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Biomedical subjects

J F Schmidt

Publications and source records attributed to J F Schmidt.

At least 37 records · Page 2Linked to original sources
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

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

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↗
PubMed1992

Radioimmunoassay of beta-endorphin in ventricular and lumbar cerebrospinal fluid.

We describe a sensitive beta-endorphin (beta-EP) radioimmunoassay specific for beta-EP 1-31 applied to human ventricular and lumbar cerebrospinal fluid (CSF). Specificity was documented by reversed-phase HPLC of CSF pools. Simultaneous ventricular and lumbar CSF samples from 13 patients suspected of having normal-pressure hydrocephalus showed median beta-EP values of 2.2 (range 1.7-4.0) and 4.8 (2.8-14.6) pmol/L, respectively. Ventricular and lumbar beta-EP concentrations were positively correlated (Spearman r = 0.72, P = 0.013). The beta-EP rostral-caudal gradient was closely related to the CSF protein gradient. HPLC profiles of beta-EP immunoreactivity were similar in ventricular and lumbar CSF with both C- and N-terminal antisera. beta-EP concentrations did not vary in the first 12 mL of lumbar CSF, tapped in 3-mL portions [F(3,32) = 0.42, P = 0.74]. The beta-EP concentration in lumbar CSF from 15 children in remission from acute leukemia [23.4 (15.0-27.1) pmol/L] was higher than in 54 healthy adults [11.7 (10.9-13.3) pmol/L; P less than 0.01]. There was no effect of sex or age on CSF beta-EP in adults. beta-EP in lumbar human CSF may indicate di- and mesencephalic beta-EP neuronal activity.

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

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

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

Intracranial pressure and cerebrospinal fluid outflow conductance in healthy subjects.

Conductance of cerebrospinal fluid (CSF) outflow (Cout) is an important parameter to be considered in patients with CSF circulation abnormalities. In patients with normal-pressure hydrocephalus it is the single most important parameter in determining if the patient needs CSF shunting. The lower normal limit for Cout has been estimated from the effect of shunting in patients with normal-pressure hydrocephalus, from patients retrospectively reevaluated after recovering from illness, and from patients with known abnormalities in the brain or the CSF system. The true value of Cout in normal individuals, however, has hitherto not been reported. In the present study, Cout has been measured by a lumbar infusion test in eight young volunteers with no suspicion of disease. The mean intracranial pressure (ICP) was 11 mm Hg and a linear relationship was found between CSF absorption and ICP. The mean Cout was 0.11 ml/min/mm Hg and the lower 95% confidence level was 0.10 ml/min/mm Hg. These values are in accordance with those obtained from previous studies.

Adult↗
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

The effect of nimodipine on ICP and CBF in patients with normal-pressure hydrocephalus.

Eight patients with normal-pressure hydrocephalus (NPH) were studied. The resting mean arterial blood pressure (MABP) was 100 (90-125) mmHg and the mean intracranial pressure (ICP) was 11 (5-17) mmHg. ICP and MABP were continuously measured intraventricularly and intra-arterially, respectively. Changes in global cerebral blood flow (CBF) were estimated by the arteriovenous oxygen difference method. Intravenous nimodipine (15 microgram/kg/hour) was given in the first 2 hours and 30 microgram/kg/hour in the next 2 hours. MABP was reduced 23 (4-47) mmHg (p less than 0.05). ICP was increased 3 (0-10) mmHg (p less than 0.05). CBF was unchanged in the group on the whole, but in 4 of patients a major drop in perfusion pressure was seen, and CBF decreased 6, 11, 23 and 34%, respectively. Thus these findings underline the importance of maintaining the perfusion pressure under treatment with nimodipine.

Aged↗
PubMed1990

Angiotensin converting enzyme inhibition, CBF autoregulation, and ICP in patients with normal-pressure hydrocephalus.

Fourteen patients with normal pressure hydrocephalus had the autoregulation of cerebral blood flow (CBF) and intracranial pressure (ICP) investigated. In 8 of the patients the effect of Captopril on ICP and CBF was also investigated. The mean arterial blood pressure (MABP) was 109 mmHg (intra-arterially), and ICP was 11 mmHg (intraventricularly). Changes in global CBF were estimated by the arterio-venous oxygen difference method. The autoregulation of CBF was present in 13 of the patients (p less than 0.01). The lower limit of CBF autoregulation was 86% of the baseline perfusion pressure. One hour after 50 mg of captopril perorally, MABP was reduced 16 mmHg, and ICP and CBF were unchanged. The autoregulation was maintained and the lower limit was decreased 19 mmHg. Thus patients would be expected to benefit from captopril treatment in hypotensive anaesthesia.

Administration, Oral↗
PubMed1990

The acute effect of dilevalol on cerebral blood flow and oxygen consumption in normotensive humans.

The antihypertensive agent dilevalol, a stereoisomer of labetalol, causes vasodilatation by combined beta-adrenergic blockade and direct beta 2-receptor agonism. The acute effect of a single oral dose of 400 mg dilevalol on cerebral blood flow (CBF), and its response to induced changes in arterial carbon dioxide tension (PaCO2), and the cerebral metabolic rate of oxygen (CMRO2) were studied after 1, 2, and 4 h in eight normotensive volunteers. Serum dilevalol 2 h after oral intake ranged between 22 and 49 ng/ml. Mean arterial blood pressure was reduced from 93 +/- 8 to 86 +/- 8 mm Hg (p less than 0.01). An analysis of variance of the successive differences of CBF during the study showed that dilevalol altered CBF significantly. After 1 h CBF had decreased by 4.4% (p less than 0.05), whereas the 2 and 4 h values were similar to the pretreatment level. CMRO2 showed a tendency for reduction (p = 0.086). The CBF response to changes in PaCO2 remained unchanged. It is concluded that a single dose of dilevalol induces a slight and short-lasting decrease in CBF, probably due to a direct effect on brain metabolism.

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↗
PubMed1990

Effect of nimodipine on cerebral blood flow in human volunteers.

The present study was undertaken to examine the effect of a clinically relevant dose of nimodipine (30 micrograms/kg/h) on the autoregulation of CBF in 12 young healthy volunteers. Mean arterial blood pressure (MABP) was measured intraarterially (i.a.), and changes in cerebral blood flow (CBF) were estimated by the arteriovenous-oxygen [(a-v)O2]-difference method. The lower limit (LL) of CBF autoregulation was calculated by a computerized program and tested for different factors for correction of the PaCO2-induced changes in CBF. MABP was increased by norepinephrine (NE) and decreased by ganglion blockade (trimethaphane camphosulfonas) in combination with lower body negative pressure. The MABP manipulations were performed 1 h after infusion of nimodipine. MABP was reduced by 13 mm Hg (8-15 mm Hg), and CBF was increased by 8% (3-12%) during nimodipine infusion. Autoregulation was preserved in 11 of the 12 volunteers. A CO2-correction factor of 1% CBF/0.1 kPa was used. The LL was 75 mm Hg (71-80 mm Hg) [SE 3 mm Hg (2-4 mm Hg)] and not significantly different from a previous control group of healthy volunteers. No side effects were observed. The present study shows a maintained autoregulation of CBF during nimodipine infusion; however, this could be obtained only by reducing the correction for changes in carbon dioxide to 1%/0.1 kPa from 3%/0.1 kPa, which was used in a similar study in healthy volunteers.

Adult↗
PubMed1990

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

The present study was undertaken to examine the effect of captopril on cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2) and CO2 reactivity in eight young healthy volunteers. The mean arterial blood pressure (MABP) was measured intraarterially, and CBF was measured by inhaled xenon-1233. The CO2 reactivity was defined as the relative change in CBF per 0.1 kPa change in arterial CO2. During the CO2 reactivity tests, the CBF changes were estimated by the arteriovenous-oxygen-difference method (CBFsat). Median CBF was 52 ml/100 g/min (50-56) and without any significant regional side-to-side asymmetries. No significant change was observed after captopril. The median resting MABP was 90 mm Hg (89-93), and was slightly reduced by 5 mm Hg (4-6) 1 h after an oral dose of captopril (50 mg). CMRO2 was 3.7 ml/100 g/min (3.5-3.8) and was unchanged after captopril. For the entire range of PaCO2 the median slope of the ln(CBFsat) versus PaCO2 regression line was 1.4 (1.3-1.6) at baseline compared to 1.4 (1.3-1.7) after captopril (p = 0.23). Considering the PaCO2 values between 4.0 and 6.5, the CO2 reactivity was 2.4%/0.1 kPa (2.1-2.4) at baseline and increased significantly to 2.9%/0.1 kPa (2.1-3.2) after captopril (p less than 0.05). No side effects were observed. The present study shows an overall unchanged CO2 reactivity; however, with an increased CO2 reactivity of the cerebral vessels for small changes in PaCO2 around the resting value of PaCO2 and a maintained coupling of CBF and CMRO2 after peroral captopril.

Adult↗