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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cervical spinal cord stimulation (cSCS) has been employed as a treatment for intractable pain for the past 20 years. Recently, we reported that cSCS increased regional cerebral blood flow (rCBF) in cats and humans. The present study was designed to examine the effects of cSCS on experimental cerebral strokes, using a cat middle cerebral artery occlusion model (MCAO). A total of 31 cats were randomly assigned to three groups; Group 1: control, Group 2: sham operation, Group 3: cSCS. Mortality of the control group was 92% as long as 4 days after MCAO. Groups 2 and 3 showed a prolongation of survival rate (44% and 56%, respectively). CSCS reduced the rate of death within 24 hours after MCAO. There was no alteration of infarct size, which was estimated by the TTC method and measured by computer technique (PDP-11/23), was found in dead cats of all groups. In cats that survived in Group 3, however, drastic prevention of an infarct progression was found, compared to Group 2. The results provide a clinical application of cSCS for stroke patients, although no evident mechanism was obtained.
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PMID:The effects of cervical spinal cord stimulation (cSCS) on experimental stroke. 247 58

Cerebrovascular damage of renovascular hypertensive rats (RHR) was observed under light microscope and electron microscope, and the cerebral collateral vessels of RHR were observed with vascular casts. In focal cerebral ischemia of RHR, the infarct volume was measured by TTC staining in combination with computer image processing and analysis. When hypertension persisting longer, there were hyalinosis in small arterial walls, luminal narrowing and basement membrane thickening in capillaries, decreased collateral vessels, and occluded microvessels. In cerebral ischemia, the infarct volume was large and could not be improved. The results demonstrated that the key to prevent stroke is to prevent and treat hypertension as early as possible.
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PMID:[Hypertension inducing cerebrovascular damage and effecting on cerebral infarction]. 806 19

Diffusion-weighted, echo-planar imaging (EPI) was used to map regional changes in the apparent diffusion coefficient (ADC) during experimental focal ischemia in the rat brain following permanent middle cerebral arterial occlusion (MCAO). Sixteen 64 x 64 diffusion-weighted EPIs were acquired in 32 s with successively increasing amplitudes of the diffusion-sensitive gradient pulses. A linear least-squares regression algorithm was used to fit 15 of the 16 two-dimensional matrices, on a pixel-by-pixel basis, to solve for the slope from which the ADC value was calculated. The correlation coefficient of the fit, R2, was used to filter the final ADC maps, and the ADCs were then scaled appropriately to be displayed in a 256 gray level format. Ranges (bins) of 0.05 x 10(-3) mm2/s were then grouped and color coded to qualify and quantify the evolution of ischemia in the MCA territory. The percentage of area in the ischemic and contralateral hemispheres in seven ADC bins were calculated at 30, 60, and 120 min after MCAO for 10 animals and demonstrated a significant increase in ADC bins below 0.45 x 10(-3) mm2/s and a decrease in bins above 0.50 x 10(-3) mm2/s over time. The postmortem infarct area, as measured by TTC staining, was highly correlated with the portion of the ischemic hemisphere falling below ADC values of 0.55 x 10(-3) mm2/s at 2 h after stroke onset. These studies suggest that focally ischemic brain tissue can be quantitatively subdivided according to ADC values and that ADC values below 0.55 x 10(-3) mm2/s 2 h following ischemia highly predict infarction in a rat permanent occlusion stroke model.
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PMID:Apparent diffusion coefficient mapping of experimental focal cerebral ischemia using diffusion-weighted echo-planar imaging. 841 2

The effects of the stable prostacyclin analogue TTC-909 on memory impairment in the water maze task and on neuronal damage were studied in rats with cerebral embolism induced by injecting polyvinyl acetate (PVA) into the right internal carotid artery and the ensuing embolism extending out into the right middle cerebral artery. Areas supplied by the lenticulostriate artery were most markedly damaged. In the water maze test, the PVA-embolized rats took longer to reach the platform than did the nontreated control rats. To some extent, repeated administrations of TTC-909 (200 ng/kg, IV) overcame this impairment in water maze learning in the rats. We assume that the vasodilating effects of TTC-909 maintain this blood supply to the ischemic area and that TTC-909 prevents the development of thrombosis around the PVA particles in the arterial capillaries, as a result of antiplatelet aggregative effects. These two mechanisms are likely to be involved in memory improvement. TTC-909 may prove effective for treating subjects with stroke and other cerebrovascular disorders.
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PMID:Prostacyclin analogue TTC-909 reduces memory impairment in rats with cerebral embolism. 854 73

The potential cerebroprotective effects of recombinant human basic fibroblast growth factor (rhbFGF) were evaluated in a feline model of acute cerebral ischemia using high-speed magnetic resonance imaging (MRI) in conjunction with immunohistology. The neuroprotective efficacy of three doses of rhbFGF was evaluated in a unilateral middle cerebral artery (MCA) occlusion/reperfusion model. Ten h following a 2 h period of MCA occlusion in control (vehicle-treated) animals, cerebral perfusion in the ischemic hemisphere was 58 +/- 17% of the contralateral normal hemisphere. Corresponding ischemic/normal perfusion ratios in rhbFGF-treated groups were not significantly different: 54 +/- 16% (14 micrograms/kg/h dose), 40 +/- 19% (42 micrograms/kg/h dose) and 75 +/- 8% (125 micrograms/kg/h dose). Triphenyltetrazolium chloride histopathological assessment demonstrated brain damage in vehicle-treated animals comprising 31 +/- 15% of the hemisphere; in rhbFGF-treated groups injury was not significantly different: 19 +/- 4% (14 micrograms/kg/h rhbFGF), 24 +/- 6% (42 micrograms/kg/h rhbFGF) and 16 +/- 10% (125 micrograms/kg/h rhbFGF). Immunohistochemical analysis of brain sections using glial fibrillary acidic protein (GFAP) revealed that in animals that showed marked perfusion deficits throughout the entire experiment (regardless of treatment), GFAP staining was elevated contralateral to the occlusion and absent ipsilaterally. While some tendency towards protection is found, particularly at higher doses of rhbFGF, it must be concluded that in the chosen stroke model and time interval, the doses used did not significantly improve reperfusion or confer significant cerebroprotective benefit. Non-invasive high-speed MRI was found to be useful for evaluation of putative cerebroprotective agents.
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PMID:Evaluation of recombinant human basic fibroblast growth factor (rhbFGF) as a cerebroprotective agent using high speed MR imaging. 861 13

The prostacyclin analogue TTC-909 is incorporated in lipid microspheres and is chemically very stable. We examined the efficacy of TTC-909 on cerebral microcirculation following focal cerebral ischaemia. Focal cerebral ischaemia was produced by the occlusion of the distal middle cerebral artery in stroke-prone spontaneously hypertensive rats. Intravenous administration of TTC-909 (100 ng/kg/day) or vehicle was started 30 minutes after the occlusion and repeated for 7 days. On day 7, cerebral blood flow and blood-brain barrier permeability were measured autoradiographically. Brain oedema was estimated by the gravimetric method. The size of the infarction was calculated from area measurements on serial histologic sections. Treatment with TTC-909 resulted in significant improvement in regional blood flow in the ischaemic rim (p < 0.01) and the surrounding area (p < 0.05). With TTC-909 treatment, the increased permeability was significantly reduced in the ischaemic centre (p < 0.01) and rim (p < 0.05). A decrease in specific gravity in the ischaemic region and the remote non-ischaemic regions was prevented by the treatment (p < 0.01). We assumed that the efficacy of TTC-909 maintains the blood supply in the ischaemic area, improves disruption of the blood-brain barrier and prevents development of ischaemic oedema.
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PMID:Stable prostacyclin improves postischaemic microcirculatory changes in hypertensive rats. 874 76

TTC-909 is a newly developed isocarbacyclin methyl ester (TEI-9090) incorporated in lipid microspheres. The neuroprotective effect of TTC-909 was histologically examined in the pyramidal cell layer of the hippocampus CA1 subfield 7 days after transient forebrain ischemia using stroke-prone spontaneously hypertensive rats. TTC-909, given intravenously 10 min after the transient forebrain ischemia, dose-dependently protected against ischemia-related delayed neuronal death. The blood pressure remained unchanged following TTC-909 administration. This finding suggests that TTC-909 has a neuroprotective action on ischemic delayed neuronal death in the hippocampus.
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PMID:Neuroprotective effect of TTC-909, an isocarbacyclin methyl ester incorporated in lipid microspheres, on hippocampal delayed neuronal death of stroke-prone spontaneously hypertensive rats. 888 35

Neutrophil activation and accumulation as a consequence of cerebral ischemia-reperfusion has been suggested to exacerbate tissue injury. The current study is designed to examine the effect of IB4, a monoclonal antibody directed against the neutrophil adhesion protein, CD18, in a rabbit model of thromboembolic stroke. New Zealand rabbits (3-3.5 kg n=8 each group), were given an autologous clot embolus, delivered to the anterior circulation of the brain via the internal carotid artery. Immediately following thromboembolism, the mean arterial pressure in all animals was reduced to 30 mmHg by controlled exsanguination for a period of 45 min. All animals were mechanically ventilated and following parameters were monitored hourly: arterial blood gases, intracranial pressure, regional cerebral blood flow, hematocrit, and core temperature. Rabbits were given either IB4 (1 mg kg(-1)), or vehicle (1 percent albumin, IV) 30 min following the thromboembolic event. The mean arterial pressure of all animals was restored to the baseline value of 50-60 mmHg for the remainder of the 4-h experiment. Following the thromboembolic event, the intracranial pressure rose in both groups, although this was significantly less in the IB4-treated group, with the final values being 195.9 +/- 38.3 vs. 135.5 +/- 26.0 percent of baseline (mean +/- SEM, p < 0.05). However, regional cerebral blood flow and infarct size (TTC staining) were virtually identical in both groups. It is concluded that blockade of the neutrophil adhesion protein, CD18, may contribute to a reduction in the intracranial pressure following cerebral ischemia and reperfusion, providing further evidence that activated neutrophils may contribute to cerebral edema.
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PMID:IB4, a monoclonal antibody against the CD18 leukocyte adhesion protein, reduces intracranial pressure following thromboembolic stroke in the rabbit. 916 74

Reduced brain tissue oxygenation is frequently seen in severe head injury and after subarachnoid hemorrhage, and this is considered a major cause of secondary ischemic brain injury. In fact, in a previous study, we found a tight correlation between low brain tissue oxygen tension and poor outcome. Therefore, we tested the hypothesis that an allosteric modifier of hemoglobin, which improves oxygen transport to tissue, could reduce the size of an acute infarct in a feline model of human stroke. This compound produces a shift in the hemoglobin dissociation curve to the right and therefore facilitates the unloading of oxygen during low oxygen tension. Seventeen adult cats were studied. Ischemic stroke was induced through a transorbital, permanent, middle cerebral artery occlusion. Seven animals received saline, and 10 received the allosteric Hb modifier RSR-13. Three different endpoints were used to determine the effect of the allosteric modifier. Delta p50 values were measured in the arterial blood; the intra-infarct oxygen tension was measured, and finally, the volume of the infarct was assessed using TTC staining. Mean delta p50 changes varied from 10.4 +/- 9.2 mmHg up to 15.0 +/- 6.8 mmHg. Mean intra-infarct oxygen tension was 27 +/- 6 mmHg for the control group and 33 +/- 7 mmHg for the drug-treated animals. The mean infarct size (measured as percentage of hemisphere volume) in the control group was 32 +/- 9% and for the RSR-13 animals 22 +/- 10% (p < 0.05). A definitive trend towards improvement in brain oxygen tension was seen, such that animals pretreated with RSR-13 showed a higher infarct oxygen tension. Infarct size was significantly reduced in the drug group. Therefore, RSR-13 is potentially beneficial in the treatment of brain ischemia. Since human studies with this compound are already completed, and other compounds which increase oxygen delivery, such as perfluorocarbons, are already being evaluated, it is likely that oxygen delivery enhancement will rapidly become the first 'neuroprotective' modality, employed in patients with severe brain injury, stroke and subarachnoid hemorrhage.
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PMID:The rationale for, and effects of oxygen delivery enhancement to ischemic brain in a feline model of human stroke. 936 91

The effects of TTC-909, the isocarbacyclin methyl ester clinprost (CAS 88931-51-5), incorporated into lipid microspheres, on ischemia-induced decrease in norepinephrine (NE) contents in stroke-prone spontaneously hypertensive rats (SHR-SP) with an occluded middle cerebral artery (MCA) were examined. Occluding of MCA led to infarction limited to the cerebral cortex and also a severe decrease in NE contents in peripheral regions of the infarction. TTC-909 was injected immediately after MCA occlusion, and then daily for 6 consecutive days. As TTC-909 in a dose of 200 ng/kg significantly (p < 0.05) prevented decreases in NE contents, TTC-909 may have cytoprotective effects on neuronal damage related to ischemia in humans.
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PMID:Effects of the isocarbacyclin methyl ester clinprost incorporated into lipid microspheres, in focal ischemia of stroke-prone spontaneously hypertensive rats. 942 73


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