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Query: UMLS:C0038454 (
stroke
)
147,016
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Laser-scanning confocal microscopy (LSCM) was used to measure at high resolution cerebral plasma volumes (perfusion) using two fluorescent plasma markers in a rat model of embolic
stroke
. This application of LSCM to study the microvascular circulation in embolic
stroke
was developed as an alternative to autoradiography to measure cerebral perfusion. An additional benefit of LSCM is that it quantitates with great accuracy the structural relationships of the microcirculation to cells and the pathological alterations of the ischemic brain. Autoradiography allows only a quantitative analysis of cerebral perfusion. For example, in order to study the microcirculation and its relationship to blood brain barrier damage, the volume of perfused cerebral capillaries was measured by administering two fluorescent plasma markers (FITC-dextran and
Evans
blue) intravenously to a rat.
Evans
blue was administered before cerebral ischemia and FITC-dextran administered post-ischemia 1 min before sacrifice. Volumes of plasma perfusion were analyzed by means of a system developed for 3D analysis of fixed and stained serial brain histologies. Plasma volumes for the non-ischemic cerebral cortex were 1.00%+/-0.38% while plasma volumes in the caudate/putamen were 0.69%+/-0.17% in good agreement with the previously published values using the autoradiography method. The architecture of the capillaries in the ischemic core showed perfusion of
Evans
blue but there was no flow of FITC dextran. Our work represents a novel application of this technology to investigation of cerebral vascular disease and identifies its potential to become an important tool for investigation of cerebral pathology.
...
PMID:High resolution quantitation of microvascular plasma perfusion in non-ischemic and ischemic rat brain by laser-scanning confocal microscopy. 1044 13
Nocardiosis is an opportunistic infection caused by gram-positive, weakly acid-fast filamentous aerobic organisms. Three species cause infection in man: N. asteroides, N. brasiliensis, and N. caviae, the first one being the most common. With increased use of immunosuppressive therapy for various autoimmune diseases, opportunistic infection by Nocardia has increasingly been reported. N. asteroides infections manifest in various ways; the lungs, skin, and brain are the organs most frequently involved. We describe a patient with
Evans' syndrome
, a disease requiring long-term immunosuppression, who acquired systemic nocardiosis. The infection was primarily pulmonary, misdiagnosed as tuberculosis, with subsequent hematogenous dissemination to the skin and central nervous system. The diagnosis of cerebral involvement was difficult to prove, as the patient presented with
stroke
-like episodes. After a positive blood culture was obtained, antibiotic therapy was introduced. The patient's condition deteriorated and the brain with infiltration of the meninges, lungs, skin, and kidneys. Nocardia is an important but often overlooked opportunistic infectious agent in immunocompromised hosts, causing diagnostic and therapeutic problems. As the mortality of cerebral nocardiosis is greater than 80%, early diagnosis and appropriate therapy are crucial.
...
PMID:Disseminated nocardiosis as a complication of Evans' syndrome. 1046 Mar 54
Magnetic resonance imaging (MRI) was utilized to obtain absolute estimates of regional brain water content (W), and results were compared with those obtained with conventional wet/dry measurements. In total, 31 male Long-
Evans
rats were studied and divided into two groups based on the surgical procedures used to induce cerebral focal ischemia: suture (n = 18) and three-vessel ligation (TVL: n = 13) groups. Both relative spin density and T1 were extracted from the acquired MR images. After correcting for radiofrequency field inhomogeneities, T2* signal decay, and temperature effects, in vivo regional brain water content, in absolute terms, was obtained by normalizing the measured relative brain spin density of animals to that of a water phantom. A highly linear relationship between MR-estimated brain water content based on the normalized spin density and wet/dry measurements was obtained with slopes of 0.989 and 0.986 for the suture (r = 0.79) and TVL (r = 0.83) groups, respectively. Except for the normal subcortex of the TVL group (P < 0.02) and the normal hemisphere of the suture group (P < 0.003), no significant differences were observed between MR-estimated and wet/dry measurements of brain water content. In addition, a highly linear relationship between MR-measured R1 (= 1/T1) and 1/W of wet/dry measurements was obtained. However, slopes of the linear regression lines in the two groups were significantly different (P < 0.02), indicating that different R1 values were associated with the same water content depending on the model. These results show that an absolute measurement of in vivo regional brain water content can be obtained with MRI and potentially serves as a noninvasive means to monitor different therapeutic interventions for the management of brain edema subsequent to
stroke
and head trauma.
...
PMID:An absolute measurement of brain water content using magnetic resonance imaging in two focal cerebral ischemic rat models. 1061 91
Experimental
stroke
using a focal cerebral ischemia and reperfusion (FCIR) model was induced in male Long-
Evans
rats by a bilateral occlusion of both common carotid arteries and the right middle cerebral artery for 30-90 min, followed by various periods of reperfusion. Oxidative DNA lesions in the ipsilateral cortex were demonstrated using Escherichia coli formamidopyrimidine DNA N-glycosylase (Fpg protein)-sensitive sites (FPGSS), as labeled in situ using digoxigenin-dUTP and detected using antibodies against digoxigenin. Because Fpg protein removes 8-hydroxy-2'-deoxyguanine (oh8dG) and other lesions in DNA, FPGSS measure oxidative DNA damage. The number of FPGSS-positive cells in the cortex from the sham-operated control group was 3 +/- 3 (mean +/- SD per mm(2)). In animals that received 90 min occlusion and 15 min of reperfusion (FCIR 90/15), FPGSS-positive cells were significantly increased by 200-fold. Oxidative DNA damage was confirmed by using monoclonal antibodies against 8-hydroxy-guanosine (oh8G) and oh8dG. A pretreatment of RNase A (100 microg/ml) to the tissue reduced, but did not abolish, the oh8dG signal. The number of animals with positive FPGSS or oh8dG was significantly (P<0.01) higher in the FCIR group than in the sham-operated control group. We detected few FPGSS of oh8dG-positive cells in the animals treated with FCIR of 90/60. No terminal UTP nicked-end labeling (TUNEL)-positive cells, as a detection of cell death, were detected at this early reperfusion time. Our data suggest that early oxidative DNA lesions elicited by experimental
stroke
could be repaired. Therefore, the oxidative DNA lesions observed in the nuclear and mitochondrial DNA of the brain are different from the DNA fragmentation detected using TUNEL.
...
PMID:Oxidative DNA damage precedes DNA fragmentation after experimental stroke in rat brain. 1078 50
In patients with thrombotic
stroke
, the occluded artery often reopens over time. This results through a natural dissolution of the occluding material, and fragments of the material may move downstream to obstruct distal arteries. The current study was undertaken to investigate the patency of brain microvessels at varying time intervals after injection of a preformed clot into the right internal carotid artery of rats. Cerebral microvessels in brain sections were visualized using immunohistochemistry for fibronectin (detecting existing microvessels) and
Evans
blue (visualizing perfused microvessels). The percentage of patent microvessels was calculated as the number of
Evans
blue-positive microvessels divided by the number of fibronectin-positive microvessels. In normal control animals, results showed that 98% +/- 3% (mean +/- SD) of microvessels in the cortex and 94% +/- 14% in the striatum were patent. In the ischemic animals, immediately after clot injection, microvessels in the cortex and striatum were occluded, mainly in the territory irrigated by the middle cerebral artery. One hour after clot injection, microvessels had reopened in most of the cortex but remained occluded in some portions of the striatum, possibly as a result of downstream movement of fragments formed from the original clot. By 3 hours after clot injection, microvessels in the cortex were patent in all animals, whereas in the striatum microvessels were patent in 50% of the animals. In the other 50%, small striatal perfusion deficits persisted. At 24 hours after clot injection, microvessels were patent in both the cortex and striatum of all animals except one. These findings suggest that intracerebral clots dissolve spontaneously in a relatively short period of time, but that fragments formed from the clot may obstruct more distal blood vessels. It is likely that clot fragments lodge in arteries with lower blood flow and poor collateral perfusion, where they continue to cause ischemia for a longer duration. These results may in part explain the resistance of the striatum to neuroprotective strategies used for the treatment of focal cerebral ischemia.
...
PMID:Patency of cerebral microvessels after focal embolic stroke in the rat. 1132 27
Magnesium probably protects brain tissue against the effects of cerebral ischemia, brain injury and
stroke
through its actions as a calcium antagonist and inhibitor of excitatory amino acids. The effects of magnesium sulfate on cerebrovascular permeability to a dye,
Evans
blue, were studied during insulin-induced hypoglycemia with hypothermia in rats. Hypoglycemia was induced by an intramuscular injection of insulin. After giving insulin, each animal received MgSO4 (270 mg/kg) ip, followed by a 27 mg/kg dose every 20 min for 2.5 h. Plasma glucose and Mg2+ levels of animals were measured. Magnesium concentrations increased in the serum following MgSO4 administration (6.05+/-0.57 vs. 2.58+/-0.14 mg/dL in the Mg2+ group, and 7.14+/-0.42 vs. 2.78+/-0.06 mg/dL in the insulin + Mg2+ group, P < 0.01). Plasma glucose levels decreased following hypoglycemia (4+/-0.66 vs. 118+/-2.23 mg/dL in the insulin group, and 7+/-1.59 vs. 118+/-4.84 mg/dL in the insulin + Mg2+ group, P < 0.01). Blood-brain barrier permeability to
Evans
blue considerably increased in hypoglycemic rats (P < 0.01). In contrast, blood-brain barrier permeability to
Evans
blue was significantly reduced in treatment of hypoglycemic rats with MgSO4 (P < 0.01). These results indicate that Mg2+ greatly reduced the passage of exogenous vascular tracer bound to albumin into the brain during hypoglycemia with hypothermia. Mg2+ could have protective effects on blood-brain barrier permeability against insulin-induced hypoglycemia.
...
PMID:Magnesium sulfate attenuates increased blood-brain barrier permeability during insulin-induced hypoglycemia in rats. 1159 80
We have previously shown that early forced overuse of the affected forelimb worsens outcome following moderately severe transient focal cortical ischemic
stroke
in rats using a distal middle cerebral artery occlusion (MCAo) model. This effect may be site-dependent, because we have also found that early forced use of the affected limb after unilateral 6-OHDA induced degeneration of ascending nigrostriatal dopamine neurons markedly enhanced functional outcome and is neuroprotective. The present study examines the effects of early overuse and disuse following a moderately severe proximal MCAo model, by means of intraluminal suture occlusion. Ischemia was produced in male Long-
Evans
rats with 60 min of occlusion, or sham surgery was performed. Early overuse or disuse of the affected forelimb was forced by immobilizing either the ipsilateral or contralateral forelimb, respectively, in a plaster cast or the animal was left uncasted. Casts were removed on day 10 and sensorimotor testing was performed weekly during days 17-38. Animals were sacrificed on day 45 and brains were fixed for later cresyl violet staining. The MCAo+contralateral cast group performed worse than all other groups on tests of forelimb sensorimotor function. All MCAo groups regardless of cast condition had significant atrophy of the ischemic striatum, but there was no significant atrophy of the ischemic cortex in any group. Forced disuse, but not overuse, of the affected forelimb immediately following proximal ischemia using the intraluminal suture model has detrimental effects on functional outcome, without exaggerating anatomical damage. The effects of disuse and overuse during the first 10 days after
stroke
differ depending on cortical or subcortical involvement.
...
PMID:Early overuse and disuse of the affected forelimb after moderately severe intraluminal suture occlusion of the middle cerebral artery in rats. 1170 49
Individuals with chronic fatigue syndrome (CFS) experience a number of somatic complaints including severe, disabling fatigue, and exercise intolerance. We hypothesized that hypovolemia, through its interaction with central hemodynamics, would contribute to the exercise intolerance associated with this disorder. We examined blood volume, peak aerobic power, habitual physical activity, fatigue level, and their interrelations to understand the physiological basis of this disorder. Seventeen patients who met the Centers for Disease Control criteria for CFS and 17 age-matched controls participated in the study. Blood volume was assessed using a single bolus injection of
Evans
blue dye. Peak oxygen consumption was measured during exercise on an upright cycle ergometer. Supine cardiac output and
stroke
volumes were measured using CO(2) rebreathing. Questionnaires were used to assess habitual physical activity and fatigue. Patients displayed a trend for a 9% lower blood volume (58.3 +/- 2.1 vs. 64.2 +/- 2.5 ml/kg, P = 0.084) and had a 35% lower peak oxygen consumption (22.0 +/- 1.2 vs. 33.6 +/- 1.9 ml/kg, P < 0.001). These two variables were highly related within the patients (r = 0.835, P < 0.001) and the controls (r = 0.850, P < 0.001). Peak ventilation and habitual physical activity were significantly lower in the patients. Fatigue level was not related to any of the measured physiological parameters within the CFS group. In conclusion, individuals with CFS have a significantly lower peak oxygen consumption and an insignificant trend toward lower blood volume compared with controls. These variables were highly related in both subject groups, indicating that blood volume is a strong physiological correlate of peak oxygen consumption in patients with CFS.
...
PMID:Blood volume and its relation to peak O(2) consumption and physical activity in patients with chronic fatigue. 1174 48
The repair of oxidative DNA lesions (ODLs) in the nucleus of ischemic cortical brain cells was examined following experimentally induced
stroke
by occluding the right middle cerebral artery and both common carotid arteries for 60-90 min followed by reperfusion in male long-
Evans
hooded rats. The control group consisted of sham-operated animals undergoing the same surgery without vessel occlusion. Using a gene-specific assay based upon the presence of Escherichia coli Fpg protein-sensitive sites, we noted that animals with
stroke
exhibited six and four ODLs per gene in the actin and DNA polymerase-beta genes, respectively. This was increased from one per four copies of each gene in the sham-operated control (p < 0.01). One half of the initial ODLs was repaired within 30 min, and 83% of them were repaired as early as 45 min of reperfusion. There was no further increase when gene repair was measured again at 2 h of reperfusion. The rates of active repair within 45 min of reperfusion were the same in these two genes (p = 0.103, ANOVA). BrdU (10 mg/kg) was administered via intraperitoneal injection at least one day before surgery. We observed that there was no significant incorporation of BrdU triphosphates into genomic DNA during active repair, but there were significant amounts of BrdU triphosphate in nuclear DNA after active repair. The result indicates that genomic repair of ODLs in the brain did not significantly incorporate BrdU, and the initiation of neurogenesis probably starts after the completion of repair in the brain.
...
PMID:Homogeneous repair of nuclear genes after experimental stroke. 1179 49
Malignant
stroke
-prone spontaneously hypertensive rats (M-SHRSP) develop hypertension and
stroke
at earlier ages than do nonmalignant SHRSP. Our previous findings suggested that reactive oxygen species were involved in the development of
stroke
in this strain. Nitric oxide (NO) which is more released at ischemia, might play a crucial role in
stroke
development by producing peroxynitrite, a neurotoxic substance. This study investigated whether the development of cerebrovascular lesion in M-SHRSP could be assessed by the fluctuation of serum NO(x) concentration, and whether peroxynitrite is associated with brain damage. Serum NO(x) levels were examined using an automated NO detector.
Stroke
-onset was temporally assessed according to a known method: changes in body weight, water intake, and neurologic symptoms. Cerebral lesions were confirmed by magnetic resonance imaging (MRI), and
Evans
blue extravasation at autopsy. MRI taken just after estimated
stroke
onset disclosed brain lesions. The baseline serum NO(x) level remained at 15-18 micromol/l, but the level gradually increased prior to
stroke
, and significantly at
stroke
onset. A marked rise in serum NO(x) occurred subsequently at poststroke. Immunohistochemical staining of nitrotyrosine, a peroxynitrite marker, was detected around vessels, neuronal cells and parenchyma in cerebral lesions.
Stroke
occurred in 50% of male M-SHRSP at 80 days of age. In conclusion, this study provides the first evidence for fluctuation of serum NO(x) at the onset of spontaneous
stroke
accompanying the appearance of peroxynitrite in brain lesions. Monitoring serum NO(x) would serve to assess the development of brain lesions at least in spontaneous
stroke
model.
...
PMID:Fluctuation of serum NO(x) concentration at stroke onset in a rat spontaneous stroke model (M-SHRSP). Peroxynitrite formation in brain lesions. 1221 10
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