Biomedical subjects

D Bereczki

Publications and source records attributed to D Bereczki.

At least 37 records · Page 2Linked to original sources

PubMed1999

[Evidence-based medicine. (Role of the Cochrane collaboration)].

The basic condition of practising evidence-based medicine is the knowledge of the evidence. Strongest of all evidences are the conclusions drawn from systematic reviews of randomized controlled trials. The over 2 million papers published annually in the biomedical literature is neither available nor possible to read for any individual, therefore it is necessary to identify and collect all relevant clinical trials, to make them available in databases, and to produce, to publish and to update systematic reviews based on the best evidence. The Cochrane Collaboration was established for these purposes in 1993. The activity of the Collaboration is summarized by a database The Cochrane Library which is updated quarterly. The user friendly Cochrane Library currently contains bibliographic data of over 218 thousand controlled trials (Cochrane Controlled Trials Register, CC-TR), and 1014 systematic reviews (Cochrane Database of Systematic reviews, CDSR) prepared by reviewers in 49 Review Groups. As the Cochrane Library contains information on much more controlled trials than any other databases including MEDLINE, decision makers in health care should be aware of this source of information. In addition to the application of the Cochrane Library as a source of information, active participation by identifying controlled trials in the Hungarian medical literature and registering them in the CCTR is another important task.

Clinical Medicine↗

PubMed1999

A systematic review of vinpocetine therapy in acute ischaemic stroke.

OBJECTIVES: To determine whether vinpocetine decreases short- and long-term case fatality and proportion of dependent survivors if administered within 2 weeks of stroke onset. METHODS: All published and unpublished trials were attempted to be identified using the standard search strategy of the Cochrane Collaboration Stroke Review Group, using MEDLINE searches performed with all known manufacturer code names and trade names of vinpocetine and by contacting manufacturers of vinpocetine to give information of all randomised controlled trials on vinpocetine in stroke. Researchers who participated in trials on vinpocetine in Hungary were asked for further information. Only truly randomised, unconfounded clinical trials that compared the effect of vinpocetine to either placebo or another reference treatment for acute stroke where treatment started no later than 14 days after stroke onset were eligible for inclusion. Data synthesis and analysis was performed using the Cochrane Review Manager software (RevMan version 3.0). RESULTS: Among the identified studies on vinpocetine in stroke, only one fulfilled the selection criteria for inclusion in the review. No death occurred in the study groups and no statistically significant difference was found in dependency between the treatment and the placebo groups. No adverse effects were reported. CONCLUSIONS: Based on only one small randomised controlled unconfounded study, presently there is not enough evidence to decide whether the administration of vinpocetine does or does not decrease case fatality and dependency in acute stroke.

Cerebrovascular Disorders↗

PubMed1999

No relationship between cerebral blood flow velocity and cerebrovascular reserve capacity and contemporaneously measured glucose and insulin concentrations in diabetes mellitus.

Blood glucose and insulin concentrations have been reported to influence cerebral hemodynamics. We studied the relationship between actual blood glucose and insulin concentrations and resting cerebral blood flow velocity in the middle cerebral artery and cerebrovascular reserve capacity after acetazolamide stimulation. Thirty-six insulin-dependent diabetic patients in a state of good glycemic control were studied. Blood samples were taken for determination of glucose and insulin concentrations. Subsequently we measured resting cerebral blood flow velocities in supine position using transcranial Doppler, administered 1 g acetazolamide intravenously, and repeated the measurements after 5, 10, 15 and 20 minutes. Cerebrovascular reserve was calculated as the maximal percent increase after acetazolamide stimulation. Multiple regression was used for statistical analysis. Blood glucose levels were not correlated with resting blood flow velocity (R = 0.21, p = 0.22) nor cerebrovascular reserve capacity (R = 0.17, p = 0.32). Similarly, no correlation was found between insulin concentrations, resting cerebral blood flow velocity (R = 0.24, p = 0.22) and cerebrovascular reserve (R = 0.26, p = 0.24). Studying patients with long-term (> 10 years) and short-term (</= 10 years) disease duration yielded the same lack of correlation. We conclude that there is no significant correlation between contemporaneously measured glucose and insulin concentrations and either cerebral blood flow velocity or cerebrovascular reserve capacity in the middle cerebral artery in type 1 diabetic patients with good control.

Acetazolamide↗

PubMed1999

Basic characteristics of hospital stroke services in Eastern Hungary.

Stroke mortality is extremely high in Central-Eastern European countries. We report basic characteristics of a stroke unit in Eastern Hungary, including age and sex distribution; the proportion of transient ischemic attacks (TIA), ischemic and hemorrhagic strokes; case fatality; application of diagnostic methods; and length of stay for all patients treated with acute cerebrovascular disease over a 12-month period. Records of all patients with acute cerebrovascular disease (n = 522) discharged in 1995 from a stroke unit with a well defined catchment area of 220,000 inhabitants in Eastern Hungary were retrospectively analyzed. Case fatality was 18.6% for all patients and 21.1% after excluding cases with TIA. Computer tomography, duplex carotid ultrasound, cerebrospinal fluid examination and electroencephalography were performed in 79%, 77%, 7% and 2% of the patients, respectively. The database of the university hospital with the same catchment area was electronically searched for patients who were discharged with the diagnosis of stroke from the three departments of internal medicine. Stroke mortality data of the catchment area based on death certificates was obtained from the Central Statistical Bureau. Two hundred twenty-eight stroke deaths were reported in the catchment area in 1995. In the same period 97 stroke deaths occurred at the stroke unit and 76 at the departments of internal medicine. If we aim to treat all patients with acute stroke at the stroke unit, with the present stroke incidence and duration of hospital stay the current capacity of the stroke unit (1 bed per 10.000 inhabitants) should be doubled.

Adult↗

PubMed1999

Screening of vascular cognitive impairment on a Hungarian cohort.

Cerebrovascular disease is a major public health problem in Eastern European countries. A Hungarian post-stroke population was examined to estimate the rate of dementia, the risk factors for cognitive impairment, and the applicability of a recently established Canadian diagnostic checklist in this cohort. Chronic cerebrovascular outpatients were screened for cognitive impairment with a combined checklist: the Diagnostic Checklist for Vascular Dementia established by the Consortium of Canadian Centres for Clinical Cognitive Research using the Mini Mental State Examination instead of the detailed neuropsychological part of the Checklist. Of the 247 consecutive patients at a cerebrovascular outpatient unit, 176 had cerebrovascular disorder diagnosed either by computed tomography (CT; n=126) or by the clinical signs. Of these, 15% were cognitively impaired and 5% fulfilled the criteria of dementia. The mean age of the patients with cognitive impairment was significantly higher than that of patients with normal cognition (68.2+/-10.2 and 60.5+/-10.5 years, P<0.001). The Barthel index was significantly lower in the cognitively affected group than in non-affected patients (92.4+/-16.0 and 97.1+/-8.7, P=0.027). Diabetes and more than two subcortical infarcts on CT or magnetic resonance imaging were more frequent in patients with cognitive loss (P=0.043 and P=0.013, respectively). Cognitive performance was also influenced by the level of education. Higher age, diabetes, motor deficits, and multiple subcortical infarcts are risk factors for cognitive impairment after stroke. The combined checklist appears to be a practical screening test for cognitive impairment in patients with chronic cerebrovascular diseases.

Age Distribution↗

PubMed1999

Screening for depressive symptoms among post-stroke outpatients in Eastern Hungary.

Patients were consecutively enrolled in a cross-sectional study to determine the severity of depressive symptoms and the rate of treated depression in a patient population returning to a stroke outpatient service during a 10-week period for a regular check-up examination after their stroke. Of the 143 stroke patients, 119 fulfilled the inclusion criteria. The 13-item Beck Depression Inventory was used to screen for depressive symptoms. The score was at least 5 in 53%, 10 or above in 26%, and 15 or above in 11% of patients. Severity of depressive symptoms did not depend on gender, age, time elapsed from stroke, or the site of the cerebral lesion. Most patients with considerable depressive symptoms did not receive antidepressant medication at the time of the screening.

Adult↗

PubMed1998

[Cerebrovascular reactivity in non-insulin dependent diabetes mellitus (preliminary results)].

AIMS: Previously numerous investigators reported about impairment of cerebrovascular reserve capacity in Type I, diabetes mellitus. However, no similar data are available about patients suffering from Type II diabetes. The goal of the study was to assess cerebrovascular reserve in Type II diabetic patients. PATIENTS AND METHODS: 14 NIDDM patients and 20 healthy controls were studied. Middle cerebral artery mean blood flow velocity was measured at rest and during 20 minutes after i.v. administration of 1 g. acetazolamide. Velocities measured after acetazolamide were compared to resting values and were expressed as the percent increase of the mean velocity. Data obtained in diabetics and healthy persons were compared using Student's t-test. The correlation between age of the patients, diabetes duration, actual blood glucose-, insulin-, glycosylated hemoglobin-, urine microalbumin concentrations and resting blood flow velocity and cerebrovascular reserve capacity was assessed using linear regression analysis. RESULTS: Resting cerebral blood flow velocities, cerebrovascular reactivity and reserve capacity did not differ from that of healthy controls. No correlation has been found between obtained laboratory parameters and resting cerebral blood flow velocities and cerebrovascular reserve capacity. CONCLUSIONS: Vasodilatory ability of the cerebral arterioles in NIDDM-patients did not differ from that of healthy control persons. Further studies are needed to find out an accurate screening method for detection of cerebral microangiopathic changes in Type II diabetes mellitus.

Acetazolamide↗

PubMed1998

Local cerebral blood flow during the first hour following acute ligation of multiple arterioles in rat whisker barrel cortex.

The objectives are to measure the early time-course of the flows of blood, red cells, and plasma in brain tissue destined to infarct following arterial occlusion. The flux of fluorescent red blood cells (fRBCs) through venules and the arteriovenous transit times (AVTT) of fluorescein-labeled plasma albumin were periodically monitored in anesthetized adult Wistar rats before and up to 60 min after permanent ligations of several small branches of the middle cerebral artery. Of note, fRBC is a function of venular erythrocyte flow and volume, whereas AVTT is a function of plasma flow and volume in visible arteriole-capillary-venule units. In another group of anesthetized rats, local cerebral blood flow (ICBF) was measured 1 h after permanent arterial occlusion by [14C]iodoantipyrine (IAP) autoradiography. With this model of focal ischemia, the lesion is highly reproducible and involves part of the whisker barrel cortex. Infarction of this area was observed in 12 of 13 rats. From 10 to 60 min after arterial occlusion, AVTT was nearly four times longer in the ischemic barrel cortex than at the same site before ligations, and fRBC flux was 25%. Neither parameter changed appreciably over this time. After 60 min of ischemia, ICBF on the ipsilateral barrel cortex was 18% of that on the contralateral side and 15% of the sham control value for the same area of the barrel cortex. Since whole blood flow in the ischemic barrel cortex was < 20% of normal at 60 min and AVTT and fRBC flux were essentially constant from 10 to 60 min, the rates of plasma and red cell flows were similarly depressed during the first hour of arteriolar occlusion. In conclusion, such lowering of red cell, plasma, and blood flows produced consistent infarctions in the barrel cortex.

Acute Disease↗

PubMed1998

Cerebral effects of a single dose of intravenous vinpocetine in chronic stroke patients: a PET study.

The effects of vinpocetine (Cavinton) on the cerebral glucose metabolism of chronic stroke patients are studied with positron emission tomography. The regional and global cerebral metabolic rates of glucose (CMRglu) and the kinetic constants related to them are quantified before and after single-dose intravenous vinpocetine treatment. These measurements are completed with transcranial Doppler sonography and single photon emission computed tomography to explore the possible mechanisms underlying the resulting changes in glucose uptake and metabolism in the brain. The authors' findings indicate that a single-dose vinpocetine treatment, although it does not affect significantly the regional or global metabolic rates of glucose, improves significantly the transport of glucose (both uptake and release) through the blood-brain barrier in the whole brain, the entire contralateral hemisphere, and in the brain tissue around the infarct area of the symptomatic hemisphere. These changes are in accord with increased blood flow in the entire contralateral hemisphere as well as decreased blood flow velocity and increased peripheral vessel resistance in the entire symptomatic hemisphere.

Aged↗

PubMed1997

Impairment of cerebrovascular reactivity in long-term type 1 diabetes.

The early preclinical detection of cerebrovascular complications in individuals with diabetes is one of the goals of care described in the St. Vincent Declaration. In accordance with this goal, the aim of the present work was to investigate whether altered cerebral microvascular function in patients suffering from type 1 diabetes can be detected with a transcranial Doppler probe after the administration of acetazolamide. A total of 72 type 1 diabetic patients and 40 healthy control subjects entered the study. Patients were divided into two groups: those with long-term diabetes (disease duration of >10 years, n = 37) and those with short-term diabetes (disease duration of < or =10 years, n = 35). Mean blood-flow velocity in the middle cerebral artery (MCAV) was measured at rest and at 5, 10, 15, and 20 min after intravenous administration of 1 g acetazolamide with a transcranial Doppler probe and expressed as the percentage change from the pretest measurement. The percentage increase in MCAV (cerebrovascular reactivity) was calculated at each time point and compared between the groups. Cerebrovascular reserve capacity (CRC), expressed as the maximal percentage increase of the MCAV, was compared between the groups. Additionally, a reproducibility study of CRC was performed in 10 patients, using intraclass correlations. Cerebrovascular reactivity in the long-term diabetes group was lower (means +/- SD: 5 min, 23.4 +/- 15.4%; 10 min, 28.8 +/- 17.0%; 15 min, 30.0 +/- 15.6%; 20 min, 24.2 +/- 17.8%) than that of the control subjects (5 min, 43.5 +/- 23.9%; 10 min, 55.3 +/- 24.0%; 15 min, 56.7 +/- 23.8%; 20 min, 54.8 +/- 25.9%) and the short-term diabetic patients (5 min, 43.6 +/- 25.9%; 10 min, 52.2 +/- 27.7%; 15 min, 55.3 +/- 32.2%; 20 min, 45.8 +/- 35.8%). CRC was lower in the long-term diabetes group than in the control group or the short-term diabetes group. Impairment of cerebrovascular reactivity was associated with retino- and nephropathy and increased levels of fibrinogen. In contrast, CRC was independent from actual glucose, insulin, glycosylated hemoglobin, von Willebrand factor antigen, and alpha-2 macroglobulin levels. Transcranial Doppler measurements of the changes in MCAV after stimulation with acetazolamide can detect altered cerebral microvascular function in patients with diabetes. Cerebrovascular reactivity and reserve capacity are reduced in patients with long-term diabetes. Further prospective studies should delineate the clinical significance of our results.

Acetazolamide↗

PubMed1996

[Low doses of acetylsalicylic acid effectively inhibits thrombocyte aggregation after ischemic stroke].

Platelet aggregation was examined in 43 patients after ischemic stroke and in 16 healthy subjects using multiparametric aggregation index (MAI). The value of MAI was significantly higher in stroke patients (3.15 in patients and 0.92 l/mumol in controls, p < 0.0001). Patients who had increased MAI (n = 26) were treated with a daily dose of 100 mg acetilsalicylic acid (ASA). Platelet activity was measured before and on the 7th and 28th day of treatment measuring three parameters: MAI, spontaneous dysaggregation and collagen induced aggregation. All 3 methods showed a significant decrease in platelet aggregation on the 7th day of treatment, but further changes were not found on the 28th day. Serum levels of thromboxane-A2 (TXA2) and prostacycline (PGI2) metabolites (TXB2 and 6-keto-prostaglandin-F1 alpha) were determined before and on the 28th day of treatment. The effect of 100 mg ASA per day proved to be selective: comparing the serum levels before and after treatment, a significant decrease of TXB2 concentration was found without changes in the concentration of 6-keto-prostaglandin-F1 alpha. Evaluating MAI and the value of dysaggregation might reflect ineffectiveness of antiplatelet therapy in patients not responding to a daily dose of 100 mg of ASA. For these patients the increase of the daily dose of ASA, or changing to another antiplatelet drug might be recommended.

Aged↗

PubMed1996

Cerebrovascular reactivity measured by transcranial Doppler in migraine.

Changes in the diameter of intracranial arteries might have a major role in the pathophysiology of migraine. Though several studies have found alterations in velocity of blood flow and in cerebral vasomotor reactivity of intracranial arteries in migraineurs in headache-free periods, as well as during migraine attacks, the results are inconclusive. To determine if intracranial hemodynamic characteristics of patients with migraine differ from those of controls, we measured baseline velocity of blood flow by transcranial Doppler in the middle cerebral arteries in headache-free periods in 51 migraine patients and in 101 age-matched controls. Cerebrovascular reactivity was measured after intravenous administration of acetazolamide in 12 migrainous patients and in 19 controls. Baseline mean velocity was significantly higher in the migraine group (70 versus 65 and 72 versus 65 cm/s with P = 0.02 and P = 0.0007 on the left and right sides, respectively). The difference stayed significant during acetazolamide stimulation, but the course of response did not differ between controls and migraineurs. Despite statistical significance, absolute differences were small. Therefore, middle cerebral artery velocity measurements and the acetazolamide test are not useful for the diagnosis of migraine in the interictal period.

Acetazolamide↗

PubMed1995

Nicotine raises the influx of permeable solutes across the rat blood-brain barrier with little or no capillary recruitment.

Nicotine (1.75 mg/kg s.c.) was administered to rats to raise local CBF (lCBF) in various parts of the brain, test the capillary recruitment hypothesis, and determine the effects of this increase in lCBF on local solute uptake by brain. lCBF as well as the local influx rate constants (K1) and permeability-surface area (PS) products of [14C]antipyrine and [14C]-3-O-methyl-D-glucose (3OMG) were estimated by quantitative autoradiography in 44 brain areas. For this testing, the finding of significantly increased PS products supports the capillary recruitment hypothesis. In 17 of 44 areas, nicotine treatment increased lCBF by 30-150%, K1 of antipyrine by 7-40%, K1 of 3OMG by 5-27%, PS product of antipyrine by 0.20% (mean 7%), and PS product of 3OMG by 0-23% (mean 8%). Nicotine had no effect on blood flow or influx in the remaining 27 areas. The increases in lCBF and K1 of antipyrine were significant, whereas those in K1 of 3OMG and in PS for both antipyrine and 3OMG were not statistically significant. The lack of significant changes in PS products implies that in brain areas where nicotine increased blood flow: (a) essentially no additional capillaries were recruited and (b) blood flow within brain capillary beds rises by elevating linear velocity. The K1 results indicate that the flow increase generated by nicotine will greatly raise the influx and washout rates of highly permeable materials, modestly elevate those of moderately permeable substances, and negligibly change those of solutes with extraction fractions of < 0.2, thereby preserving the barrier function of the blood-brain barrier.

3-O-Methylglucose↗

PubMed1994

Slightly altered permeability-surface area products imply some cerebral capillary recruitment during hypercapnia.

To test the capillary recruitment hypothesis in brain, cerebral blood flow was raised markedly in rats by exposure to 8% CO2 (hypercapnia), and capillary permeability-surface area (PS) products were measured. Local cerebral blood flow (LCBF), volume of radiolabeled blood in parenchymal microvessels (also referred to as the blood space or Vb), plus the local capillary influx rate constants (K1) and PS products of [14C]antipyrine and 3-O-[14C]methyl-D-glucose (3OMG) were estimated in 44 brain areas. Hypercapnia raised PaO2 to 140 mm Hg, elevated LCBF by two- to threefold through out the brain, and increased Vb from 5 to 33% (mean = 22%) in 42 of 44 brain areas; hypercapnia did not, however, alter microvessel hematocrit. With hypercapnia, the influx of antipyrine was increased by 40-65% in all brain areas, and the PS products of antipyrine were elevated from 0-35% (mean = 17%). The PS products of antipyrine plus the parenchymal blood spaces suggest modest (< 30%) capillary recruitment in most brain areas as well as some microvessel dilation, mainly in forebrain gray matter and white matter areas. In contrast, hypercapnia did not appreciably alter K1 nor PS of 3OMG; it slightly but not significantly raised the blood levels of glucose. In view of the blood space and antipyrine evidence for modest capillary recruitment and vasodilation, the lack of change in PS of 3OMG implies that glucose transporter activity was lowered by hypercapnia, an effect similar to that reported for high-dose pentobarbital. Finally, the microvessel hematocrit and 3OMG data suggest that cerebral capillary permeability (P) was not increased by hypercapnia. Overall, hypercapnia seems to increase LCBF mainly by raising the velocity of blood flow; capillary recruitment and dilation appear to play relatively minor roles in this flow increase.

3-O-Methylglucose↗

PubMed1994

A simple technique for the estimation of regional blood content in brain.

A simple and inexpensive technique is described for the assessment of regional cerebral blood volume (CBV) using a color reaction based on the pseudoperoxidase activity of hemoglobin. Cryostat sections are placed on a commercially available reagent strip originally designed for quantitative estimation of blood content in urine. After melting of the brain section, a blue color reaction appears which is darker in areas with higher hemoglobin content. The image is analyzed by a computerized image-processing system and evaluated by standards prepared from brain homogenate with different hemoglobin content. From the optical density data, regional CBV is calculated with correction for the difference between microvascular and large vessel hematocrit. The method was validated by a radiolabel procedure. Values of regional CBV are reported in gray matter areas of control rabbits and in brains embolized by autologous clot. This simple inexpensive technique is a useful supplementary tool in multiparametric metabolic studies.

Animals↗

PubMed1994

Virtually unaltered permeability-surface area products imply little capillary recruitment in brain with hypoxia.

OBJECTIVE: To test the capillary recruitment hypothesis for the brain with control and hypoxic rats. METHODS: Local cerebral blood flow (LCBF) was sharply raised by respiring 10% O2 (hypoxia). LCBF as well as local influx rate constants (K1) and permeability-surface area (PS) products of 14C-antipyrine and 14C-3-O-methyl-D-glucose (30MG) were estimated for capillary systems in 44 brain areas. RESULTS: With this testing, an increase in PS product would be suggestive of capillary recruitment. In all brain areas, LCBF was increased by 30-90% by hypoxia. Hypoxia modestly raised the influx of antipyrine in brain but did not appreciably alter its PS products. With hypoxia, K1's and PS products of 30MG were significantly lowered (5-25%) throughout the brain, and the blood levels of glucose were sizeably raised. The latter increase would diminish the transfer of 30MG across the blood-brain barrier by the hexose transporter because of increased glucose competition. By applying a glucose-concentration correction to the data, the apparent PS product of 30MC for the hypoxic group became equal to that for the controls, which agrees with the antipyrine PS product results. CONCLUSIONS: Hypoxia, thus, leads to virtually no increase in PS products and no capillary recruitment in brain, and elevates LCBF mainly, perhaps exclusively, by raising the velocity of flow through already perfused capillaries.

3-O-Methylglucose↗

PubMed1993

Spatial and temporal changes in tissue pH and ATP distribution in a new model of reversible focal forebrain ischemia in the rat.

The effects of reversible middle cerebral artery occlusion on regional pH and ATP distribution were studied in a new stroke model in rats by a planimetric method. Thirty minutes of ischemia was followed by 2, 4 and 24 hours of reperfusion. Ischemia resulted in acidosis and ATP depletion. In some areas tissue pH reached the threshold of the umbelliferone method (about pH 6.0). Areas with ATP depletion were significantly smaller than regions of pH alteration not only at the end of ischemia but during the first 4 hours of recirculation as well. By 4 hours of reperfusion large areas with altered pH were associated with ATP depletion in smaller regions, mostly in the hippocampus and the frontal cortex. The areas of ATP depletion were acidic initially, but by 4 hours alkaline pH could also be detected. Twenty four hours after ischemia alkaline areas (pH > 7.4) were found with ATP depletion, suggesting irreversible tissue damage, in cortical areas, in the hippocampus, and in the thalamus. By 24 hours of reperfusion there was no significant difference between the size of areas with altered pH and ATP depletion.

Adenosine Triphosphate↗

PubMed1993

Hypoxia increases velocity of blood flow through parenchymal microvascular systems in rat brain.

The postulation that hypoxia increases local cerebral blood flow (lCBF) mainly by perfusing more capillaries (the capillary recruitment hypothesis) was tested in awake adult male Sprague-Dawley rats exposed to 10% O2 and control rats. The [14C]iodoantipyrine technique was used to measure lCBF. Local cerebral blood volume was determined by measuring plasma and red cell distribution spaces within the brain parenchyma with 125I-labeled serum albumin (RISA) and 55Fe-labeled red cells (RBC), respectively. Tissue radioactivity in 44 brain areas was estimated by quantitative autoradiography. Hypoxia raised lCBF by 25-90% in all brain areas. In about one-quarter of the brain areas, the rise in blood flow was associated with a small increase in microvascular plasma and blood volumes. This change in blood volume, which could be the result of perfusing more parenchymal microvessels and/or increasing parenchymal microvessel diameter, is not sufficient to account for the observed rise in lCBF. In the remaining areas the RISA, RBC, and blood spaces were either unchanged or only marginally increased by hypoxia. For this hypoxic perturbation, the major mechanism of raising blood flow appears to be increased velocity of microvessel perfusion and not perfusion of more capillaries. These findings provide only limited support for the capillary recruitment hypothesis.

Animals↗