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At least 109 records · Page 6Linked to original sources
PubMed2005

Focal brain ischemia in rat: acute changes in brain tissue T1 reflect acute increase in brain tissue water content.

Several recent studies have reported changes of brain tissue T(1) in ischemic models during the first minutes after occlusion of the middle cerebral artery (MCA). In order to assess whether these tissue T(1) changes are related to an increase in tissue water content, we performed T(1) (7 T) and tissue water content measurements in a rat model (n = 10, Sprague-Dawley) of focal cerebral ischemia (intraluminal occlusion model). The tissue water content was determined using a gravimetric technique. The animals were divided into two groups: an ischemic group, with an effective MCA occlusion (n = 6) and a control group, with animals having undergone sham surgery but no MCA occlusion (n = 4). In the ipsilateral cortex, the tissue water content was 81.1 +/- 0.7% at 2 h 15 min following ischemic insult (contralateral value: 79.3 +/- 0.5%). Concomitantly, the tissue T(1) in the ipsilateral cortex was 2062 +/- 60 ms at ischemia onset + 1 h (contralateral 1811 +/- 28 ms) and 2100 +/- 38 ms at ischemia onset + 2 h (contralateral 1807 +/- 18 ms). The tissue T(1) and tissue water content values measured in the contralateral area do not differ from the values obtained in the control group. A significant T(1) increase is observed at ischemia onset + 1 h (+ 14%) and ischemia onset (+ 2 h) + 16%, together with a significant increase in tissue water content (+ 2.3%). This suggests that there is an increase in tissue water content concomitant with cell swelling during the first hours of ischemia.

Animals↗
PubMedDate not supplied

[The effects of combined electrolytic brain stem-orbitofrontal and brain stem-hippocampal damages to the rat brain].

Morphofunctional studies of animals with associated electrolytic orbitofrontal and hippocampal brainstem lesions as compared to variants of isolated brainstem coagulation showed participation and specific role of orbitofrontal cortex and hippocampus in adaptive-compensatory brain reactions of rats with brainstem lesions. Associated brainstem-orbitofrontal damages result in aggravation of the animals' condition and highly probable lethality within the first two weeks after surgery due to blood circulation dysregulation of hemorrhagic type and probably due to secondary hypothalamus dysfunction. Associated brainstem-hippocampal coagulation intensifies primarily brainstem neurologic symptoms and prolongs time of their reverse development, i.e. supports the brainstem centre of stable pathological activity.

Animals↗
PubMedDate not supplied

Laboratory of Caribbean Brain Research Organization in the decade of the brain midpoint. Results in reaching behavior--interferences of subcortical motor centers, neurotransmitter blocking and brain function modeling.

CARIBRO was founded in response to the United Nations declaration that the 1990s be designated the Decade of the Brain. The Program of Action is: 1. Annual meetings; 2. Training courses of the Caribbean School of Neurosciences; 3. Network scientific programs; 4. Fellowship programs; and 5. Dissemination of information on neuroscience. In the same program, a CARIBRO Laboratory was created in one of the Medical Faculties of Havana with the aim to teach students from the Caribbean in neuroscience research. As part of this program, we have been working in lateralized motor functions. Preliminary results in rats show that reaching acquisition allows classification of the animals as right-handed (40%), left-handed (40%), and ambidextrous (20%). Electrolytic lesion of caudate nucleus or amygdala impairs lateralized response. Contralateral lesions increase reaching attempts. Ipsilateral lesions to the preferred forepaw do not affect the reaction. The results remain the same 10, 20, and 90 d after the interference. Pharmacological experiments showed that trihexiphenidil (0.1 mg/kg i.p.) induced handedness reversion in 50% if the animals, whereas haloperidol (1 mg/kg i.p.) produced immobility, tremor, and autonomic symptoms. This effect remained the same in young as well as in old animals. We are also working on mathematical modelation. In this sense, preliminary reports about a model for synaptic modification in the framework of the Fukushima hypothesis is discussed.

Animals↗
PubMed2005

Sleep is of the brain, by the brain and for the brain.

Sleep is a widespread biological phenomenon, and its scientific study is proceeding at multiple levels at the same time. Marked progress is being made in answering three fundamental questions: what is sleep, what are its mechanisms and what are its functions? The most salient answers to these questions have resulted from applying new techniques from basic and applied neuroscience research. The study of sleep is also shedding light on our understanding of consciousness, which undergoes alteration in parallel with sleep-induced changes in the brain.

Animals↗
PubMed1996

Brain parenchyma PO2, PCO2, and pH during and after hypoxic, ischemic brain insult in dogs.

OBJECTIVES: 1) The investigation of fiberoptic PO2, PCO2, and pH sensor technology as a monitor of brain parenchyma during and after brain injury, and 2) the comparison of brain parenchyma PO2, PCO2, and pH with intracranial pressure during and after hypoxic, ischemic brain insult. DESIGN: Prospective, controlled, animal study in an acute experimental preparation. SETTING: Physiology laboratory in a university medical school. SUBJECTS: Fourteen mongrel dogs (20 to 35 kg), anesthetized, room-air ventilated. INTERVENTIONS: Anesthesia was induced with thiopental and maintained after intubation using 1% to 1.5% halothane in room air (FiO2 0.21). Mechanical ventilation was established to maintain end-tidal PCO2 approximately 35 torr (-4.7 kPa). Intravenous, femoral artery, and pulmonary artery catheters were placed. The common carotid arteries were surgically exposed, and ultrasonic blood flow probes were applied. A calibrated intracranial pressure probe was placed through a right-side transcranial bolt, and a calibrated intracranial chemistry probe with optical sensors for PO2, PCO2, and pH was placed through a left-side bolt into brain parenchyma. Brain insult was induced in the experimental group (n = 6) by hypoxia (FiO2 0.1), ischemia (bilateral carotid artery occlusion), and hypotension (mean arterial pressure [MAP] approximately 40 mm Hg produced with isoflurane approximately 4%). After 45 mins, carotid artery occlusion was released, FiO2 was reset to 0.21, and anesthetic was returned to halothane (approximately 1.25%). The control group (n = 5) had the same surgical preparation and sequence of anesthetic agent exposure but no brain insult. MEASUREMENTS AND MAIN RESULTS: Monitored variables included brain parenchyma PO2, PCO2, and pH, which were monitored at 1-min intervals, and intracranial pressure, MAP, arterial hemoglobin oxygen saturation (by pulse oximetry), end-tidal PCO2, and carotid artery blood flow rate, for which data were collected at 15-min intervals for 7 hrs. Arterial and mixed venous blood gas analyses were done at approximately 1-hr intervals. Baseline data agreed closely with other published results: brain parenchyma PO2 of 27 +/- 7 (SD) torr (3.6 +/- 0.9 kPa); brain parenchyma PCO2 of 69 +/- 12 torr (9.2 +/- 1.6 kPa); and brain parenchyma pH of 7.13 +/- 0.09. Postcalibration data were accurate, indicating stability and durability over several hours. In six experiments, during the brain insult, brain parenchyma PO2 decreased to 16 +/- 2 torr (2.1 +/- 0.3 kPa), brain parenchyma PCO2 increased to 105 +/- 44 torr (14 +/- 5.9 kPa) (p < .05), and brain parenchyma pH decreased to 6.75 +/- 0.08 (p < .05). Intracranial pressure (ICP) remained nearly constant (baseline 16 +/- 6 to 14 +/- 5 mm Hg at the end of the brain insult). Cerebral perfusion pressure (CPP = MAP - ICP) decreased (baseline 95 +/- 15 to 28 +/- 8 mm Hg; p < .05). On release of brain insult stresses, ICP increased to 30 +/- 9 mm Hg and CPP increased to 71 +/- 19 mm Hg (p < .05). A biphasic recovery was observed for brain parenchyma pH, which had the slowest recovery of the monitored variables. On average, brain parenchyma pH gradually returned toward baseline, and was no longer significantly different from baseline 3 hrs after release of insult stresses. Brain parenchyma PCO2 continued to decrease rapidly after brain insult and then remained approximately 52 +/- 10 torr (approximately 6.9 +/- 1.3 kPa) (p < .05). Brain parenchyma PO2 increased from a minimum at the end of brain insult to a maximum of 43 +/- 17 torr (5.7 +/- 2.3 kPa) within 1.25 hrs (p < .05), and then gradually decreased to approximately 35 +/- 10 torr (approximately 4.7 +/- 1.3 kPa). Cerebral perfusion pressure gradually decreased as ICP increased 3 to 5 hrs after insult. CONCLUSIONS: Intracranial chemistry probes with optical sensors demonstrated stable, reproducible monitoring of brain parenchyma PO2, PCO2, and pH in dogs for periods lasting > 8 hrs. Significant changes in brain p

Anesthesia↗
PubMed2000

[Brain hypothermia treatment for the management of severe pediatric brain injury].

In the management of severe pediatric brain injury, attention has previously been paid to brain edema, ICP elevation and low cerebral perfusion pressure (CPP). However, in the acute stage within 3-6 hours after trauma, brain hypoxia and hyperglycemia associated with diffuse brain injury are often observed. We have pointed out brain thermo-pooling (elevation of brain tissue temperature) and brain hypoxia caused by defective release of oxygen from hemoglobin (due to decrease in red blood cell enzyme (DPG)) as a new mechanism of brain injury. To treat these pathologic changes, we have developed a brain hypothermia treatment, the major purpose of which is to prevent brain hypoxia, brain thermo-pooling, neurohormonal changes causing cytokine encephalopathy, and a selective, radical-mediated damage of the dopamine A10 nervous system. The brain tissue temperature is initially adjusted to 35 degrees C with adequate cerebral oxygenation, followed by brain hypothermia at 34 degrees C for 1 weeks to prevent brain hypoxia, free radical reactions, brain edema and ICP elevation. What is most difficult in the pediatric brain hypothermia treatment is to maintain metabolic balance in the injured brain tissue and pulmonary infections associated with an immune crisis. When a rapid elevation of serum glucose is noted it is critical to lower the value because glucose quickly penetrates the blood-brain barrier and increases pyruvate and lactate by inhibiting the TCA cycle metabolism. Thus, hyperglycemia during brain hypothermia treatment is one of the major target of management. Another problem is immune crisis associated with secondary pulmonary infections. To prevent them, early enteral nutrition and replacement of L-arginine were most useful, as well as preconditioning for rewarming as follows: serum albumin > 3.0 g/dl; lymphocyte > 1500/mm3; T-H (CD4) lymphocytes > 55%; serum glucose, 120-140 mg/dl; vitamin A > 50 mg/dl; Hb > 12 g/dl and 2,3 DPG, 10-15 mumol/gHb; O2 ER, 23-25% and AT-III, > 100%. The clinical benefit of this therapy is still controversial.

Acute-Phase Reaction↗
PubMed1994

A critique of the role of the blood-brain barrier in the chemotherapy of human brain tumors.

There is general agreement that most chemotherapy agents achieve only relatively low concentrations in the normal central nervous system, that the blood-brain barrier is variably disrupted in malignant brain tumors, and that the concentration of chemotherapy drugs in the brain adjacent to tumor is intermediate between concentrations achieved in brain tumors vs normal brain. However, there is substantial controversy regarding the role of the blood-brain barrier in resistance to chemotherapy of intracerebral tumors. Many chemotherapy agents achieve concentrations in brain tumors that are comparable to those in extracerebral tumors, and drugs that cross the intact blood-brain barrier only poorly may be active against intracerebral tumors. Furthermore, the hypothesis that the brain is a pharmacological sanctuary where metastases may grow while tumor is responding in other parts of the body may be flawed: there are only 2 or 3 types of malignancies (out of all those that are sensitive to chemotherapy) in which the risk of isolated central nervous system relapse is moderately high, and even in these 2 or 3, effective central nervous system prophylaxis has minimal or no impact on overall survival. Furthermore, drugs that cross the BBB do not appear to be more effective than other drugs at reducing the risk of brain metastases, and brain metastases at the time of diagnosis do not necessarily convey a worse prognosis than metastases to various other sites. While average drug concentrations in brain adjacent to tumor are lower than those within brain tumors, very small numbers of tumor cells may be capable of inducing local leakiness in blood vessels, and there is little information on drug concentrations achieved in individual tumor cells within the brain adjacent to tumor. Furthermore, any limitation of uptake of drugs into brain tumors could be at least partially due to increased tissue pressure within tumors rather than being due to blood-brain barrier phenomena. This distinction could be important, since strategies that one might use to increase drug delivery to brain tumors might differ depending on whether the reduced delivery were due to barrier phenomena vs blood flow phenomena. The role of the blood-brain barrier in resistance of intracerebral tumors to chemotherapy remains unclear: while it may well play some role (and perhaps even a major one), self-fulfilling prophecies and unintentional bias in data selection and interpretation may have previously made it appear more important than it actually is.(ABSTRACT TRUNCATED AT 400 WORDS)

Antineoplastic Agents↗
PubMed1999

Barrier mechanisms in the brain, II. Immature brain.

1. It is widely believed that 'the' blood-brain barrier is immature in foetuses and newborns. 2. Much evidence in support of this belief is based on experiments that were unphysiological and likely to have disrupted fragile blood vessels of the developing brain. Some confusion about barrier development arises from insufficient recognition that the term 'blood-brain barrier' describes a complex series of mechanisms controlling the internal environment of the brain. 3. We present evidence showing that the brain develops within an environment that, particularly with respect to protein, is different from that of the rest of the body and that possesses a number of unique features not present in the adult. 4. Barriers to protein at blood-brain and blood-cerebrospinal fluid (CSF) interfaces (tight junctions) are present from very early in development; immunocytochemical and permeability data show that proteins are largely excluded from extracellular space in developing brain. 5. Cerebrospinal fluid in developing brain contains high concentrations of proteins largely derived from plasma. This protein is transferred from blood by an intracellular mechanism across the epithelial cells of the immature choroid plexus. Only a small proportion of choroid plexus cells is involved. The route is an intracellular system of tubulo-endoplasmic reticulum continuously connected across the epithelial cells only early in brain development. 6. High concentrations of proteins in CSF in developing brain are largely excluded from the brain's extracellular space by barriers at the internal and external CSF-brain interfaces. These consist of membrane specializations between surfaces of cells forming these interfaces (neuroependyma on the inner surface; radial glial end feet on the outer surface). In contrast with tight junctions present at the blood-brain and blood-CSF barriers, at the CSF-brain barriers of the immature brain, other junctional types are involved: strap junctions in the neuroependyma and a mixture of junctions at the outer CSF-brain barrier (plate junctions, strap junctions and wafer junctions). These barriers are not present in the adult. 7. Permeability to small lipid-insoluble molecules is greater in developing brain; more specific mechanisms, such as those involved in transfer of ions and amino acids, develop sequentially as the brain grows.

Adult↗
PubMed1991

Relationship between body and brain temperature in traumatically brain-injured rodents.

Recent work has shown that mild to moderate levels of hypothermia may profoundly reduce the histological and biochemical sequelae of cerebral ischemic injury. In the present study, the authors examined the effect of fluid-percussion injury on brain temperature in anesthetized rats and the effect of anesthesia on brain temperature in uninjured rats. The relationship between the brain, rectal, and temporalis muscle temperatures during normothermia, hypothermia, and hyperthermia was studied following a moderate magnitude of fluid-percussion brain injury (2.10 to 2.25 atmospheres) in rats. The results showed that mean brain temperature in 10 anesthetized injured rats, in 21 anesthetized uninjured rats, and in 10 unanesthetized uninjured rats was a mean (+/- standard error of the mean) of 36.04 degrees +/- 0.20 degrees C, 36.30 degrees +/- 0.08 degrees C, and 37.95 degrees +/- 0.09 degrees C, respectively. There was no significant difference in temperature under general anesthesia between injured and uninjured rats (p greater than 0.05). In the absence of brain injury, mean brain temperature was significantly lower in anesthetized rats than in unanesthetized rats (p less than 0.001). In anesthetized brain-injured rats, temporalis muscle temperature correlated well with brain temperature over a 30 degrees to 40 degrees C range, even when brain temperature was rapidly changed during induction of hypothermia or hyperthermia (r = 0.9986, p less than 0.0001). In contrast, rectal temperature varied inconsistently from brain temperature. These observations indicated that: 1) brain injury itself does not influence brain temperature in this model; 2) anesthesia alone decreases brain temperature to levels producing cerebral protection in this model; and 3) external monitoring of temporalis muscle temperature can provide a reliable indirect measure of brain temperature in the course of experimental brain injury. The authors believe that it is essential to monitor or control brain temperature in studies of experimental brain injury.

Animals↗
PubMed2005

Gender and environmental effects on regional brain-derived neurotrophic factor expression after experimental traumatic brain injury.

Alterations in brain-derived neurotrophic factor expression have been reported in multiple brain regions acutely after traumatic brain injury, however neither injury nor post-injury environmental enrichment has been shown to affect hippocampal brain-derived neurotrophic factor gene expression in male rats chronically post-injury. Studies have demonstrated hormone-related neuroprotection for female rats after traumatic brain injury, and estrogen and exercise both influence brain-derived neurotrophic factor levels. Despite recent studies suggesting that exposure post-traumatic brain injury to environmental enrichment improves cognitive recovery in male rats, we have shown that environmental enrichment mediated improvements with spatial learning are gender specific and only positively affect males. Therefore the purpose of this study was to evaluate the effect of gender and environmental enrichment on chronic post-injury cortical and hippocampal brain-derived neurotrophic factor protein expression. Sprague-Dawley male and cycling female rats were placed into environmental enrichment or standard housing after controlled cortical impact or sham surgery. Four weeks post-surgery, hippocampal and frontal cortex brain-derived neurotrophic factor expression were examined using Western blot. Results revealed significant increases in brain-derived neurotrophic factor expression in the frontal cortex ipsilateral to injury for males (P=0.03). Environmental enrichment did not augment this effect. Neither environmental enrichment nor injury significantly affected cortical brain-derived neurotrophic factor expression for females. In the hippocampus ipsilateral to injury brain-derived neurotrophic factor expression for both males and females was half (49% and 51% respectively) of that observed in shams housed in the standard environment. For injured males, there was a trend in this region for environmental enrichment to restore brain-derived neurotrophic factor levels to sham values. However, there were robust increases in hippocampal brain-derived neurotrophic factor expression ipsilateral to the injury for injured females in environmental enrichment compared with both sham and injured females placed in standard housing (P<or=0.005). In the hippocampus contralateral to injury, there were also significant injury-related increases in brain-derived neurotrophic factor expression for females (P<or=0.05) that were not further augmented by environmental enrichment. These results show significant, region-specific gender differences in brain-derived neurotrophic factor expression with both injury and environmental enrichment that may be important for recovery. However, these data do not support a critical role for brain-derived neurotrophic factor in environmental enrichment mediated improvements with spatial learning.

Actins↗
PubMed2004

Blood-brain barrier transport of morphine in patients with severe brain trauma.

AIMS: In experimental studies, morphine pharmacokinetics is different in the brain compared with other tissues due to the properties of the blood-brain barrier, including action of efflux pumps. It was hypothesized in this clinical study that active efflux of morphine occurs also in human brain, and that brain injury would alter cerebral morphine pharmacokinetics. METHODS: Patients with traumatic brain injury, equipped with one to three microdialysis catheters in the brain and one in abdominal subcutaneous fat for metabolic monitoring, were studied. The cerebral catheter locations were classified as 'better' and 'worse' brain tissue, referring to the degree of injury. Morphine (10 mg) was infused intravenously over a 10-min period in seven patients in the intensive care setting. Tissue and plasma morphine concentrations were obtained during the subsequent 3-h period with microdialysis and regular blood sampling. RESULTS: The area under the concentration-time curve (AUC) ratio of unbound morphine in brain tissue to plasma was 0.64 (95% confidence interval 0.40, 0.87) in 'better' brain tissue (P < 0.05 vs. the subcutaneous fat/plasma ratio), 0.78 (0.49, 1.07) in 'worse' brain tissue and 1.00 (0.86, 1.13) in subcutaneous fat. The terminal half-life and T(max) were longer in the brain vs. plasma and fat, respectively. The relative recovery for morphine was higher in 'better' than in 'worse' brain tissue. The T(max) value tended to be shorter in 'worse' brain tissue. CONCLUSIONS: The unbound AUC ratio below unity in the 'better' human brain tissue demonstrates an active efflux of morphine across the blood-brain barrier. The 'worse' brain tissue shows a decrease in relative recovery for morphine and in some cases also an increase in permeability for morphine over the blood-brain barrier.

Adult↗
PubMed1985

Relationship of brain glutamine and brain neutral amino acid concentrations after portacaval anastomosis in rats.

Evidence from several sources suggest that blood-brain transport of the large neutral amino acids (NAA) is abnormal in animals with a portacaval anastomosis (PCA) and in patients with liver cirrhosis and portal-systemic shunting and encephalopathy, but the underlying mechanisms are unknown. After PCA, the concentration of glutamine (Gln) in brain is markedly increased as a by-product of cerebral ammonia detoxification, and the rate of efflux of Gln from brain is also increased. The following studies were undertaken to clarify the relationships among plasma and brain concentrations of NAA after PCA in rats and to examine the relationship of brain Gln concentration to plasma and brain NAA concentrations. After PCA plasma phenylalanine, tyrosine and histidine were elevated and leucine, isoleucine and valine were lowered. In brain, phenylalanine, tyrosine, histidine and methionine were markedly elevated after PCA and their concentrations in brain far exceeded the concentrations in plasma. Analyses of single, partial and multiple correlations of plasma NAA ratios expressed as plasma competitor function (PCF), brain NAA and brain Gln showed significant correlations between PCF nd brain NAA in shunted rats. A better correlation was found between brain NAA and brain Gln. Correlation coefficients obtained from multiple correlation analysis equalled or exceeded those obtained in the partial correlation or in the single correlation, suggesting that the effects of PCF and brain Gln on brain NAA were separate and additive. Gln was shown to compete with other NAA for blood brain transport by inhibiting brain 14C phenylalanine uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1996

Brain death diagnosed by forensic analysis of drug distribution in human tissues-II--Distribution of caffeine in brain dead patients.

Caffeine concentrations in human tissues of 6 brain death cases as well as 5 non-brain death cases were examined in order to assess the possibility of diagnosing brain death based on an analysis of this compound. Concentrations of caffeine in human tissues were determined using gas chromatography/mass spectrometry. The tissue-to-blood concentration ratios were used to evaluate the distribution pattern in each case. In non-brain death cases, the ratios in all examined tissues were similar, and the values were close to 1 in all tissues except adipose, of which the value was near 0.3. In brain death cases, the ratios in all tissues except brain and adipose were similar to those in non-brain death cases. The ratios in the brain were higher than those of non-brain death cases, in 5 brain death cases, and lower in 1 brain death case to whom blood transfusion was done in a hospital. The ratios in the adipose were slightly higher in brain death cases than those in non-brain death cases. The discorded distribution of caffeine in brain death cases was presumably related to cessation of cerebral blood circulation at the time of brain death. Therefore, comparing caffeine concentrations in the brain with those in the other tissues can be useful for a forensic diagnosis of brain death.

Adult↗