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PubMed2004

Novel therapeutic strategy to treat brain ischemia: overexpression of hepatocyte growth factor gene reduced ischemic injury without cerebral edema in rat model.

BACKGROUND: Although cerebral occlusive disease leads to cerebral ischemic events, an effective treatment has not yet been established. An ideal therapeutic approach to treat ischemia might have both aspects of enhancement of collateral formation and prevention of neuronal death. Hepatocyte growth factor (HGF) is a potent angiogenic factor that also acts as a neurotrophic factor. Thus, in this study, we examined the therapeutic effects of HGF on brain injury in a rat permanent middle cerebral artery occlusion model. METHODS AND RESULTS: Gene transfer into the brain was performed by injection of human HGF gene with hemagglutinating virus of Japan-envelope vector into the cerebrospinal fluid via the cisterna magna. Overexpression of the HGF gene resulted in a significant decrease in the infarcted brain area as assessed by triphenyltetrazolium chloride staining, whereas rats transfected with control vector exhibited a wide area of brain death after 24 hours of ischemia. Consistently, the decrease in neurological deficit was significantly attenuated in rats transfected with the HGF gene at 24 hours after the ischemic event. Stimulation of angiogenesis was also detected in rats transfected with the HGF gene compared with controls. Of importance, no cerebral edema or destruction of the blood-brain barrier was observed in rats transfected with the HGF gene. CONCLUSIONS: Overall, the present study demonstrated that overexpression of the HGF gene attenuated brain ischemic injury in a rat model, without cerebral edema, through angiogenic and neuroprotective actions. In particular, the reduction of brain injury by HGF may provide a new therapeutic option to treat cerebrovascular disease.

Animals↗
PubMed1994

Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia.

Naturally occurring cell death (NOCD) is a prominent feature of the developing nervous system. During this process, neurons express bcl-2, a major regulator of cell death whose expression may determine whether a neuron dies or survives. To gain insight into the possible role of bcl-2 during NOCD in vivo, we generated lines of transgenic mice in which neurons overexpress the human BCL-2 protein under the control of the neuron-specific enolase (NSE) or phosphoglycerate kinase (PGK) promoters. BCL-2 overexpression reduced neuronal loss during the NOCD period, which led to hypertrophy of the nervous system. For instance, the facial nucleus and the ganglion cell layer of the retina had, respectively, 40% and 50% more neurons than normal. Consistent with this finding, more axons than normal were found in the facial and optic nerves. We also tested whether neurons overexpressing BCL-2 were more resistant to permanent ischemia induced by middle cerebral artery occlusion; in transgenic mice, the volume of the brain infarction was reduced by 50% as compared with wild-type mice. These animals represent an invaluable tool for studying the effects of increased neuronal numbers on brain function as well as the mechanisms that control the survival of neurons during development and adulthood.

Animals↗
PubMed1985

Homing and circulation of indium-111-labelled leucocytes. A post-mortem study.

The history of a patient with a suspected ischemic brain infarct undergoing an indium-111-tropolone white cell labelled test is reported. The patient, who died 12 h after injection of the labelled cells, suffered of a brain haemorrhage. The post-mortem examination has allowed for the first time the measurement of radioactivity in different organs following the injection of indium-111-labelled leucocytes. High radioactivity was found only in tissues affected by inflammatory processes and in the lymphonodes draining the corresponding areas. This report clearly indicates the importance of this method for the study of white cell localization and circulation to the sites of infections.

Cerebral Hemorrhage↗
PubMed1992

[Multi-infarct and Alzheimer dementia--problems of differential diagnosis].

The differential diagnosis of Alzheimer's and so-called multi-infarct dementia is still a major problem in clinical dementia research. It was Binswanger who in 1894 pointed out that a subtype of vascular dementia exists which is characterized by subcortical arteriosclerotic encephalopathy. It is this type that can most easily be mistaken for Alzheimer's dementia, presented for the first time in 1906, which may be associated with congophilic angiopathy leading to brain infarction. Beyond clinical criteria, which in part are summarized in Hachinski's ischemic score, further advancement of brain imaging techniques, especially those yielding perfusion or metabolic data, has facilitated and substantiated clinical in vivo distinction.

Alzheimer Disease↗
PubMed1996

Induction of thymosin beta(4) mRNA following focal brain ischemia.

Thymosin beta 4 is a protein expressed in most rodent and human tissues, including the brain, and is thought to participate in neurite outgrowth during development by sequestration of G-actin necessary for growth cone extension. Under normal conditions in the adult rat brain, the gene has been suggested to be expressed in microglia and CA1-CA2 hippocampal pyramidal cells. Here we show by using in situ hybridization that t beta 4 is dramatically up-regulated in the infarcted brain area after focal ischaemia. In addition, moderate t beta 4 induction is detected in the perifocal zone, substantia nigra and CA1-CA3 hippocampal pyramidal neurones. Macrophages are probably responsible for t beta 4 induction in the infarcted region, and activated non-neuronal cells probably contribute to the induction seen in the thalamus, substantia nigra and perifocal zone. However, the pyramidal neurones in the hippocampus show t beta 4, upregulation which may be related to restoration of neurite circuits after focal ischemic damage.

Animals↗
PubMed1991

Cerebral infarction: early detection by means of contrast-enhanced cerebral arteries at MR imaging.

The authors describe a new magnetic resonance (MR) imaging sign of acute cerebral ischemia/infarction. Abnormally contrast material-enhanced curvilinear structures were demonstrated in eight patients in the evolving area of cerebral ischemia/infarction within 26 hours after the ictus on contrast-enhanced, high-field-strength (1.5-T), T1-weighted spin-echo images. The abnormal enhancement is considered to represent cortical arterial vessels of markedly slowed circulation in areas of underlying brain injury, which will eventually progress to frank brain infarction. This was demonstrated at computed tomographic (CT) and follow-up MR examinations. Characteristically, the degree of the contrast enhancement of vessels appeared most intense in the proximal portions, and the intensity of enhancement gradually diminished in the more distal portions of these vessels as they pass over the convexities and finally disappear.

Acute Disease↗
PubMed1988

Cerebral blood flow requirement for brain viability in newborn infants is lower than in adults.

Measurements of regional cerebral blood flow (CBF) with positron emission tomography in adult humans with cerebrovascular disease have demonstrated consistently that values below 10 ml/(100 gm.min) occur only in infarcted brain. Although experimental data suggest that the newborn brain may be more resistant to ischemic injury than the adult brain, the minimum CBF necessary to sustain neuronal viability in newborn infants is unknown. We have measured CBF with positron emission tomography in 16 preterm and 14 term newborn infants and have determined the relationship between CBF and subsequent brain function as assessed by neurological examination and developmental assessment. The range of mean CBF in the preterm infants was 4.9 to 23 ml/(100 gm.min) and the range of mean CBF in the term infants was 9.0 to 73 ml/(100 gm.min). Five preterm infants and one term infant with mean CBF less than 10 ml/(100 gm.min) survived. Three of these 5 preterm infants, with mean CBF of 4.9, 5.2, and 9.3 ml/(100 gm.min), respectively, have normal neurological examinations and Bayley Scales of 80 or greater at 6, 6, and 24 months of age, respectively. One (mean CBF 6.9) has normal cognitive development (Bayley 103) and a mild spastic diplegia at age 19 months, and one infant (mean CBF 6.2) has a left hemiparesis and a Binet IQ score of 70 at age 33 months. The term infant, with a mean CBF of 9.0 ml/(100 gm.min), was developing normally when he died of sepsis at age 5 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain↗
PubMed2001

Design, synthesis, SAR, and biological evaluation of highly potent benzimidazole-spaced phosphono-alpha-amino acid competitive NMDA antagonists of the AP-6 type.

A series of 2-amino-(phosphonoalkyl)-1H-benzimidazole-2-alkanoic acids was synthesized and evaluated for NMDA receptor affinity using a [3H]CPP binding assay. Functional antagonism of the NMDA receptor complex was evaluated in vitro using a stimulated [3H]TCP binding assay and in vivo by employing an NMDA-induced seizure model. Several compounds of the AP-6 type demonstrated potent and selective NMDA antagonistic activity both in vitro and in vivo. In particular, [R(-)]-2-amino-3-(5-chloro-1-phosphonomethyl-1H-benzoimidazol-2-yl)-propionic acid (1) displayed an IC(50) value of 7.1 nM in the [3H]CPP binding assay and an ED(50) value of 0.13 mg/kg (ip) in the NMDA lethality model. Compound 1, when administered intravenously as a single bolus dose of 3 mg/kg following permanent occlusion of the middle cerebral artery in the rat, reduced the volume of infarcted brain tissue by 45%. These results support a promising therapeutic potential for compound 1 as a neuroprotective agent.

Animals↗
PubMed1988

Increase of plasma methionine-enkephalin levels in patients at the acute stage of cerebral infarction.

We investigated the participation of endogenous opioid peptide in cerebral ischaemia. In 13 patients with supratentorial infarction, the plasma immunoreactive methionine-enkephalin concentration at the acute stage (30.77 +/- 3.54 pg/ml) was significantly higher than that at the chronic stage (20.37 +/- 2.07 pg/ml) or that of the control subjects (19.64 +/- 1.71 pg/ml). However, it was unrelated to infarct size or patient severity. The increased methionine-enkephalin, which appears to originate from the sympatho-adrenal system or infarcted brain, may play a role in the evolution of cerebral ischaemia.

Aged↗
PubMed2002

Proximal and distal hyperattenuating middle cerebral artery signs at CT: different prognostic implications.

PURPOSE: To determine whether a proximal (M1-segment) or distal (M2- and/or M3-segment) hyperattenuating middle cerebral artery (MCA) sign in patients with ischemic infarction in the territory of the MCA indicates a worse short-term prognosis than that in patients without a hyperattenuating MCA sign. MATERIALS AND METHODS: We retrospectively reviewed the records of 352 patients who were diagnosed with ischemic brain infarction in the territory of the MCA. Of these patients, 186 patients met our final criteria and were included in this study. Nonenhanced computed tomography (CT) was performed for the entire brain, with a 5-mm section thickness in all patients, within 24 hours after symptom onset. The presence and location of a hyperattenuating MCA sign was correlated with neurologic deficit at discharge from the hospital (ie, short-term prognosis) by using the chi(2) test to detect differences between patient groups. RESULTS: Patients with a hyperattenuating MCA sign at CT have a worse short-term prognosis than do patients without a hyperattenuating MCA sign (P <.05). Patients with a proximal hyperattenuating MCA sign have a significantly (P <.01) worse short-term prognosis than do patients with a distal hyperattenuating MCA sign. CONCLUSION: A proximal hyperattenuating MCA sign is a reliable predictor of poor short-term prognosis in patients who experience acute stroke.

Acute Disease↗
PubMed1999

Oxygen delivery during retrograde cerebral perfusion in humans.

UNLABELLED: Retrograde cerebral perfusion (RCP) potentially delivers metabolic substrate to the brain during surgery using hypothermic circulatory arrest (HCA). Serial measurements of O2 extraction ratio (OER), PCO2, and pH from the RCP inflow and outflow were used to determine the time course for O2 delivery in 28 adults undergoing aortic reconstruction using HCA with RCP. HCA was instituted after systemic cooling on cardiopulmonary bypass for 3 min after the electroencephalogram became isoelectric. RCP with oxygenated blood at 10 degrees C was administered at an internal jugular venous pressure of 20-25 mm Hg. Serial analyses of blood oxygen, carbon dioxide, pH, and hemoglobin concentration were made in samples from the RCP inflow (superior vena cava) and outflow (innominate and left carotid arteries) at different times after institution of RCP. Nineteen patients had no strokes, five patients had preoperative strokes, and four patients had intraoperative strokes. In the group of patients without strokes, HCA with RCP was initiated at a mean nasopharyngeal temperature of 14.3 degrees C with mean RCP flow rate of 220 mL/min, which lasted 19-70 min. OER increased over time to a maximal detected value of 0.66 and increased to 0.5 of its maximal detected value 15 min after initiation of HCA. The RCP inflow-outflow gradient for PCO2 (slope 0.73 mm Hg/min; P < 0.001) and pH (slope 0.007 U/min; P < 0.001) changed linearly over time after initiation of HCA. In the group of patients with preoperative or intraoperative strokes, the OER and the RCP inflow-outflow gradient for PCO2 changed significantly more slowly over time after HCA compared with the group of patients without strokes. During RCP, continued CO2 production and increased O2 extraction over time across the cerebral vascular bed suggest the presence of viable, but possibly ischemic tissue. Reduced cerebral metabolism in infarcted brain regions may explain the decreased rate of O2 extraction during RCP in patients with strokes. IMPLICATIONS: Examining the time course of oxygen extraction, carbon dioxide production, and pH changes from the retrograde cerebral perfusate provided a means to assess metabolic activity during hypothermic circulatory arrest.

Adult↗
PubMed2006

[Adult bacterial meningitis complicated by cerebral infarction: report of three cases].

Fatality rates and the number of patients suffering from the after sequelae of bacterial meningitis have still remained high despite the development of new antibiotics. Cerebrovascular complications have been reported less frequently in adult cases than in child cases. We experienced 3 consecutive cases of bacterial meningitis in adults complicated by brain infarction. Primary causative organism were the Group B Streptococci in one case and the Streptococcus pneumoniae in other two cases. MRI, especially with FLAIR method and of coronal view, disclosed abnormal intensity areas near the brain surface. Conventional angiography and MR-angiography in the two cases showed tapering and stenosis of arteries. These cases suggest that routine use of MRI/ MRA in bacterial meningitis reveal neuro-vascular complications more frequently and easily. The benefits of adjunctive steroid therapy in the treatment of bacterial meningitis might be beneficial to suppression of these neurovascular complication cased by inflammatory vasculitis.

Aged↗
PubMed2006

Intracranial carotid artery calcification on head CT and its association with ischemic changes on brain MRI in patients presenting with stroke-like symptoms: retrospective analysis.

INTRODUCTION: Our purpose was to study the association between the intracranial arterial calcifications observed on head CT and brain infarcts demonstrated by MRI in patients presenting with acute stroke symptoms. METHODS: Institutional review board approval was obtained for this retrospective study which included 65 consecutive patients presenting acutely who had both head CT and MRI. Arterial calcifications of the vertebrobasilar system and the intracranial cavernous carotid arteries (intracranial carotid artery calcification, ICAC) were assigned a number (1 to 4) in the bone window images from CT scans. These four groups were then combined into high calcium (grades 3 and 4) and low calcium (grades 1 and 2) subgroups. Brain MRI was independently evaluated to identify acute and chronic large-vessel infarcts (LVI) and small-vessel infarcts (SVI). The relationship between ICAC and infarcts was evaluated before and after adjusting for demographics and cardiovascular risk factors. RESULTS: Statistical analysis could not be performed for the vertebrobasilar system due to an insufficient number of patients in the high calcium group. Of the 65 patients, 46 (71%) had a high ICAC grade on head CT. They were older and had a higher prevalence of cardiovascular risk factors. Acute SVI (P = 0.006), chronic SVI (P = 0.006) and acute LVI (P = 0.04) were associated with a high ICAC grade. After adjustment for age and other risk factors, only acute SVI was associated with a high ICAC grade (P = 0.002). CONCLUSION: Although age emerged as the most important determinant of ischemic cerebral changes, there were rather complex interactions among multiple risk factors with different infarct types. A high ICAC grade demonstrated a correlation with acute SVI in our patients independent of these risk factors.

Aged↗
PubMed1992

Photothrombosis in rabbit brain cortex: follow up by continuous pO2 measurement.

Continuous recording of changes in local pO2 during and after brain infarction in surviving animals which can be followed for months or years, may provide interesting information concerning pathophysiology and treatment of stroke and thrombosis. We performed such measurements before, during and till 4 weeks after photochemical induction of a cerebrocortical infarction in three rabbits. Rose bengal--a photosensitive dye which sticks to endothelial cells and gives rise to endothelial damage and thrombosis when illuminated--was injected intravenously. After injection, a circular area (diameter 3 mm) of the brain cortex was illuminated using an optic fiber conducting light from a halogen lamp, whether or not filtered by heat and colour filters. In order to enable pO2 measurement in and near the infarct zone, we constructed a transparent plastic frame in which pO2 electrodes were fixed beneath and 1 mm besides a shaft permitting mounting of the optic fiber. A black adhesive ring (inner diameter 3 mm) was attached to the bottom of the frame providing a perfectly demarcated illumination area. After fixation the electrodes were calibrated and the frame was implanted in the rabbit's skull. Ten days later an infarction was induced; pO2 was monitored continuously before, during and till 4 hours after this induction. Furthermore, pO2 was recorded 24 hours, 48 hours, 5 days, 14 days and 4 weeks after infarction. Parameters describing the time course of pO2 were determined. In the illuminated area pO2 decreased after a certain latency time to reach a very low level, probably zero level, where it remained for at least 24 hours. Gradually, recovery was observed during the following days, and four weeks after infarction both level and pattern of electrode current appeared to be normal again. In the border zone pO2 decreased but did not reach zero level. Recovery was observed earlier than in the illuminated area.

Animals↗
PubMed2005

Stroke in patients on maintenance hemodialysis: a 22-year single-center study.

BACKGROUND: Few studies have reported the detailed clinical features of stroke in patients with end-stage renal disease. We examined the frequency of the subtypes, mechanism, and outcome of stroke in patients receiving hemodialysis (HD). METHODS: We studied 151 consecutive patients who developed an acute stroke among the maintenance HD population in our kidney center during 22 years, divided into the initial 17-year (n = 61) and the more recent 5-year (n = 90) groups. For purposes of comparison, we also studied 1,017 stroke patients with normal renal function. RESULTS: Stroke patients receiving HD were younger (age, 64 +/- 10 versus 67 +/- 13 years; P < 0.02) and more frequently had hypertension (87% versus 43%; P < 0.0001) and diabetes (53% versus 23%; P < 0.0001) compared with stroke patients with normal renal function. In the initial HD group, brain hemorrhage was the major subtype of stroke (52%), whereas in the more recent group, brain infarction (BI) replaced hemorrhage as the leading subtype (68%; P < 0.005). In patients with BI, large-artery atherosclerosis was more prevalent in the more recent group than in the initial HD group (33% versus 12%; P < 0.05). A vertebrobasilar territory infarct was more prevalent for HD patients than for those with normal renal function (48% versus 33%; P < 0.05). BI (especially large-artery atherosclerosis and cardioembolism) occurred more frequently during or less than 30 minutes after the dialysis procedure (34%) than brain hemorrhage (19%; P < 0.05). Receiving HD was an independent indicator for poor functional outcome and mortality after stroke. CONCLUSION: In our maintenance HD population, stroke showed several unique characteristics compared with the control population, including a predominance of vertebrobasilar arterial territory infarcts. The dialysis procedure itself seems to be associated more frequently with ischemic rather than hemorrhagic strokes.

Aged↗
PubMed1999

[Brain metastases of lung cancer: diagnostic accuracy of positron emission tomography with fluorodeoxyglucose (FDG-PET)].

The value of FDG-PET in oncology is currently investigated in clinical studies. There is only limited information on the usefulness of FDG-PET in the evaluation of distant metastases of lung cancer. The purpose of the present prospective investigation was to determine the diagnostic accuracy of FDG-PET in the detection of brain metastases of lung cancer. After intravenous injection of 220 +/- 50 MBq F-18-deoxyglucose PET acquisition was carried out using an ECAT ART scanner (CTI Siemens). Images were reconstructed using a filtered backprojection with a Hanning filter. PET data were analyzed by visual interpretation of coronal, sagittal and transversal slices. PET scans were interpreted by two experienced nuclear medicine physicians without prior knowledge of the results of other imaging studies or clinical data. Between March 1997 and July 1998 whole-body PET was performed in 417 patients with suspected lung cancer. 402 patients were used for statistical analysis. Based on conventional brain imaging with CT (occasionally MRI), brain metastases were suspected in 17 patients (prevalence 4.2%). For FDG-PET alone, sensitivity was 82% (14/17) and specificity 38% (14/37). Therefore, diagnostic accuracy of FDG-PET in detection of brain metastases was 93.5%. The low specificity of FDG-PET can be explained by reduced tracer uptake mainly due to brain infarction or vascular encephalopathy in this group of elderly patients. Our results indicate that due to its low specificity FDG-PET is not useful for the evaluation of brain metastases in the primary staging of patients with lung cancer.

Adult↗
PubMed1982

Reduction of regional cerebral blood flow during brain retraction pressure in the rat.

The use of brain retractors in intracranial operations may lead to focal cerebral ischemia and thereby cause brain infarction. To estimate the risk of ischemic damages, the authors investigated the regional cerebral blood flow (rCBF) in rats by means of autoradiography with 14C-iodoantipyrine at different brain retractor pressures (BRP). A reduction in rCBF to between 10 and 75 ml/100 gm/min with 20 mm Hg of BRP for 30 minutes was found in brain cortex lying under the retractor (normal 55 to 150 ml/100 gm/ min). With a BRP of 30 mm Hg for 30 minutes, rCBF was reduced to between 0 and 40 ml/100 gm/min, and with a BRP of 40 mm Hg for 15 minutes rCBF was 0 to 15 ml/100 gm/min. The rCBF in the basal ganglia remained unchanged. Even with a BRP of 20 mm Hg for 30 minutes, there seemed to be a risk of focal ischemic damage.

Animals↗