect of different levels of sleep into consideration, show that light sleep (stage II) is characterized by global levels of CBF and CMR only slightly reduced by 3-10% below the level associated with wakefulness, whereas CBF and CMR during deep sleep (stage III-IV) is dramatically reduced by 25-44%. Furthermore, recent data indicate that global levels of CBF and CMR are about the same during REM sleep as in wakefulness. On the regional level, deep sleep seems to be associated with a uniform decrease in regional CBF and CMR. Investigations concerning regional CBF and CMR during REM sleep are few but data from recent investigations seem to identify site-specific changes in regional CBF and CMR during REM sleep. CBF and CMR are reflections of cerebral synaptic activity and the magnitude of reduction in these variables associated with deep sleep indicates that overall cerebral synaptic activity is reduced to approximately one-half the level associated with wakefulness, while cerebral synaptic activity levels during REM sleep are similar to wakefulness. However, even though the new understanding of CBF and CMR during sleep provides significant and important information of the brain's mode of working during sleep, it does not at its current state identify the physiological processes involved in sleep or the physiological role of sleep.

Animals↗
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↗
PubMed1990

Computerized analysis of cerebral blood flow autoregulation in humans: validation of a method for pharmacologic studies.

Cerebral blood flow (CBF) autoregulation in the supine position without tilting using systemic ganglion-blockade (trimetaphane camphosulfonas) combined with lower body vacuum is evaluated. Automatic computerized curve-fitting analysis for assessment of the lower limit (LL) of autoregulation is introduced. Global CBF was evaluated using the arteriovenous-O2-difference method in 12 volunteers and in seven patients with chronic arterial hypertension. Classic autoregulatory curves were found in all cases. The LL of CBF autoregulation was 85 +/- 5 mm Hg in the volunteers and 113 +/- 7 mm Hg in the hypertensive patients. In seven of the volunteers, the autoregulatory study was performed twice in 1 day; a small but significant shift of LL toward higher blood pressure (BP) values was observed in the second test (3 mm Hg). In five of the hypertensive patients, regional CBF (rCBF) was measured by single-photon emission computed tomography (SPECT) of inhaled xenon-133. The median global CBF decreased from 62 to 45 ml/100 g/min during the mean arterial BP (MABP) decrease from 110 to 68 mm Hg. The regional distribution of CBF was normal at baseline as well as during hypotension. The method is suitable for pharmacologic studies of cerebral autoregulation.

Adult↗
PubMed1989

Neuronal pH regulation: constant normal intracellular pH is maintained in brain during low extracellular pH induced by acetazolamide--31P NMR study.

The intracellular pH in the brain was studied in six healthy volunteers before and immediately after the administration of 2 g of acetazolamide. Phosphorus-31 nuclear magnetic resonance spectroscopy by a 1.5 tesla whole-body scanner was used. The chemical shift between the inorganic phosphate and the phosphocreatine resonance frequencies was used for indirect assessment of the intracellular pH. The mean baseline intracellular pH was 7.05 +/- 0.04 (SD). The mean pH changes obtained at 15-min intervals within the first hour of acetazolamide administration were -0.03 +/- 0.04 (SD), -0.02 +/- 0.03 (SD), and 0.00 +/- 0.04 (SD), i.e., no statistically significant pH decrease was observed during the period where extracellular pH is known to drop markedly. Although several factors contribute to the lack of change of the intraneuronal pH, we will discuss that this observation in addition might suggest a direct intracerebral effect of acetazolamide.

Acetazolamide↗
PubMed1989

Cerebral blood flow abnormalities in cerebral palsied children with a normal CT scan.

Cerebral palsy (CP) is often a consequence of a hypoxic-ischemic encephalopathy and/or intracerebral hemorrhage secondary to pre- and peri-natal asphyxia. Hypodense lesions on the CT-scan are found in about 70 to 80% of CP-patients. In the present study, regional cerebral blood flow (CBF) was measured in CP-patients having a normal CT-scan. The aim was to correlate the CBF changes with the clinical and the etiologic findings. CBF was measured by xenon-133 inhalation and single photon emission computer tomography. The mean CBF value in 20 CP-patients, age 6-19 years, was 67 +/- 11 (1 SD) ml/100g/min, the same value as found in the 9 normal children. However, 16 of the 20 CP-patients had focal hypoperfused areas on the tomographic flow map. In the preterm infants (n = 7) the hypoperfused areas were mainly located in the posterior watershed areas, often in one hemisphere only. In the term infants (n = 13) both asymmetrical and symmetrical hypoperfused areas were observed in the anterior and posterior watershed areas. In addition, several children had larger low flow areas in the frontal and fronto-parietal lobes. In both groups, a relatively poor concordance was observed between the clinical findings and the expected location of the low flow area.

Adolescent↗
PubMed1989

Angiotensin-converting enzyme inhibition and regional cerebral blood flow in acute stroke.

The effect of the angiotensin-converting enzyme (ACE) inhibitor captopril on regional cerebral blood flow (rCBF) was studied in 12 patients within 5 days after their first acute stroke. rCBF was studied by xenon-133 inhalation and single-photon emission computed tomography (SPECT) scan before and 1 h after oral administration of 25 mg captopril. No increase in rCBF was observed in any of the 12 patients included in the study. In only one patient was there a slight redistribution of blood flow in favor of the low-flow area, but the absolute flow value did not increase. Captopril did not cause any significant change in mean hemispheric blood flow, mean arterial blood pressure (MAP), or end-expiratory CO2 fraction (FECO2). The assumption that ACE inhibition might increase cerebral blood flow in the periinfarct zone and preserve some still viable brain tissue could not be verified in the present study.

Acute Disease↗
PubMed1989

Hemodilution increases cerebral blood flow in acute ischemic stroke.

We measured cerebral blood flow in 10 consecutive, but selected, patients with acute ischemic stroke (less than 48 hours after onset) before and after hemodilution. Cerebral blood flow was measured by xenon-133 inhalation and emission tomography, and only patients with focal hypoperfusion in clinically relevant areas were included. Hemodilution was done according to the hematocrit level: for a hematocrit greater than or equal to 42%, 500 ml whole blood was drawn and replaced by the same volume of dextran 40; for a hematocrit between 37% and 42%, only 250 ml whole blood was drawn and replaced by 500 cc of dextran 40. Mean hematocrit was reduced by 16%, from 46 +/- 5% (SD) to 39 +/- 5% (SD) (p less than 0.001). Cerebral blood flow increased in both hemispheres by an average of 20.9% (p less than 0.001). Regional cerebral blood flow increased in the ischemic areas in all cases, on an average of 21.4 +/- 12.0% (SD) (p less than 0.001). In three patients, a significant redistribution of flow in favor of the hypoperfused areas was observed, and in six patients, the fractional cerebral blood flow increase in the hypoperfused areas was of the same magnitude as in the remainder of the brain. In the last patient, cerebral blood flow increased relatively less in the ischemic areas. Our findings show that cerebral blood flow increases in the ischemic areas after hemodilution therapy in stroke patients. The marked regional cerebral blood flow increase seen in some patients could imply an improved oxygen delivery to the ischemic tissue.

Acute Disease↗
PubMed1989

Angiotensin converting enzyme inhibition and cerebral blood flow autoregulation in normotensive and hypertensive man.

The acute effect on the lower limit of cerebral blood flow (CBF) autoregulation of an angiotensin converting enzyme (ACE) inhibitor, captopril, was studied in normotensive volunteers and in hypertensive patients. Baseline CBF was measured using xenon-133 inhalation tomography, and changes in CBF were measured using the arterio-venous oxygen difference method. Cerebral blood flow autoregulation was studied in two separate normotensive groups, one group of 12 volunteers serving as a control, and one group of 12 volunteers studied after the administration of captopril 50 mg. In a group of seven hypertensive patients CBF autoregulation was studied before and 1 h after the administration of captopril 25 mg. In the normotensive volunteers the median lower limit of CBF autoregulation was 83 and 74 mmHg in the untreated and the captopril-treated group, respectively, with no significant difference between the two groups. In five of the hypertensive patients the lower limit of CBF autoregulation was lowered by captopril, in median by 22 mmHg. However, in two patients it was increased, by 3 and 13 mmHg, respectively. It is proposed that the shift in the lower limit of CBF autoregulation seen in some of our cases, and which has previously been documented in experimental studies, may be dependent on the activity of the sympathetic nervous system.

Adult↗
PubMed1989

CBF decreases after calcium antagonist treatment in acute ischemic stroke.

The effect of the possible influence of a new calcium antagonist, PY 108-068, on regional cerebral blood flow (CBF) was studied in patients suffering acute ischemic stroke. The dosage was 1.5 + 2.5 mg intravenously in six patients (series 1) and 2.5 + 5.0 mg intravenously in five other patients (series 2). CBF was measured before and after treatment by xenon-133 inhalation and single photon emission computed tomography (Tomomatic 64). In the first series, no changes in hemispheric CBF, arterial blood pressure, or clinical symptoms were noted after treatment, but one patient showed an increase of CBF in part of the peri-infarct area. In the second series, slight increases in mean hemispheric flow values were seen, but in three of the five patients CBF decreased even further in the ischemic area. Arterial blood pressure decreased by 13%, and the clinical symptoms were unchanged. In conclusion the results shows, that calcium antagonist may be harmful in acute ischemic strokes since it can decrease the cerebral blood flow further in the ischemic areas. A potential beneficial metabolic effect of an calcium antagonist in ischemic tissue may thus be overshadowed by a harmful flow decrease.

Acute Disease↗