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PubMed2006

Microsphere embolism-induced endothelial nitric oxide synthase expression mediates disruption of the blood-brain barrier in rat brain.

Microsphere embolism (ME)-induced up-regulation of endothelial nitric oxide synthase (eNOS) in endothelial cells of brain microvessels was observed 2-48 h after ischemia. eNOS induction preceded disruption of the blood-brain barrier (BBB) observed 6-72 h after ischemia. In vascular endothelial cells, ME-induced eNOS expression was closely associated with protein tyrosine nitration, which is a marker of generation of peroxynitrite. Leakage of rabbit IgG from microvessels was also evident around protein tyrosine nitration-immunoreactive microvessels. To determine whether eNOS expression and protein tyrosine nitration in vascular endothelial cells mediates BBB disruption in the ME brain, we tested the effect of a novel calmodulin-dependent NOS inhibitor, 3-[2-[4-(3-chloro-2-methylphenyl)-1-piperazinyl]ethyl]-5,6-dimethoxy-1-(4-imidazolylmethyl)-1H-indazole dihydrochloride 3.5 hydrate (DY-9760e), which inhibits eNOS activity and, in turn, protein tyrosine nitration. Concomitant with inhibition of protein tyrosine nitration in vascular endothelial cells, DY-9760e significantly inhibited BBB disruption as assessed by Evans blue (EB) excretion. DY-9760e also inhibited cleavage of poly (ADP-ribose) polymerase as a marker of the apoptotic pathway in vascular endothelial cells. Taken together with previous evidence in which DY-9760e inhibited brain edema, ME-induced eNOS expression in vascular endothelial cells likely mediates BBB disruption and, in turn, brain edema.

Animals↗
PubMed1997

Brain abscess and brain tumor: discrimination with in vivo H-1 MR spectroscopy.

PURPOSE: To determine the ability to differentiate brain abscess from cystic or necrotic brain tumor with hydrogen-1 magnetic resonance (MR) spectroscopy. MATERIALS AND METHODS: H-1 MR spectroscopy was prospectively performed in seven consecutive patients with pyogenic brain abscess and in seven consecutive patients with necrotic or cystic brain tumor (five patients with glioblastoma and one each with pilocytic astrocytoma and metastasis from lung cancer) in whom radiologic images depicted ring-shaped areas of contrast material enhancement (indicative of a cystic or necrotic mass). Assignment of resonance peaks to metabolites was based on reports in the literature. RESULTS: In six of seven patients with abscess, there were various resonances attributed to lactate, valine, alanine, leucine, acetate, succinate, and unidentified metabolites (2.2, 2.9, 3.2, 3.4, and 3.8 ppm). In six of seven patients with tumor, there was only a resonance attributed to lactate. One patient with a tumor had an unidentified peak at 0.9 ppm (presumably attributed to lipid) in addition to the peak attributed to lactate. CONCLUSION: Spectral patterns from in vivo H-1 MR spectroscopy may permit differentiation of brain abscess from necrotic or cystic tumor.

Adult↗
PubMed1998

Platelet-activating factor is an important mediator in hypoxic ischemic brain injury in the newborn rat. Flunarizine and Ginkgo biloba extract reduce PAF concentration in the brain.

Hypoxic-ischemic encephalopathy is still a very important cause of neonatal mortality and morbidity. Recently, platelet-activating factor (PAF) has been accused of being responsible for the neuronal damage in hypoxic-ischemic brain. We investigated tissue PAF concentrations in hypoxic-ischemic brain injury in immature rats. Endogenous PAF concentration in brain tissue showed a marked increase in hypoxic-ischemic pups (85.6 +/- 15.5 pg/mg protein) when compared to that of control (9.05 +/- 3.1 pg/mg protein). In addition, we examined the effects of flunarizine, a selective calcium channel blocker, and Ginkgo biloba extract (EGb 761) on endogenous PAF concentration in hypoxic-ischemic brain injury. Endogenous PAF concentrations in both flunarizine-pretreated (16.6 +/- 4.8 pg/mg protein) and EGb 761-pretreated (33.5 +/- 8.9 pg/mg protein) pups were significantly lower than the untreated group. These results indicate that PAF is an important mediator in immature rat model of cerebral hypoxic-ischemic injury. The suppressor effect of flunarizine and EGb 761 on PAF production may open new insight into the treatment of hypoxic-ischemic brain injury.

Animals↗
PubMed1995

Conditionally immortalized oligodendrocyte cell lines migrate to different brain regions and elaborate 'myelin-like' membranes after transplantation into neonatal shiverer mouse brains.

Five immortalized oligodendrocyte cell lines, representing a spectrum of different stages of oligodendrocyte maturation, were transplanted into neonatal shiverer mouse brains and examined for their ability to survive, multiply, and migrate in vivo. Each of the cell lines migrated to different regions of the brain with remarkable consistency when injected into the mouse forebrain, suggesting that the cells might be responding to different environmental cues present in the neonatal mouse brain. These results are consistent with the fact that cells at different stages in the oligodendrocyte lineage probably possess different sets of surface molecules and receptors. Significant differences were also observed in the survival and proliferation of the lines examined, even when the lines tested had quite similar in vitro phenotypes. Interestingly, the cell line with the most mature in vitro phenotype, N20.1, appeared to elaborate membranous processes when transplanted into the brain, reminiscent of oligodendrocytes ensheathing axonal segments. The experiments suggest that these immortalized cells could be useful models to study the cellular and molecular mechanisms involved in the development, maturation and possibly formation of myelin by oligodendrocytes in the mammalian brain.

Animals↗
PubMed1999

Genes encoding atrial and brain natriuretic peptides as candidates for sensitivity to brain ischemia in stroke-prone hypertensive rats.

-Previous studies suggested that atrial natriuretic peptide gene (Anp) and brain natriuretic peptide gene (Bnp) are plausible candidate genes for susceptibility to stroke and for sensitivity to brain ischemia in the stroke-prone spontaneously hypertensive rat (SHRSP). We performed structural and functional analyses of these 2 genes in SHRSP from Glasgow colonies (SHRSPGla) and Wistar-Kyoto rats from Glasgow colonies (WKYGla) and developed a radiation hybrid map of the relevant region of rat chromosome 5. Sequencing of the coding regions of the Anp and Bnp genes revealed no difference between the 2 strains. Expression studies in brain tissue showed no differences at baseline and at 24 hours after middle cerebral artery occlusion. Plasma concentrations of atrial natriuretic peptide (ANP) did not differ between the SHRSPGla and WKYGla, whereas concentrations of brain natriuretic peptide were significantly higher in the SHRSPGla as compared with the WKYGla (n=11 to 14; 163+/-21 pg/mL and 78+/-14 pg/mL; 95% confidence interval 31 to 138, P=0.003). We did not detect any attenuation of endothelium-dependent relaxations to bradykinin or ANP in middle cerebral arteries from the SHRSPGla; indeed the sensitivity to ANP was significantly increased in arteries harvested from this strain (WKYGla: n=8; pD2=7. 3+/-0.2 and SHRSPGla: n=8; pD2=8.2+/-0.15; P<0.01). Moreover, radiation hybrid mapping and fluorescence in situ hybridization allowed us to map the Anf marker in the telomeric position of rat chromosome 5 in close proximity to D5Rat48, D5Rat47, D5Mgh15, and D5Mgh16. These results exclude Anp and Bnp as candidate genes for the sensitivity to brain ischemia and pave the way to further congenic and physical mapping strategies.

Amino Acid Substitution↗
PubMedDate not supplied

Brain edema and blood-brain barrier permeability following quantitative cerebral microembolism.

Cerebral microemboli were formed in rats by injecting 4,000 carbonized microspheres, 50 +/- 10 mu in diameter, labelled with 85Sr, into the internal carotid artery. The use of radioactive microspheres as embolic agents enabled the number of microspheres to be determined in each cerebral hemisphere. The microspheres were mainly distributed in the cerebral hemisphere on the side of the injection. In 61 rats this hemisphere contained 582 +/- 20 microspheres against 99 +/- 9 in the contralateral hemisphere. Brain edema was assessed by measuring brain content of water, sodium and potassium. Blood-brain barrier (BBB) permeability was determined by brain accumulation of 125I-albumin. In the ipsilateral hemisphere brain edema and an increase in BBB permeability appeared 6 hours after embolization and progressed up to 48 hours. Twenty-four hours after embolization, significant correlations were observed between the microsphere content of the cerebral hemispheres and 1) the increases in water and sodium levels, 2) the decrease in potassium level, 3) the increase in BBB permeability. The study of these correlations should make it possible to ignore the poor reproducibility of embolizations and to analyze with increased accuracy the results of various experiments.

Animals↗
PubMed1993

Difluoromethylornithine decreases postischemic brain edema and blood-brain barrier breakdown.

Brain polyamines have been associated with posttraumatic vasogenic edema and blood-brain barrier (BBB) breakdown seen in some models of brain injury. We hypothesized that the inhibition of the enzyme responsible for polyamine production with the decarboxylase difluoromethylornithine (DFMO) may decrease BBB breakdown after a focal brain ischemic stroke. Thirty-two cats underwent 8 hours of middle cerebral artery occlusion and one of four treatments: sham operation (Sham), ischemia (Isc), ischemia/DFMO (Isc/DF), and ischemia/DFMO/putrescine (Isc/DF/PU). The regional brain specific gravity and the volume of Evans blue (EB) extravasation were measured at the time of death. The groups were monitored for temperature, heart rate, blood pressure, and arterial blood gases, and the values did not differ outside normal physiological ranges. EB results were expressed as the percentage of the hemisphere stained and showed the following: Sham, 2.23%; Isc, 32.8%; Isc/DF, 5.6%; Isc/DF/PU, 36.3%. As a measure of BBB, ischemia increased EB staining; DFMO pretreatment decreased the amount of EB staining to control levels; and the polyamine putrescine abolished the protective effect of DFMO (all significant at P = 0.05). DFMO pretreatment also resulted in a significant (P = 0.05) return to control values for specific gravity in the EB-stained regions (1.0328) of ischemic animals. This effect was present primarily in the white matter. Treatment with DFMO, an ornithine decarboxylase inhibitor, significantly decreased postischemic BBB breakdown and vasogenic edema in this model.

Animals↗
PubMed2004

Hyperglycemia and brain tissue pH after traumatic brain injury.

OBJECTIVE: Hyperglycemia occurring after head injury is associated with poor neurological outcome. We tested the hypothesis that blood glucose levels are associated with brain tissue pH (pH(b)) and that the correction of hyperglycemia would result in an improvement in pH(b). METHODS: This is a retrospective analysis of a prospectively collected database. Thirty-four patients in a tertiary care neuroscience critical care unit with major traumatic brain injury underwent pH(b) monitoring. RESULTS: A total of 428 glucose measurements were recorded during pH(b) monitoring. Mean glucose level was 7.1 mmol/L (range, 2.8-21.7 mmol/L) and median (interquartile range) pH(b) was 7.11 mmol/L (7.00-7.19 mmol/L). To account for the correlated, unbalanced nature of the data, a linear generalized estimating equation model was created. This model predicted that for each 1 mmol/L increase in blood glucose, pH(b) changed by -0.011 mmol/L (95% confidence interval, -0.016 to -0.005 mmol/L; P < 0.001). This relationship remained significant in a multivariable model that included cerebral perfusion pressure, brain tissue oxygen and carbon dioxide tension, and brain temperature. Twenty-one episodes of significant hyperglycemia (>or=11.1 mmol/L) treated with intravenous insulin were identified. Insulin therapy significantly reduced blood glucose concentration from a median (interquartile range) of 11.9 mmol/L (range, 11.4-13.6 mmol/L) to 8.8 mmol/L (range, 7.3-9.6 mmol/L; P < 0.001). Baseline pH(b) was not significantly different from pH(b) associated with the subsequent glucose reading of less than 11.1 mmol/L (P = 0.29), but there was a suggestion of improvement if the change in blood glucose was large. CONCLUSION: Blood glucose is associated with brain tissue acidosis in patients with major head injury. Prospective studies are required to confirm these results and to determine whether treatment of hyperglycemia improves outcome.

Adolescent↗
PubMed1983

Osmotic blood-brain barrier modification: clinical documentation by enhanced CT scanning and/or radionuclide brain scanning.

Results of initial clinical trials of brain tumor chemotherapy after osmotic blood-brain barrier disruption are promising. In general, the procedure is well tolerated. The major complication has been seizures. In this report, data are presented which indicate that the etiology of these seizures is related to the use of contrast agent (meglumine iothalamate) to monitor barrier modification. A series of 19 patients underwent a total of 85 barrier modification procedures. Documentation of barrier disruption was monitored by contrast-enhanced computed tomographic (CT) scanning, radionuclide brain scanning, or a combination of both techniques. In 56 procedures (19 patients) monitored by enhanced CT, seizures occurred a total of 10 times in eight patients. Twenty-three barrier modification procedures (in nine of these 19 patients) documented by nuclear brain scans alone, however, resulted in only one focal motor seizure in each of two patients. In eight of the 19 patients who had seizures after barrier disruption and enhanced CT scan, four subsequently had repeat procedures monitored by radionuclide scan alone. In only one of these patients was further seizure activity noted; a single focal motor seizure was observed. Clearly, the radionuclide brain scan does not have the sensitivity and spatial resolution of enhanced CT, but at present it appears safer to monitor barrier modification by this method and to follow tumor growth between barrier modifications by enhanced CT. Four illustrative cases showing methods, problems, and promising results are presented.

Adult↗
PubMed1994

Experimental intracerebral hemorrhage: relationship between brain edema, blood flow, and blood-brain barrier permeability in rats.

There have been few investigations of brain edema formation after intracerebral hemorrhage (ICH), despite the fact that mass effect and edema are important clinical complications. The present study was designed to investigate the time course for the formation and resolution of brain edema and to determine how changes in cerebral blood flow (CBF) and blood-brain barrier (BBB) permeability are temporally related to edema formation following ICH. Anesthetized adult rats received a sterile injection of 100 microliters of autologous blood into the caudate nucleus. Water and ion contents were measured immediately, at 4 and 12 hours, and daily to Day 7 (10 time points, six rats at each time) after experimental ICH. The water content of the ipsilateral basal ganglia increased progressively (p < 0.002) over the first 24 hours, then remained constant until after Day 5, when the edema began to resolve. Edema was most severe in the tissue immediately surrounding the hemorrhage; however, it was also present in the ipsilateral cortex, the contralateral cortex, and the basal ganglia. Measurements of local CBF (using [14C]-iodoantipyrine) and BBB permeability (using [3H]-alpha-aminoisobutyric acid) were obtained in separate groups of six to eight rats at various time intervals between 1 and 48 hours after ICH. Cerebral blood flow was reduced to 50% of control at 1 hour, returned to control values by 4 hours, but then decreased to less than 50% of control between 24 and 48 hours after ICH. The BBB permeability increased significantly prior to the occurrence of significant edema in the tissue surrounding the clot. However, BBB permeability in the more distant structures remained normal despite the development of edema. These results demonstrate a time course for the formation and resolution of brain edema following ICH similar to that observed during focal ischemia. Brain edema forms in the immediate vicinity of the clot as a result of both BBB disruption and the local generation of osmotically active substances and then spreads to adjacent structures. While local ischemia, due to the mass effect of the hemorrhage, may play a role in producing cytotoxic and vasogenic edema, the release of toxic substances from the clot should also be considered. Since edema is nearly maximal by 24 hours after ICH, therapy directed at reducing edema formation must be instituted within the 1st day.

Aminoisobutyric Acids↗
PubMed2000

[Diagnosis of brain tumor with proton MR spectroscopy--the quantification of gliomas compared with normal brain].

We conducted quantification of proton MR spectroscopy (MRS) using water signal as an internal standard, in order to quantify the concentrations of metabolites in normal adult brains and in gliomas in vivo. Single-voxel spectra were acquired using a point-resolved spectroscopic (PRESS) pulse sequence as part of the Probe. P spectroscopy package on a GE Signa Horizon Hispeed LX1.5T scanner (TR/TE/Ave = 3000 msec/30 msec/64). The volume of interest (VOI) varied from 15.0 x 15.0 x 15.0 mm3 to 20.0 x 20.0 x 20.0 mm3 for the brain. The present study included 26 healthy volunteers and 12 patients with gliomas, whose diagnoses were verified by histologic examination. The calculated concentrations of N-acetyl-aspartate (NAA), creatine (Cre) and choline (Cho) in normal hemispheric white matter were 23.66 +/- 1.94 mM (mean +/- SD), 12.97 +/- 1.44 mM, and 4.38 +/- 0.60 mM, respectively. We found they were not necessarily uniform in different parts of the brain, for example, in the pons and basal ganglia. The concentrations of NAA and Cre decreased in all gliomas (p < 0.001). Cho concentration also decreased in the glioma (p < 0.005). The NAA/Cre, NAA/Cho, and Cre/Cho ratios can distinguish normal brain from gliomas, and NAA/Cho ratio can distinguish low-grade astrocytoma from the high-grade group. The results indicate that this noninvasive method offers reasonable estimation of metabolite concentrations in the brain in vivo and therefore is useful in diagnoses of gliomas.

Adult↗
PubMed2002

Brain atrophy in mild or moderate traumatic brain injury: a longitudinal quantitative analysis.

BACKGROUND AND PURPOSE: Although mild or moderate traumatic brain injury (TBI) is known to cause persistent neurologic sequelae, the underlying structural changes remain elusive. Our purpose was to assess decreases in the volume of brain parenchyma (VBP) in patients with TBI and to determine if clinical parameters are predictors of the extent of atrophy. METHODS: We retrospectively assessed the total VBP in 14 patients with mild or moderate TBI at more than 3 months after injury and in seven patients at two time points more than 3 months apart. VBP was calculated from whole-brain MR images and then normalized by calculating the percent VBP (%VBP) to correct for intraindividual variations in cranial size. Clinical parameters at the time of trauma were evaluated for potential predictors of atrophy. Findings were compared with those of control subjects of similar ages. RESULTS: In the single time-point analysis, brain volumes, CSF volumes, and %VBP were not significantly different between patients and control subjects. In the longitudinal analysis, the rate of decline in %VBP (0.02 versus 0.0064 U/day, P =.05) and the change in %VBP between the first and second time points (-4.16 +/- 1.68 versus -1.49 +/- 1.7, P =.022 [mean +/-SD]) were significantly greater in patients. Change in %VBP was significantly greater in patients with loss of consciousness (LOC) than in those without LOC (P =.023). CONCLUSION: Whole-brain atrophy occurs after mild or moderate TBI and is evident at an average of 11 months after trauma. Injury that produces LOC leads to more atrophy. These findings may help elucidate an etiology for the persistent or new neurologic deficits that occur months after injury.

Adult↗
PubMed2002

CT densitometry of the brain: a novel method for early detection and assessment of irradiation induced brain edema.

The purpose of the study was to examine if the CT densitometric analysis during radiotherapy (RT) of brain tumors is suitable for the early detection of RT induced brain edema (BE), predicting related neurological progress, and assessing the effects of different edema therapies. Planimetric CT-densitograms were constructed by modifying the "High-Lighting" method. Three theoretical density regions were defined and color-coded on the images of the brain. These were defined as edema (10-20 HU), mild edema, and normal brain (29-38 HU). Corresponding axial CT slices were created at the mid-level of the lesion and that of the periventricular white matter to verify the changes in perifocal and diffuse BE. The monitoring was performed on 50 solitary brain tumor patients treated with RT. During RT courses weekly CT-densitometric examinations were carried out. We experienced that changes in densitograms coincided with clinical symptoms, furthermore, preceded the latter. With the use of preventive edema medication based on diuretics and along with adjunctive edema medication adopted to densitograms, the 5-7 week irradiation was completed without ultimate worsening in performance state in 49 of 50 cases and besides we succeeded in avoiding the routine usage of steroids. Based on our findings the CT-densitometry is suitable for early detection and continuous assessment of BE and preventing patient distress during RT. This simple, reproducible and non-invasive procedure could provide an additional clinical tool for new treatment strategies.

Adult↗
PubMed2002

[Changes of dynorphinA1-13 on the treatment of hypoxic-ischemic brain injury by the brain-derived neurotrophic factor in neonatal rats].

OBJECTIVE: To explore changes and role of dynorphinA(1 - 13) on the experimental treatment of hypoxic-ischemic brain injury (HIBI) by intracerebral transplantation of genetically modified myoblasts expressing and secreting brain-derived neurotrophic factor (BDNF) in neonatal rats. METHODS: Seven-day-old Sprague-Dawley rats were randomly divided into HIBI + BDNF group (A), HIBI + BDNF + U50, 488H group (B), HIBI group (C) and sham-operated group (D). Pups were intracerebroparenchymally transplanted with either genetically modified myoblasts producing and secreting BDNF (A, B) or their parent cells (C) at 0.8 microl (4 x 10(4)/microl) followed by a cerebroventricular microinjection of opioid kappa receptor agonist U50, 488H (0.5 microg, B) or vehicles (A, C) shortly after HIBI undergone by a permanent ligation of left common carotid artery followed by a 2.5 h inhalation of humidified 8%O(2) + 92%N(2) at 37 degrees C. Water contents of the brain, levels of malondiadehye (MDA) and cell apoptosis were investigated 1 d after the procedure. Contents of dynorphinA(1 - 13)-like immunoreactivity (ir-DynA(1 - 13)) at the left and right cortex and hippocampus were tested by radioimmunoassay 0, 1, 3 d postinjury. RESULTS: Levels of ir-DynA(1 - 13) in left cortex were markedly increased in group A, B or C when compared to group D different times after the procedure and markedly decreased in group A or B vs group C 1, 3 d after the procedure. Levels of ir-DynA(1 - 13) in left hippocampus were also markedly increased in group A, B and C (0 d), B, C (1 d) and C (3 d) when compared to group D and markedly decreased in group A (1 d) and B (3 d) vs group C, respectively. Water contents, MDA levels and percentage of cell apoptosis were significantly higher in group A, B or C than those in group D and these parameters were obviously lowered in group A compared to group C in the left brain 1 d after the procedure. There were no significant differences of water contents and levels of MDA between group B and C but significantly lowered percentage of cell apoptosis in group B was seen when compared to group C in the left brain. CONCLUSION: It is suggested that dynorphinA(1 - 13) participates in the pathophysiological process of HIBI. One of the pathways of the beneficial effects of intracerebral transplantation of genetically modified myoblasts producing BDNF on HIBI lies on the inhibition of the function of dynorphin A(1 - 13) through the binding of kappa opioid receptor.

Animals↗
PubMed2004

Topodiagnostic investigations on the sympathoexcitatory brain stem pathway using a new method of three dimensional brain stem mapping.

OBJECTIVES: To study the incompletely understood sympathoexcitatory pathway through the human brain stem, using a new method of three dimensional brain stem mapping on the basis of digitally postprocessed magnetic resonance imaging (MRI). METHODS: 258 consecutive patients presenting with acute signs of brain stem ischaemia underwent biplane T2 and EPI diffusion weighted MRI, with slice orientation parallel and perpendicular to a transversal slice selection of the stereotactic anatomical atlas of Schaltenbrand and Wahren, 1977. The individual slices were digitally normalised and projected onto the appropriate slices of the anatomical atlas. For correlation analysis lesions were imported into a three dimensional model of the human brain stem. RESULTS: 31 of the 258 patients had Horner's syndrome caused by acute brain stem ischaemia. Only four of the patients with Horner's syndrome had pontine infarctions, 12 had pontomedullary lesions, and 15 had medullary lesions. Correlation analysis showed significantly affected voxels in the dorsolateral medulla but not in the pons. A statistical comparison with infarct topology in patients with medullary lesions but without Horner's syndrome indicated that involvement of the medial and ventral part of affected voxels located in the ventrolateral medullary tegmentum was specific for Horner's syndrome. CONCLUSIONS: Based on this first in vivo topodiagnostic study, the central sympathoexcitatory pathway probably descends through the dorsal pons before converging on specific generators in the ventrolateral medullary tegmentum at a level below the IX and X nerve exits.

Aged↗
PubMed2004

[The renin-angiotensin system in human brain and brain tumors: a function unrelated to blood pressure control?].

The renin-angiotensin system (RAS), in addition to controlling blood pressure and the sodium-water balance, may be involved in cell growth and/or death in the brain. In order to address this issue, we compared the expression of RAS components in surgical specimens of human brain tumors and adjacent tissue. Human brain tumor cells and rat brain cells in culture were used to evaluate RAS functions. We found evidence that the RAS may be involved in maintaining the functions of the cerebral vasculature (the blood-brain-barrier) by controlling the ratio between angiotensin II and angiotensin III production, and by playing a more direct role in the survival of astroglial cells.

Angiotensin II↗
PubMedDate not supplied

Alterations in brain-stem auditory responses induced by head down tilting in hypertensives with supine brain-stem disorders.

The influence of head down (HD) tilting on brain-stem auditory evoked responses (BAER) was studied in hypertensives with supine brain-stem disorders (occipital headache, vertigo, nausea, diplopia, blurred vision occurring after night recumbency), in hypertensives without such phenomena and in normotensives. In the latter two categories of subjects HD tilting had no effect on BAER. On the contrary, in hypertensives with supine brain-stem disorders the manoeuvre induced a constant prolongation of I-V and III-V intervals and a depression in the amplitude of wave V; the alterations of BAER produced by HD tilting reveal probably a dysfunction of the superior brain-stem area and might be due to the impaired cerebral venous draining subsequent to the manoeuvre. The study of BAER after HD tilting seems to be a proper means to attest the supine brain-stem disorders displayed by some hypertensives.

Brain Ischemia↗
PubMed1988

[Immunoenzymatic detection of specific brain antigens as a criterion of the permeation of blood-brain barrier in rats with acute cerebral ischemia].

EIA detection system for the measurement of alpha 2 M globulin and GFAP antigen has been developed. The limit of the sensibility was only 1 ng/ml for alpha 2M and 0.8 ng/ml for GFAP. The system was used for the studies of the penetration through the blood-brain barrier in rats with experimental acute brain ischemia. The measurement of alpha 2M and GFAP antigens by EIA technique 16-20 hours after the occlusion of the carotid artery has revealed disturbances in the blood-brain barrier permeability for specific brain proteins. The method is recommended for indirect evaluation of the blood-brain barrier functional disorders.

Animals↗