Brain Cerebral Blood Flow Research Articles

Influence of Hypoxia and Sex on Hyponatremic Encephalopathy

Over the past 20 years it has become increasingly apparent that hyponatremic encephalopathy is a major cause of inhospital morbidity and mortality, particularly in postoperative patients. The factors that may lead to death or permanent brain damage and the susceptible patient groups have been gradually elucidated. Hyponatremic encephalopathy most commonly leads to brain damage in young women and in prepubescent children. The causes of brain damage include brain edema, cerebral hypoxemia, decreased brain blood flow, increased intracranial pressure, and improper therapy. Cerebral hypoxia occurs through a combination of impaired brain adaptation and cerebral vasoconstriction. Brain adaptation consists largely of brain cell loss of sodium and potassium by means of the Na-K adenosine triphosphatase (ATPase) system. There is also loss of organic osmolytes. The brain Na-K ATPase system is impaired by a combination of vasopressin plus estrogen and is stimulated by testosterone. Similarly, vasopressin plus estrogen leads to cerebral vasoconstriction, resulting in a decrement of brain oxygen utilization and cerebral blood flow. Vasopressin also directly decreases brain production of ATP. The combination leads to hypoxic brain damage, which appears to be the major cause of brain damage associated with hyponatremic encephalopathy. Measurement of arterial P o 2 in patients with symptomatic hyponatremia usually demonstrates a P o 2 <50 mm Hg. Improper therapy is another possible cause of brain damage in patients with hyponatremic encephalopathy. The type and distribution of such lesions are similar to those found in patients with hyponatremic encephalopathy who have severe hypoxia. Current scientific knowledge indicates that patient survival can be improved through aggressive treatment of hypoxia associated with hyponatremic encephalopathy, particularly in young women.

Brain Neuroimaging in Cannabis Use: A Review

In this study, the authors systematically reviewed structural and functional neuroimaging studies of cannabis use. Structural abnormalities generally have not been identified with chronic use. Regular users demonstrate reciprocal changes in brain activity globally and in cerebellar and frontal regions. Abstinence results in decreases, and administration results in increases correlating with subjective intoxication. Chronic use and cannabis administration result in attenuated brain activity in task-activated regions or activation of compensatory regions. Findings correlate partially with neuropsychological data, but generalization is limited by the lack of use of diagnostic criteria, appropriately paired neuropsychological testing or means to better quantify cannabis use and abstinence.

Multimodal Monitoring During Emergency Hemicraniectomy for Vein of Labbe Thrombosis

Cortical venous thrombosis is a rarely encountered mechanism for intracerebral hemorrhage. Multimodal monitoring may guide neurosurgical and critical care treatment in the setting of cerebral venous thrombosis. We report a 37-year-old service member who was admitted to a local field hospital for complaints of severe headache and left ear pain during Operation Iraqi Freedom. CT scan revealed a left temporal intracranial hematoma and subarachnoid hemorrhage. Angiogram revealed thrombosis of the vein of Labbe. Intracranial pressure (ICP), brain tissue oxygenation (PbO2), and cerebral blood flow (CBF) were monitored. There was a progressive increase in ICP despite ventricular drainage, sedation, and intubation. There was an ominous decrease in brain tissue oxygen and CBF became undetectable concomitantly with the increase in ICP. There was a dramatic decrease in ICP and improvement in brain tissue oxygenation and CBF after decompression and evacuation of the hematoma. Six weeks after the hemorrhage, the patient was able to follow simple commands and complete short sentences. To our knowledge, this is the first description of the use of ICP, PbO2, and laser Doppler method for obtaining CBF in the same setting. Information obtained from monitoring may lead to timely decompression and avoidance of poor outcome.

S -Ketamine Anesthesia Increases Cerebral Blood Flow in Excess of the Metabolic Needs in Humans

Animal studies have demonstrated neuroprotective properties of S-ketamine, but its effects on cerebral blood flow (CBF), metabolic rate of oxygen (CMRO2), and glucose metabolic rate (GMR) have not been comprehensively studied in humans. Positron emission tomography was used to quantify CBF and CMRO2 in eight healthy male volunteers awake and during S-ketamine infusion targeted to subanesthetic (150 ng/ml) and anesthetic (1,500-2,000 ng/ml) concentrations. In addition, subjects' GMRs were assessed awake and during anesthesia. Whole brain estimates for cerebral blood volume were obtained using kinetic modeling. The mean +/- SD serum S-ketamine concentration was 159 +/- 21 ng/ml at the subanesthetic and 1,959 +/- 442 ng/ml at the anesthetic levels. The total S-ketamine dose was 10.4 mg/kg. S-ketamine increased heart rate (maximally by 43.5%) and mean blood pressure (maximally by 27.0%) in a concentration-dependent manner (P = 0.001 for both). Subanesthetic S-ketamine increased whole brain CBF by 13.7% (P = 0.035). The greatest regional CBF increase was detected in the anterior cingulate (31.6%; P = 0.010). No changes were detected in CMRO2. Anesthetic S-ketamine increased whole brain CBF by 36.4% (P = 0.006) but had no effect on whole brain CMRO2 or GMR. Regionally, CBF was increased in nearly all brain structures studied (greatest increase in the insula 86.5%; P < 0.001), whereas CMRO2 increased only in the frontal cortex (by 15.7%; P = 0.007) and GMR increased only in the thalamus (by 11.7%; P = 0.010). Cerebral blood volume was increased by 51.9% (P = 0.011) during anesthesia. S-ketamine-induced CBF increases exceeded the minor changes in CMRO2 and GMR during anesthesia.

Cerebral Oxygenation, Central Drive And Force Output During Passive Heating And Cooling

Alterations in brain activity and cerebral blood flow occur with increased hypothalamic temperatures. Recently, it has been demonstrated that motor unit activation and force output decrease as a result of having an elevated core temperature per se, independent of exercise and maximal cardiovascular strain. The mechanisms behind this hyperthermic fatigue are not well understood, although some researchers postulate that changes in cerebral function play a role. PURPOSE To investigate whether changes in cerebral oxygenation influence the brain's ability to effectively recruit motor units and thus, sustain maximal isometric force output during passive hyperthermia. METHODS Five healthy males (age 22 ± 3 yrs: mean ± SD) were seated on a kneeextensor myograph in an environmental chamber (∼35°C) and their core temperature (Tre) was monitored via a rectal thermistor. A Near-Infrared Spectroscopy (NIRS) probe was placed over the left frontal lobe of the forehead and a liquid conditioning garment was worn in which 50°C water was circulated over the skin to passively increase core temperature. With every 0.5°C increase in Tre from baseline (∼37°C) to 39.0°C, muscle function was assessed via an isometric 10 s maximum voluntary contraction (MVC) of the knee extensors, and the interpolated-twitch technique was used to estimate motor unit activation (MUA). Subjects were then cooled (8°C water) and repeated the contraction protocol for every Tre decrease of 0.5°C until the ∼37°C baseline was reached. RESULTS Cardiovascular strain was moderate, with heart rate increasing (P<0.05) from 80 ± 13 to 139 ± 32 bpm at 39.0°C, before decreasing with cooling (75 ± 15 bpm). Mean arterial pressure decreased during heating from 94 ± 3 to 79 ± 5 mmHg before returning to 96 ± 9 mmHg. Force output decreased from 553 ± 133 at Tre 37°C to 430 ± 176 N at Tre of 39.0°C and remained depressed (474 ± 111 N) with cooling. MUA was attenuated in heat (from 90 ± 5 to 84 ± 6%) before returning to 91 ± 5 %. Cerebral oxygenation (cOX) levels during MVC did not differ significantly throughout passive heating. Cooling increased MVC cOX from −16.3 ± 5.2 μM to −6.7 ± 9.4 μM although cooling baseline measures remained depressed compared to the start of the protocol (4.0 ± 3.8 μM). CONCLUSIONS Although the magnitude of cerebral oxygenation changes throughout the cooling protocol, these changes do not coincide with decreases observed in MAP, force output or MUA with increased core temperature. Supported by an NSERC Discovery Grant.

Rapid Brain Cooling by Hypothermic Retrograde Jugular Vein Flush

Although whole-body hypothermia recently has been reported effective in improving the neurologic outcome after cardiac arrest, it is contraindicated in the management of trauma patients with hemorrhagic shock. To provide selective brain cooling in this situation, the authors speculated about the feasibility of hypothermic retrograde jugular vein flush (HRJVF). This preliminary study was conducted to test the effectiveness of brain cooling after HRJVF in rats without hemorrhagic shock. After jugular vein cannulation with cranial direction, Sprague-Dawley rats were randomized into a normal control group, a group that underwent flush with cold saline at 4 degrees C, or a group that underwent flush with saline at a room temperature of 24 degrees C. A Servo-controlled heat lamp was applied for all the rats to keep their rectal temperature at 37 +/- 0.5 degrees C. Their brain temperature and cerebral blood flow were checked. Within the 10-minute period of cold saline flush (1.7 mL/100 g), brain temperature was immediately decreased, and this cooling effect could be maintained for at least 20 minutes. Cerebral blood flow was significantly increased after HRJVF, then returned gradually to the baseline as brain temperature elevated. This study successfully demonstrated a significant cooling effect in rat brain by HRJVF. For preservation of brain function, HRJVF may be useful in resuscitation for trauma patients with hemorrhagic shock after further studies on animals with shock.

Effect of cerebral perfusion pressure augmentation on regional oxygenation and metabolism after head injury*

In this study we have used O positron emission tomography, brain tissue oxygen monitoring, and cerebral microdialysis to assess the effects of cerebral perfusion pressure augmentation on regional physiology and metabolism in the setting of traumatic brain injury. Prospective interventional study. Neurosciences critical care unit of a university hospital. Eleven acutely head-injured patients requiring norepinephrine to maintain cerebral perfusion pressure. Using positron emission tomography, we have quantified the response to an increase in cerebral perfusion pressure in a region of interest around a brain tissue oxygen sensor (Neurotrend) and microdialysis catheter. Oxygen extraction fraction and cerebral blood flow were measured with positron emission tomography at a cerebral perfusion pressure of approximately 70 mm Hg and approximately 90 mm Hg using norepinephrine to control cerebral perfusion pressure. All other aspects of physiology were kept stable. Cerebral perfusion pressure augmentation resulted in a significant increase in brain tissue oxygen (17 +/- 8 vs. 22 +/- 8 mm Hg; 2.2 +/- 1.0 vs. 2.9 +/- 1.0 kPa, p < .001) and cerebral blood flow (27.5 +/- 5.1 vs. 29.7 +/- 6.0 mL/100 mL/min, p < .05) and a significant decrease in oxygen extraction fraction (33.4 +/- 5.9 vs. 30.3 +/- 4.6 %, p < .05). There were no significant changes in any of the microdialysis variables (glucose, lactate, pyruvate, lactate/pyruvate ratio, glycerol). There was a significant linear relationship between brain tissue oxygen and oxygen extraction fraction (r = .21, p < .05); the brain tissue oxygen value associated with an oxygen extraction fraction of 40% (the mean value for oxygen extraction fraction in normal controls) was 14 mm Hg (1.8 kPa). The cerebral perfusion pressure intervention resulted in a greater percentage increase in brain tissue oxygen than the percentage decrease in oxygen extraction fraction; this suggests that the oxygen gradients between the vascular and tissue compartments were reduced by the cerebral perfusion pressure intervention. Cerebral perfusion pressure augmentation significantly increased levels of brain tissue oxygen and significantly reduced regional oxygen extraction fraction. However, these changes did not translate into predictable changes in regional chemistry. Our results suggest that the ischemic level of brain tissue oxygen may lie at a level below 14 mm Hg (1.8 kPa); however, the data do not allow us to be more specific.

Proton magnetic resonance spectroscopy and single photon emission computed tomography study of the brain in asymptomatic young hyperlipidaemic Asian Indians in North India show early abnormalities.

To evaluate brain metabolism and cerebral blood flow in young patients with hyperlipidaemia. Proton magnetic resonance spectroscopy ((1)H MRS) and single photon emission computed tomography (SPECT) of the brain was carried out in 19 asymptomatic young patients with hyperlipidaemia (mean age 32.6 +/- 6.0 years, range 22-45 years) and 21 age-matched healthy controls divided into the following three groups; (i) hyperlipidaemics on pharmacological treatment (group 1, n = 13), (ii) hyperlipidaemics not on pharmacological treatment (group 2, n = 6) and (iii) control group of healthy subjects (group 3, n = 21). No statistical difference was observed in the brain metabolite ratios between controls and hyperlipidaemic patients (both treatment naive and treated) in the (1)H NMR study. Two hyperlipidaemic patients showed a lactate peak and one had a lipid peak. The SPECT study was abnormal in seven hyperlipidaemic patients. In the pooled data, 50% subjects with high serum triglyceride (TG) levels as opposed to 14% subjects with normal serum TG levels showed cerebral hypoperfusion. The choline/creatine (Cho/Cr) ratio of the occipital region of the brain showed correlation with the excess percentage of body fat (%BF) and low levels of high density lipoprotein cholesterol (HDL-C) compared to those with normal %BF and normal HDL-C levels, respectively, in pooled data of all subjects. The N-acetyl aspartate (NAA)/Cho ratio also showed correlation with hypercholesterolaemia. Serum TG levels were positively correlated with the NAA/Cr ratio (r = 0.62, P < 0.05) and the Cho/Cr ratio (r = 0.63, P < 0.05) in the parieto-temporal area in group 1 patients. The study revealed no difference in the brain metabolite ratios between controls and hyperlipidaemic patients, while some hyperlipidaemic patients showed abnormalities of cerebral blood flow. Brain metabolite ratios were also influenced by certain parameters of body composition and lipids. As abnormal body composition, hypertriglyceridaemia and low levels of HDL-C are prevalent in Asian Indians, such data are important and indicate a need for further study.

Nonneuronal origin of CO2-related DC EEG shifts: an in vivo study in the cat.

We studied the mechanisms underlying CO(2)-dependent DC potential shifts, using epicranial, epidural, epicortical, intraventricular, and intraparenchymal (intraneuronal, intraglial, and field) recordings in ketamine-xylazine-anesthetized cats. DC shifts were elicited by changes in artificial ventilation, causing end-tidal CO(2) variations within a 2-5% range. Hypercapnia was consistently associated with negative scalp DC shifts (average shift -284.4 microV/CO(2)%, range -216 to -324 microV/CO(2)%), whereas hypocapnia induced positive scalp DC shifts (average shift 307.8 microV/CO(2)%, range 234 to 342 microV/CO(2)%) in all electrodes referenced versus the nasium bone. The former condition markedly increased intracranial pressure (ICP), whereas the latter only slightly reduced ICP. Breakdown of the blood-brain barrier (BBB) resulted in a positive DC shift and drastically reduced subsequent DC responses to hypo-/hypercapnia. Thiopental and isoflurane also elicited a dose-dependent positive DC shift and, at higher doses, hypo-/hypercapnia responses displayed reverted polarity. As to the possible implication of neurons in the production of DC shifts, no polarity reversal was recorded between scalp, various intracortical layers, and deep brain structures. Moreover, the membrane potential of neurons and glia did not show either significant or systematic variations in association with the scalp-recorded CO(2)-dependent DC shifts. Pathological activities of neurons during spike-wave seizures produced DC shifts of significantly smaller amplitude than those generated by hyper-/hypocapnia. DC shifts were still elicited when neuronal circuits were silent during anesthesia-induced burst-suppression patterns. We suggest that potentials generated by the BBB are the major source of epicortical/cranial DC shifts recorded under conditions affecting brain pH and/or cerebral blood flow.

Brain temperature and cerebral blood flow imaging in patients with severe subarachnoid hemorrhage: report of two cases

Background Temperature reversal, which is defined as observation of higher brain temperature than systemic temperature followed by lower brain temperature than systemic temperature, implies a poor prognosis in patients with severe subarachnoid hemorrhage (SAH). Serial regional cerebral blood flow (CBF) imaging using single-photon emission tomography (SPECT) was performed in 2 patients with severe SAH who showed temperature reversal. Case description 54-year-old woman and a 55-year-old man with severe SAH underwent ventricular drainage using a catheter that allowed monitoring of the brain temperature. SPECT imaging in these two patients showed that CBF was preserved before the occurrence of the temperature reversal and was exhausted afterwards. These patients died within 2 to 3 days. Conclusions Temperature reversal may indicate the exact time when absence of brain perfusion occurs, causing irreversible brain damage.

Regulation of NO-dependent cyclic GMP formation by inflammatory agents in neural cells

In the CNS, NO is an important physiological messenger involved in the modulation of brain development, synaptic plasticity, neuroendocrine secretion, sensory processing, and cerebral blood flow [Annu. Rev. Physiol. 57 (1995) 683]. These NO actions are largely mediated by cyclic GMP (cGMP) formed by stimulation of soluble guanylyl cyclase (sGC). NO has also been recognized as a neuropathological agent in conditions such as epilepsy, stroke and neurodegenerative disorders. In these conditions, NO may contribute to excitotoxic cell death and neuroinflammatory cell damage [Brain Res. Bull. 41 (1996) 131; Glia 29 (2000) 1]. NO can be formed in every type of CNS parenchymal cell, however, cGMP appears to be formed mainly in neurons and astroglia [Annu. Rev. Physiol. 57 (1995) 683]. There is a large body of information about the regulation of NO formation in brain cells under both normal and pathological conditions but much less is known about the control of cGMP generation, in particular during neuroinflammation when there is a high NO output. Here we briefly review our present knowledge on the regulation of NO-dependent cGMP formation in brain cells under inflammatory conditions.

Cerebral activation during vagus nerve stimulation: a functional MR study.

To study the short-term effects of vagus nerve stimulation (VNS) on brain activation and cerebral blood flow by using functional magnetic resonance imaging (fMRI). Five patients (three women, two men; mean age, 35.4 years) who were treated for medically refractory epilepsy with VNS, underwent fMRI. All patients had a nonfocal brain MRI. The VNS was set at 30 Hz, 0.5-2.0 mA for intervals of activation of 30 s on and 30 s off, during which the fMRI was performed. Statistical parametric mapping (SPM) was used to determine significant areas of activation or inhibition during vagal nerve stimulation (p < 0.05). VNS-induced activation was detected in the thalami bilaterally (left more than right), insular cortices bilaterally, ipsilateral basal ganglia and postcentral gyri, right posterior superior temporal gyrus, and inferomedial occipital gyri (left more than right). The most robust activation was seen in the thalami (left more than right) and insular cortices. VNS-induced thalamic and insular cortical activation during fMRI suggests that these areas may play a role in modulating cerebral cortical activity, and the observed decrease in seizure frequency in patients who are given VNS may be a consequence of this increased activation.

In vivo imaging of anaesthetic action in humans: approaches with positron emission tomography (PET) and functional magnetic resonance imaging (fMRI)

In vivo imaging of anaesthetic action in humans: approaches with positron emission tomography (PET) and functional magnetic resonance imaging (fMRI)

Quantitative local cerebral blood flow change after cerebrospinal fluid removal in patients with normal pressure hydrocephalus measured by a double injection method with N-isopropyl-p-[(123)I] iodoamphetamine.

The efficacy of cerebrospinal fluid (CSF) shunting surgery for normal pressure hydrocephalus (NPH) is difficult to predict. The CSF removal test is useful but quantification of the results is difficult. A method to quantitatively measure cerebral blood flow (CBF) by single photon emission computed tomography twice within 30 min after double injection of N-isopropyl-p-[(123)I] iodoamphetamine using a background subtraction method to correct for the temporal profile was utilized in tandem with CSF removal via a lumbar spinal tube in 22 patients of NPH to produce maps of baseline CBF and quantitative CBF change after CSF removal. All 22 patients with NPH underwent ventriculoperitoneal shunting surgery and were divided into two groups according to improvement in clinical symptoms and signs (responder group, N=15; nonresponder group, N=7). Baseline clinical characteristics and baseline CBF values were not significantly different between the two groups. Regional and whole brain CBF changes in the responder group (range 98-105%, whole brain 101+/-39%) were significantly higher than those in the nonresponder group (range 41-48%, whole brain 46+/-40%) (P<0.01). Discrimination analysis showed that an increase of more than 80% in CBF after CSF removal was predictive of response to shunt surgery with 77% accuracy. This new quantitative CSF removal test could be useful for selecting good candidates for CSF shunting surgery among patients with NPH.

Differences in brain temperature and cerebral blood flow during selective head versus whole-body cooling.

To compare brain temperature and cerebral blood flow (CBF) during head and body cooling, with and without systemic hypoxemia. Seventeen newborn swine were studied for either measurement of brain temperature alone (n = 9) or measurement of brain temperature and CBF (n = 8). All animals were ventilated and instrumented, and temperature probes were inserted into the rectum, into the brain at depths of 2 and 1 cm from the cortical surface, and on the dural surface. Blood flow was measured with microspheres. The protocol consisted of a control period, an interval of either head or body cooling, and cooling with 15 minutes of superimposed hypoxia. After a 1-hour recovery period, animals were exposed to the same sequence except that the alternate mode of cooling was evaluated. Head cooling with a constant rectal temperature resulted in an increase in the temperature gradient across the brain from the warmer central structures to the cooler periphery (brain 2 cm - dura temperature: 1.3 +/- 1.1 degrees C at control to 7.5 +/- 3.5 degrees C during cooling). Hypoxia superimposed on head cooling decreased the temperature gradient by at least 50%. In contrast, body cooling was associated with an unchanged temperature gradient across the brain (brain 2 cm - dura temperature: 1.5 +/- 1.2 degrees C at control to 1.1 +/- 0.9 degrees C during cooling). Hypoxia superimposed on body cooling did not change brain temperature. Both modes of brain cooling resulted in similar reductions of global CBF ( approximately 40%) and O(2) uptake. Brain hypothermia achieved through head or body cooling results in different brain temperature gradients. Alterations in systemic variables (ie, hypoxemia) alters brain temperature differently in these 2 modes of brain cooling. The mode of brain cooling may affect the efficacy of modest hypothermia as a neuroprotective therapy.

Inducible cyclooxygenase-2 expression after experimental intracerebral hemorrhage

Cyclooxygenase-2 (COX-2) is an inducible isoform of cyclooxygenase, which catalyzes the conversion of arachidonic acid to prostaglandins and thromboxane. Recent evidence suggests it has a pathological role in cerebral insults, but its involvement in intracerebral hemorrhage (ICH) is unknown. The present study investigates the temporal and anatomic distribution of COX-2 as well as the effect of the selective COX-2 inhibitor NS-398 on brain edema formation and cerebral blood flow in a rat model of ICH. Immunohistochemistry for COX-2 was performed in control rats and 6 h, as well as 1, 3, 7 and 10 days after the injection of 100 μl autologous blood into the right basal ganglia. Double-labeling immunohistochemistry was used to determine the type of COX-2 immunoreactive microvascular-associated cells. Western blot analysis was used to quantify COX-2 protein. The effect of NS-398 on brain water content, ion concentration and cerebral blood flow were assessed 24 h after ICH. The results demonstrated that COX-2 protein was expressed in control brain tissue and induced significantly in the ipsilateral hemisphere at 6 h, as well as 1 and 3 days after ICH. Increased staining of COX-2 in neurons was observed around the blood clot with a peak at 6 h. COX-2 was induced in endothelial cells, perivascular cells as well as infiltrating leukocytes 1 day after ICH. Brain water and ion contents and cerebral blood flow were unaffected by NS-398 administration. Thus, although COX-2 expression was increased in the ipsilateral hemisphere after an autologous blood injection, its products do not appear to be major regulators of blood flow or edema formation following ICH.

Room E, 10/16/2000 2: 00 PM - 4: 00 PM (PS) Brain Tissue Oxygenation and Cerebral Blood Flow during Hemodilution and Hypoxia

<b>Room E, 10/16/2000 2: 00 PM - 4: 00 PM (PS) Brain Tissue Oxygenation and Cerebral Blood Flow during Hemodilution and Hypoxia</b>

Glucose transporters, hexokinase, and phosphofructokinase in brain of rats with perinatal asphyxia.

Transport by glucose transporters from blood to the brain during hypoxic-ischemic conditions is well studied. However, the recent availability of a clinically related animal model of perinatal asphyxia and the fact that no concomitant determination of glucose transporters, parameters for glucose utilization, brain glucose, and cerebral blood flow (CBF) have been reported and the early phase of perinatal asphyxia has never been studied led us to perform the following study. Cesarean section was performed on full-term pregnant rats. The obtained pups within patent uterus horns were placed into a water bath at 37 degrees C from which they were subsequently removed after 5-20 min of graded asphyxia. Brain pH, brain tissue glucose, CBF, mRNA and activity of hexokinase and phosphofructokinase, and mRNA and protein of the glucose transporters GLUTI and GLUT3 were determined. Brain pH decreased and brain tissue glucose and CBF increased with the length of the asphyctic period; hexokinase and phosphofructokinase mRNA and activity were unchanged during the observation period. The mRNA and protein of both glucose transporters were comparable between normoxic and asphyctic groups. We show that glucose transport and utilization are unchanged in the early phase of perinatal asphyxia at a time point when CBF and brain glucose are already significantly increased and severe acidosis is present.

Glycerol attenuates the adherence of leukocytes in rat pial venules after transient middle cerebral artery occlusion

Intravenous infusion of glycerol has been used in patients with a cerebral infarction, expecting improvement in brain edema and cerebral blood flow (CBF). However, the mechanism of the improvement of CBF has not been clearly demonstrated. The aim of this study in the rat pial microvasculature after transient middle cerebral artery occlusion (MCAO) is to examine the effects of glycerol on leukocyte- endothelium interaction, which plays a critical role in the pathogenesis of brain injury by ischemia/ reperfusion and concerns induction of secondary brain damage. Rhodamine 6G-labeled leukocytes at the brain surface were visualized with intra-vital fluorescence videomicroscopy through a closed cranial window and an analysis was made of the number of adherent leukocytes and the centerline leukocyte velocity in the venule before MCAO, after reperfusion of MCAO and after infusion of glycerol (Croup 1) or saline (Croup 2). The number of adherent leukocytes decreased and the centerline leukocyte velocity increased statistically significantly immediately after the infusion of glycerol in Croup I, but there was no significant change in Croup 2. The infusion of glycerol washes away the adherent leukocytes and prevents them from interfering with the blood cell and plasma flow. Furthermore, secondary brain damage may be relieved by decreasing the adherence of leukocytes. In conclusion, modulating the adherence of leukocytes is one of the important factors in the neuroprotective effect of glycerol. [Neurol Res 1999; 21: 785-790]

103 Monitoring Brain Tissue PO2 and Cerebral Blood Flow during Isovolemic Hemodilution in Rabbits

103 Monitoring Brain Tissue PO2 and Cerebral Blood Flow during Isovolemic Hemodilution in Rabbits