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PubMed2003

Beneficial effect of pharmacological mobilization of bone marrow in experimental cerebral ischemia.

Bone marrow stem cells are able to differentiate into nervous and endothelial cells. In our study, we found that administration of a bone marrow-stimulating factor (granulocyte colony-stimulating factor; G-CSF 50 microg/kg) decrease the brain infarct volume and enhance survival rate in a model of cerebral ischemia. Taken together, these data suggest a beneficial effect of a pharmacological endogenous bone marrow mobilization in the course of cerebral ischemia and open a new direction for cellular therapy strategy in stroke.

Animals↗
PubMed1990

Beneficial effect of 1,3-butanediol on cerebral energy metabolism and edema following brain embolization in rats.

We assessed the effect of 1,3-butanediol on cerebral energy metabolism and edema after inducing multifocal brain infarcts in 108 rats by the intracarotid injection of 50-microns carbonized microspheres. An ethanol dimer that induces systemic ketosis, 25 mmol/kg i.p. butanediol was injected every 3 hours to produce a sustained increase in the plasma level of beta-hydroxybutyrate. Treatment significantly attenuated ischemia-induced metabolic changes by increasing the concentrations of phosphocreatine, adenosine triphosphate, and glycogen and by reducing the concentrations of pyruvate and lactate. Lactate concentration 2, 6, and 12 hours after embolization decreased by 13%, 44%, and 46%, respectively. Brain water content increased from 78.63% in six unembolized rats to 80.93% in 12 saline-treated and 79.57% in seven butanediol-treated rats 12 hours after embolization. (p less than 0.05). The decrease in water content was associated with significant decreases in the concentrations of sodium and chloride. The antiedema effect of butanediol could not be explained by an osmotic mechanism since equimolar doses of urea or ethanol were ineffective. Our results support the hypothesis that the beneficial effect of butanediol is mediated through cerebral utilization of ketone bodies arising from butanediol metabolism, reducing the rate of glycolysis and the deleterious accumulation of lactic acid during ischemia.

3-Hydroxybutyric Acid↗
PubMed1994

Conjunctival oxygen tension is influenced by plasma and blood volume, and flow through the external carotid artery.

An investigation of the feasibility and validity of measurement of the conjunctival oxygen tension as a monitor of peripheral circulation, blood and extracellular fluid volume and cerebral circulation was carried out in 7 healthy volunteers and 5 unconscious critical care patients with proven total cerebral infarction. The healthy volunteers were subjected to changes in hydration achieved by the administration of furosemide and subsequent rehydration by administration of normal saline. Conjunctival oxygen tension was found to be a sensitive indicator of changes in the degree of hydration presumably by its ability to detect changes in peripheral circulation depending upon circulating blood and extracellular fluid volume. A drawback is that other stimuli of the sympatho-adrenergic system such as temperature and pain, interfere with measurement in the conscious volunteer. In patients with presumed total brain infarction the conjunctival PO2 cannot be used as a reliable monitor of cerebral blood flow because of varying perfusion of the palpebral conjunctiva from the external carotid artery in the occasional patient.

Adult↗
PubMed2005

ATP extracellular concentrations are increased in the rat striatum during in vivo ischemia.

Interest is growing in the role of adenosine triphosphate (ATP) on P2 receptors during hypoxic/ischemic events in the brain. However, there is no direct evidence of an increase in extracellular ATP levels during cerebral ischemia in vivo. The aim of the present study was to evaluate ATP outflow from the rat striatum by the microdialysis technique associated with focal cerebral ischemia in vivo by intraluminal occlusion of the right middle cerebral artery (MCA). Between 1 and 4h after ischemia, rats showed a clear turning behavior contralateral to the ischemic side. Twenty-four hour after MCA occlusion, ischemic rats had definite neurological deficit and striatal and cortical damage. The ATP concentration (mean+/-S.E.M.) in the striatum of normoxic rats (n = 8) was 3.10+/-0.34 nM. During 220 min after MCA occlusion, the extracellular ATP levels significantly increased two-fold, being 5.90+/-0.61 nM (p < 0.01 versus normoxic level). ATP outflow showed a tendency to increase over time during the 220 min of ischemia. Since extracellular ATP is rapidly metabolized to adenosine, we also assessed ATP outflow in the presence of the ecto-5'-nucleotidase inhibitor, alpha,beta-methylene-adenosine diphosphate (AOPCP, 1 mM) directly perfused into the striatum. The ATP concentration in normoxic rats (n = 8) was increased three-fold in the presence of the ecto-5'-nucleotidase inhibitor (9.57+/-0.26 nM). During 220 min of ischemia, extracellular ATP levels significantly increased 1.3-fold in AOPCP-treated rats (12.62+/-0.65 nM, p < 0.01 versus normoxic level). The present study confirms that ATP is continuously released in the brain and demonstrates for the first time that ATP outflow increases during ischemia in vivo. These results confirm that ATP may be an important mediator in brain ischemia.

5'-Nucleotidase↗
PubMed2002

Specific ligand for a central type prostacyclin receptor attenuates neuronal damage in a rat model of focal cerebral ischemia.

The neuroprotective effect of a central type prostacyclin receptor ligand was examined in a rat model of focal cerebral ischemia. Under halothane anesthesia, male Sprague-Dawley rats were subjected to left middle cerebral artery occlusion. A selective central type prostacyclin receptor ligand, 15-deoxy-(16-m-tolyl)-17,18,19,20-tetranorisocarbacyclin methylester, or a peripheral type prostacyclin receptor ligand, iloprost methylester, were administered intravenously immediately after ischemia. Twenty-four hours after ischemia, brain damage was evaluated. In separate experiments, concentrations of 15-deoxy-(16-m-tolyl)-17,18,19,20-tetranorisocarbacyclin in ischemic brain tissue were measured by injection of a tritium labeled compound. Treatment with 15-deoxy-(16-m-tolyl)-17,18,19,20-tetranorisocarbacyclin methylester (0.03 mg/kg) significantly (P<0.05) reduced the volume of brain damage by 35%. With this treatment, the concentration of this compound in the brain was more than 10 nM. Treatment with iloprost methylester did not show a neuroprotective effect. These results indicated that activation of a central type prostacyclin receptor attenuates ischemic brain damage. The present study demonstrated that the intravenous application of a central type prostacyclin receptor ligand could be a novel therapeutic agent for acute stroke.

Animals↗
PubMed1998

Cobalt-57 as a SPET tracer in the visualization of ischaemic brain damage in patients with middle cerebral artery stroke.

In PET studies we have shown the usefulness of cobalt radionuclides for the visualization and quantification of ischaemic damage in stroke. In the present study, we explored 57Co2+ as a SPET tracer. Uptake of radioactivity was estimated by using a cobalt enhancement ratio defined as the ratio of cobalt uptake in the affected region versus a similar volume in the non-affected contralateral side. Clinical status was assessed with the Orgogozo stroke score at the time of scanning and at least 60 days after admission. Nineteen patients (11 men, 8 women) with a middle cerebral artery stroke were examined with 57Co2+ SPET 0-30 days after stroke onset. Our investigations show enhanced cobalt uptake in the infarcted brain tissue in patients with a major stroke and little clinical improvement. There was a significant correlation between the cobalt enhancement ratio and the Orgogozo score at the time of scanning and discharge. Our results suggest that 57Co2+ SPET is suitable for determining the extent of (possibly calcium-mediated) damage in stroke and in the assessment of potential therapeutic interventions.

Adult↗
PubMed2005

Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemia.

Mitochondrial permeability transition (PT) is a phenomenon induced by high levels of matrix calcium and is characterized by the opening of the PT pore (PTP). Activation of the PTP results in loss of mitochondrial membrane potential, expansion of the matrix, and rupture of the mitochondrial outer membrane. Consequently, PT has been implicated in both apoptotic and necrotic cell death. Cyclophilin D (CypD) appears to be a critical component of the PTP. To investigate the role of CypD in cell death, we created a CypD-deficient mouse. In vitro, CypD-deficient mitochondria showed an increased capacity to retain calcium and were no longer susceptible to PT induced by the addition of calcium. CypD-deficient primary mouse embryonic fibroblasts (MEFs) were as susceptible to classical apoptotic stimuli as the WT, suggesting that CypD is not a central component of cell death in response to these specific death stimuli. However, CypD-deficient MEFs were significantly less susceptible than their WT counterparts to cell death induced by hydrogen peroxide, implicating CypD in oxidative stress-induced cell death. Importantly, CypD-deficient mice displayed a dramatic reduction in brain infarct size after acute middle cerebral artery occlusion and reperfusion, strongly supporting an essential role for CypD in an ischemic injury model in which calcium overload and oxidative stress have been implicated.

Animals↗
PubMed1997

Brain temperature monitoring and modulation in patients with severe MCA infarction.

BACKGROUND: Brain temperature has been measured only occasionally in humans. After head trauma, a temperature gradient in brain temperature compared with body temperature of up to 3 degrees C degrees higher in the brain has been reported. Elevated temperature facilitates neuronal injury after ischemia. At present, no information concerning changes in brain temperature after acute stroke is available. METHODS: In 15 patients who had suffered severe ischemic stroke in the MCA territory, intracerebral temperature was recorded with use of two different thermocouples, with intraventricular, epidural, and parenchymatous measurements. Body-core temperature (Foley catheter temperature) and jugular bulb temperature (n = 5) were recorded simultaneously. Measures for reducing brain temperature were compared. RESULTS: In all patients, brain temperature exceeded body-core temperature by at least up to 1 degrees C (range, 1.0 to 2.1 degrees C). Temperature in the ventricles exceeded epidural temperature by up to 2.0 degrees C. Brain temperature modulation was independent of single pharmacologic (paracetamol, metamizol) treatments. Only systemic cooling was effective and sustained hypothermic (33 to 34 degrees C) brain temperatures. CONCLUSION: After MCA stroke, human intracerebral temperature is higher than central body-core temperature. There is also a temperature gradient within the brain, with the ventricles warmer than the surface. Mild hypothermia in the treatment of severe cerebral ischemia with use of cooling blankets is both easy to perform and effective in the therapy of severe hemispheric infarction.

Adult↗
PubMed1981

Cyclic AMP concentrations in plasma, cerebrospinal fluid and urine in patients with acute cerebral hemispheric infarction.

Plasmas, cerebrospinal fluid and urine were sampled from 22 patients with cerebral hemispheric infarction and analyzed for cyclic AMP. The following observations were made: (1) In mild cases with slight dysarthria and/or hemiparesis but without disturbance of consciousness (Group I), cyclic AMP in peripheral venous plasma (PVP) remained over the normal lowest level more than 10 days after the onset. Patients with apparent neurological deficits could be divided into two groups. In one group, cyclic AMP in PVP decreased to a subnormal level within about 5 days after the onset of stroke (Group II). In another group (Group III), such a decrease was not observed. Brain isotope scintigrams were revealed negative in Group I. The size of brain infarct as judged by isotope uptake was larger in Group III than in Group II, except for a few cases in which the lesion was restricted in the basal ganglionic region. (2) No clinical significance was, however, found in the time course of cyclic AMP levels in internal jugular venous or femoral arterial plasma, or in cerebrospinal fluid, or of the daily amount of cyclic AMP excretion into urine. (3) Cerebral arterio-venous difference of cyclic AMP was negative in most of the cases.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMedDate not supplied

Molecular and cellular mechanisms of neuroprotection by vascular endothelial growth factor.

The present view of the neuroprotective functions and mechanisms of action of vascular endothelial growth factor (VEGF) is based on studies of neuronal ischemic/hypoxic models in vivo and in vitro. Endogenous neuronal VEGF increases in the ischemic brain and plays a neuroprotective role in the pathophysiologic processes that follow stroke. Exogenous VEGF, directly administered or overexpressed by gene delivery into rat brains, reduces ischemic brain infarct and decreases hypoxic neuronal death. The main neuroprotective mechanisms of VEGF include: (1) modulation of the phosphatidylinositol 3'-kinase (PI3K)/Akt/nuclear factor-kappaB signaling pathway, inhibition of caspase-3 activity, and reduction of ischemic neuronal apoptosis; (2) inhibition of outward delayed rectifier potassium channel currents and increase of ischemia-induced tyrosine phosphorylation of Kv1.2 potassium channel proteins via activation of the PI3K pathway; and (3) enhancement of proliferation and migration of neural progenitors in the subventricular zone and improvement of striatal neurogenesis and maturation of newborn neurons in adult rat brains after stroke.

Animals↗
PubMed2003

The methionine-homocysteine cycle and its effects on cognitive diseases.

Homocysteine, a sulfur-containing amino acid, is a metabolite of the essential amino acid methionine, and exists at a critical biochemical intersection in the methionine cycle - between S-adenosylmethionine, the indispensable ubiquitous methyl donor, and vitamins B12 and folic acid. High blood levels of homocysteine signal a breakdown in this vital process, resulting in far-reaching biochemical and life consequences. The link between homocysteine and cardiovascular disease is well established, and decreasing plasma total homocysteine by providing nutritional cofactors for its metabolism has been shown to reduce the risk of cardiovascular events. Information has been emerging regarding a connection between homocysteine metabolism and cognitive function, from mild cognitive decline (age-related memory loss) to vascular dementia and Alzheimer's disease. Significant deficiencies in the homocysteine re-methylation cofactors cobalamin (B12) and folate, as well as the trans-sulfuration cofactor vitamin B6, are commonly seen in the elderly population, with a resultant increase in homocysteine with advancing age. Hyperhomocysteinemia has been shown to be an independent risk factor for cognitive dysfunction. Indirect and direct vascular damage can be caused by homocysteine, which has been implicated in vascular dementia, with an increased risk of multiple brain infarcts and dementia as homocysteine levels rise. A significant correlation has been found between risk of Alzheimer's disease and high plasma levels of homocysteine, as well as low levels of folic acid, and vitamins B6 and B12. All of these disease associations are thought to be interrelated via increased homocysteine and S-adenosylhomocysteine and subsequent hypomethylation of numerous substances, including DNA and proteins, that render vascular structures and neurons more susceptible to damage and apoptosis. Providing the nutritional cofactors for proper functioning of the methionine cycle may improve methylation and protect the brain from damage. Further studies need to be performed to assess whether this will also reduce the risk of cognitive diseases and/or improve cognitive functioning.

Alzheimer Disease↗
PubMed2000

Atorvastatin upregulates type III nitric oxide synthase in thrombocytes, decreases platelet activation, and protects from cerebral ischemia in normocholesterolemic mice.

BACKGROUND AND PURPOSE: Thrombosis superimposed on atherosclerosis causes approximately two thirds of all brain infarctions. We previously demonstrated that statins protect from cerebral ischemia by upregulation of endothelial type III nitric oxide synthase (eNOS), but the downstream mechanisms have not been determined. Therefore, we investigated whether antithrombotic effects contribute to stroke protection by statins. METHODS: 129/SV wild-type and eNOS knockout mice were treated with atorvastatin for 14 days (0.5, 1, and 10 mg/kg). eNOS mRNA from aortas and platelets was measured by reverse-transcriptase polymerase chain reaction. Platelet factor 4 (PF 4) and beta-thromboglobulin (beta-TG) in the plasma were quantified by ELISA. Transient cerebral ischemia was induced by filamentous occlusion of the middle cerebral artery followed by reperfusion. RESULTS: Stroke volume after 1-hour middle cerebral artery occlusion/23-hour reperfusion was significantly reduced by 38% in atorvastatin-treated animals (10 mg/kg) compared with controls. Serum cholesterol levels were not affected by the treatment. eNOS mRNA was significantly upregulated in a dose-dependent manner in aortas and in thrombocytes of statin-treated mice compared with controls. Moreover, indices of platelet activation in vivo, ie, plasma levels of PF 4 and beta-TG, were dose-dependently downregulated in the treatment group. Surprisingly, atorvastatin-treatment did not influence PF 4 and beta-TG levels in eNOS knockout mice. CONCLUSIONS: The synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor atorvastatin upregulates eNOS in thrombocytes, decreases platelet activation in vivo, and protects from cerebral ischemia in normocholesterolemic mice. Antithrombotic and stroke-protective effects of statins are mediated in part by eNOS upregulation. Our results suggest that statins may provide a novel prophylactic treatment strategy independent of serum cholesterol levels.

Animals↗
PubMed2004

Histochemical detection of ultrasmall superparamagnetic iron oxide (USPIO) contrast medium uptake in experimental brain ischemia.

Recently, macrophage infiltration in different central nervous system (CNS) pathologies has been visualized with ultrasmall particles of iron oxide (USPIO) as a new cell-specific contrast medium for MRI. However, validation of these findings at the histological level has been hampered by the fact that the in situ detection of iron uptake by conventional Prussian blue staining is not sensitive enough to detect low amounts of iron in the brain. Here, an improved method for the histochemical detection of USPIO uptake in ischemic brain lesions is reported. The procedure relies on the sequential enhancement of Prussian blue staining by diaminobenzidine and silver/gold impregnation. After photothrombotic cortical brain infarction, this method allowed sensitive in situ detection of iron-laden macrophages which matched both macrophage immunostaining and USPIO-induced signal alterations in high-resolution 7 T MRI. This staining method provides a basis for correlative histological assessment of USPIO-enhanced MRI in a broad spectrum of CNS pathologies.

Animals↗
PubMed2006

Neuroprotection of nicotiflorin in permanent focal cerebral ischemia and in neuronal cultures.

Nicotiflorin is a single component extracted from traditional Chinese medicine Flos Carthami. In this study, we investigated its neuroprotection in permanent focal cerebral ischemia model in rats, and in an in vitro model of ischemia. At doses of 2.5, 5 and 10 mg/kg, nicotiflorin administered immediately after the onset of ischemia markedly reduced brain infarct volume and neurological deficits. For primarily cultured neurons suffered 2 h hypoxia followed by 24 h reoxygenation, nicotiflorin significantly attenuated cell death and reduced LDH release. Morphological observation also directly confirmed its protective effect on neuron. These results provided strong pharmacological basis for its potential therapeutic role in cerebral ischemic illness.

Animals↗
PubMed2005

Safety and therapeutical benefit of hemicraniectomy combined with mild hypothermia in comparison with hemicraniectomy alone in patients with malignant ischemic stroke.

INTRODUCTION: Both for hemicraniectomy and for hypothermia, several reports describe a beneficial effect in patients with malignant supratentorial cerebral ischemia. We compared the safety and the clinical outcome in patients with a malignant supratentorial infarction who were treated with hemicraniectomy alone (HA) or received a combination therapy with hemicraniectomy and hypothermia of 35 degrees C (HH), respectively. METHODS: In a prospective and randomized study, 25 consecutive patients were treated after an ischemic infarction of more than two thirds of one hemisphere by HA (n=13 patients) or the HH combination therapy (n=12 patients). Safety parameters were compared between both treatment groups, the clinical outcome was assessed during treatment and after 6 months. RESULTS: Age, cranial CT or MRI findings, initial National institutes of Health Stroke Scale Score (NIHSSS) and level of consciousness were not significantly different between both groups. Hemicraniectomy was performed within 15+/- 6 h after the ischemic event. Hypothermia was induced immediately after surgery. Overall mortality was 12% (2/13 vs. 1/12 in the two groups), but none of these 3 patients died due to treatment-related complications. There were no severe side effects of hypothermia. Duration of need for intensive care or for mechanical ventilation and infectious status did not differ significantly between both groups, but the need for catecholamine application was increased in the HH group. The clinical outcome showed a tendency for a better outcome in the HH compared with the HA group with respect to status after 6 months, as assessed by the NIHSSS (10+/-1 vs. 11+/-3, p<0.08). DISCUSSION: The present study suggests that a combined therapy of mild hypothermia and hemicraniectomy in malignant brain infarction does not imply additional risks by side effects and improves functional outcome as compared with hemicraniectomy alone.

Adult↗
PubMed2004

Preconditioning with prolonged oxygen exposure induces ischemic tolerance in the brain via oxygen free radical formation.

PURPOSE: To determine if 100% oxygen (O2) inhalation induces ischemic tolerance to focal cerebral ischemia and if the effect is induced via O2 free radical formation. METHODS: Experiment 1: 36 rats were randomly assigned to four groups (n = 9 each): Group A, control rats inhaled air for 24 hr; Groups B, C and D animals inhaled 100% O2 for six hours, 12 hr and 24 hr respectively. Experiment 2: 32 rats were randomly assigned to four groups (n = 8 each): Groups E and F rats received normal saline (5 mL.kg(-1) intraperitoneally) and then inhaled air (Group E) or 100% O2 (Group F) for 24 hr; Groups G and H animals received 10% dimethylthiourea (500 mg.kg(-1) intraperitoneally) and then inhaled 100% O2 (Group G) or air (Group H) for 24 hr. Twenty-four hours after the treatments, the right middle cerebral artery was occluded in all rats for 120 min. The neurologic deficit scores (NDS) and brain infarct volumes were evaluated at 24 hr after reperfusion. RESULTS: Experiment 1: the infarct volume and NDS of Group D were smaller than in controls (P = 0.004 and 0.042 respectively). The infarct volume was reduced by 47% in Group D. There was no statistical difference among Groups A, B and C. Experiment 2: the infarct volume and NDS in Group F were less than in controls (Group E; P = 0.001 and 0.036 respectively). The infarct volume was reduced by 60% in Group F. There was no difference among Groups E, G and H. CONCLUSION: Our study demonstrates that preconditioning with 100% O2 for 24 hr can induce ischemic tolerance via formation of O2 free radicals in transient focal cerebral ischemia in rats.

Animals↗
PubMed2000

Survival and histological evaluation of therapeutic window of post-ischemia treatment with magnesium sulfate in embolic stroke model of rat.

The neuroprotective window of magnesium for up to 8 h after ischemic insult was evaluated in a clinically relevant model of focal cerebral ischemia subjected to embolization of the right middle cerebral artery (MCA) with an autologous thrombus. The animals were treated with either vehicle or 5% magnesium sulfate (90 mg/kg) intravenously at 2, or 6, or 8 h after ischemic insult. Survival rate significantly increased only in animals treated with magnesium sulfate in treatment groups at 2 h after MCA embolization but improvement in neurological outcome was observed in all medicated groups. Compared with animals in control group, post-ischemia treatment with magnesium sulfate significantly reduced brain infarct volume (P<0.01) except the 8 h group. These data indicate that the therapeutic window for neuroprotection of magnesium can be extended up to 6 h in the focal cerebral ischemia model of this study. The long window of opportunity for effective dosing may be explained with the proposed multiple mechanisms of actions for magnesium.

Animals↗
PubMed2004

[A case of a subclavian-vertebral junction arterial aneurysm with brain stem thromboembolism].

Subclavian artery aneurysm is relatively rare, but, we can scarcely find mention in the literature of a subclavian-vertebral junction aneurysm. We report a case of a 73-year-old man with a left subclavian-vertebral junction arterial aneurysm of 11 mm in diameter which caused a brain stem thromboembolism. He showed right hemiparesis and dysarthria on admission. On the 5th day after admission, his hemiparesis worsened and he could not even walk. In order to prevent further embolic attack on the vertebro-basilar system and rupture from the aneurysm, we embolized the aneurysm successfully with some GDC coils. During the operation, no further brain infarction occurred, and we maintained blood circulation in the left subclavian-vertebral artery. This aneurysm appeared on angiography to be atherosclerotic in its clinical characteristics, and we have scheduled follow-up angiography in two years time. As his hemiparesis had improved, he was discharged from the hospital on foot.

Aged↗