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

We used a photochemical technique which induces thrombotic infarction by intravenous injection of the fluorescein derivative Rose Bengal and focal illumination of the intact skull surface. Following such photochemically induced infarcts in the sensorimotor neocortex of rats, posttreatment with flunarizine, a class IV calcium antagonist, within a critical period of the first 6 h after infarction, results in marked sparing of sensorimotor function (tactile/proprioceptive limb placing reactions), while animals remain normoglycemic and are free of drug-induced behavioral toxicity. This could reflect flunarizine-induced coping of neuronal tissue with ischemia-related ionic shifts. It is argued that photochemical thrombosis and middle cerebral artery occlusion can fruitfully complement each other as experimental stroke models.
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PMID:Animal models of cerebral stroke: pharmacological protection of function. 218 Jul 13

Unilateral photochemical infarcts were produced in the hind limb sensorimotor neocortex of 243 rats by intravenous injection of the fluorescein derivative Rose Bengal and focal illumination of the intact skull surface. Facial contact stimuli governed the degree and recovery rate of contralateral tactile/proprioceptive forelimb placing reactions. Contralateral forelimb placing recovered, whereas hind limb placing was resistant to recovery. Infarcted rats displayed marked recovery of spontaneous limb usage (beam traversing). However, deficits in isolated tactile/proprioceptive hind limb placing reactions endured. Posttreatment with the class IV calcium antagonist flunarizine after neocortical infarction protected sensorimotor function in a dose-dependent manner. This protective effect may be due to the peculiar ionic channel blocking profile of flunarizine. Scopolamine hydrobromide reinstated contralateral placing errors in infarcted rats at a dosage that did not affect neurologically intact rats. The cognitive enhancer sabeluzole, a novel benzothiazol derivative, dose-dependently blocked the anticholinergic-induced deterioration of a sensorimotor deficit in rats.
Stroke 1990 Nov
PMID:Ionic channels, cholinergic mechanisms, and recovery of sensorimotor function after neocortical infarcts in rats. 223 75

This study was carried out with a recently developed model of focal cerebral ischemia in the rat based on the photochemical induction of thrombotic stroke using the dye Rose Bengal. We examined the change in the volume of the lesion and brain water content, in separate groups of rats, at different times (1, 4, 24, 72, and 168 h) after the induction of the ischemic lesion. The volume of ischemic damage increased rapidly between 1 and 24 h after the ischemic insult and decreased between 24 and 168 h. The lesion at 168 h was significantly larger than that following 1 h of ischemia and similar to that obtained at 4 h, suggesting that the maximum extent of tissue damage (without the involvement of significant edema) was reached within the first 4 h in this model. The enlargement of the lesion after 4 h correlated closely with changes in brain water content.
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PMID:Quantitation of photochemically induced focal cerebral ischemia in the rat. 333 8

A photochemical method using the Rose Bengal dye as thrombogenic agent was employed to induce focal cerebral ischemia in frontoparietal cortex of rats. A transcerebral microdialysis probe was used to collect samples from ischemic cortical area. An increase in glutamate (6-fold) and in taurine (4-fold) within the first hour occurred. Neuropathological investigations demonstrate a reproducible damaged area surrounded by a thin peripheral area showing neuronal apoptotic phenomena. The method represents a reproducible model of focal cerebral ischemia with neuropathological aspects superimposable to those characteristic of thrombogenic stroke in man. This method could also be relevant in the study of neurotransmitters during the evolution of ischemia. Furthermore, the presence of apoptotic phenomena in the perilesional halo confirms an ischemic penumbra suggesting the significance of preclinical pharmacological trials.
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PMID:Aminoacid recovery via microdialysis and photoinduced focal cerebral ischemia in brain cortex of rats. 756 38

In experimental stroke research one of the key questions is whether animals models truly reflect human disease. One important reason for modelling stroke is to produce tissue changes that can be used to validate the correlation between the results of advanced radiological imaging and pathology. The aim of this study was to compare two minimally invasive rat models of focal ischaemic stroke as to their ability to simulate clinical stroke reproducibly. In one model a focal infarct was induced using the photochemical Rose Bengal technique. The second model was based on transvascular occlusion of the middle cerebral artery using a cervical approach. In all animals we performed MRI at different times with two different paramagnetic contrast agents. The time course of blood-brain-barrier disruption in the Rose Bengal model differed entirely from that in human brain ischaemia. The experimental stroke showed marked contrast enhancement in the first hour after the onset of ischaemia. On the other hand, the MRI changes in the suture occlusion model were very similar to the changes observed in human brain ischaemia: no early disruption of the blood-brain-barrier and increased T2-signal 4-6 h after the onset of stroke. We hope that the suture occlusion model will be used for research not only by basic and clinical scientists but also by radiologists, who, using modern imaging methods, may greatly influence the diagnosis as well as the management of this devastating disease.
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PMID:MRI monitoring of experimental cerebral ischaemia: comparison of two models. 806 66

Focal ischaemia in the rat cerebral cortex was produced by means of a photochemically induced thrombosis of cerebral arteries. This was achieved by intravenous infusion of the photosensitive dye Rose Bengal and illumination of the skull with focused green light. Initial experiments justified the use of tetrazolium staining as an index of infarct damage. Using this technique it was demonstrated that chlormethiazole (200 mg/kg, i.p.) given 5 min post ischaemia markedly reduced the area of infarcted cortical tissue. A second experiment replicated this observation and showed that, in contrast, nimodipine (0.5 mg/kg, i.p.) given 5 min post infarct was without effect on infarct size. The pattern of Evans Blue extravasation indicated that the infarct developed over a 24-h period with the major damage occurring in the first 4.5 h. The spread of the infarct beyond the initial core of damage was decreased by an estimated value of almost 50% by injection of chlormethiazole (200 mg/kg, i.p.) 5 min after the light exposure. These data indicate that chlormethiazole is an effective drug in protecting against the effects of focal ischaemia in the rat and, taken with earlier observations that chlormethiazole protects against the effects of global ischaemia in the gerbil, suggest that the drug may be an effective treatment against the ischaemic cell death that can occur following a stroke or cardiac arrest.
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PMID:The effects of chlormethiazole and nimodipine on cortical infarct area after focal cerebral ischaemia in the rat. 848 58

Intracerebral hemorrhage is the major complication associated with antithrombotic and thrombolytic therapy. Despite efforts directed toward achieving hemorrhagic infarction, an ideal animal model of cerebral hemorrhage has not yet to be established. Using the photothrombotic technique in rabbits, we developed a model of cerebral hemorrhage by inducing cyclic flow reductions in the middle cerebral artery (MCA). Furthermore, the hemorrhage increased 4-fold after infusion of heparin at a dose prolonging activated partial thromboplastin time by about three times that of control animals. The photothrombotic occlusion of the MCA is based on a thrombosis induced by endothelial injury through singlet oxygen produced by Rose Bengal injection and green light irradiation (Acta Neuropathol. 72 (1987) 315; Acta Neuropathol. 72 (1987) 326; J. Pharmacol. Toxicol. Methods. 29 (1993) 165). Using a pulse Doppler flowmeter, spontaneous reperfusion of the MCA after the thrombotic occlusion following cyclic flow reductions was observed within 2 h in the majority of animals. This model is unusual with respect to the development of clinical stroke, because of the MCA cyclic flow reductions. Thus it is different from permanent or ischemia/reperfusion MCA occlusion in rodents and may be suitable for studying hemorrhagic risks associated with the use of antithrombotic agents.
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PMID:A novel MCA occlusion model of photothrombotic ischemia with cyclic flow reductions: development of cerebral hemorrhage induced by heparin. 1203 27

The present study evaluated the effect of galanthamine, a selective competitive cholinesterase inhibitor, on histological and functional outcome after experimental stroke in rats. Cholinesterase inhibitors are commonly used as cognitive enhancers for dementia in aged people, including those who may sustain ischemic attacks. Young adult (5 months) and aged (24 months) rats were treated with saline or galanthamine at a dose of 2.5 mg/kg (i.p., once a day). Drug treatment started 4 days before focal cortical photothrombosis (Rose Bengal, 20 mg/kg) and continued for 21 days thereafter. Sensorimotor recovery was assessed by a new beam-walking test and spatial learning by the Morris water-maze over a 3-week follow-up period. Infarct volumes were measured from nitroblue tetrazolium-stained sections at the end of follow-up. Infarct volumes in the cortex were similar in ischemic controls and ischemic rats treated with galanthamine. In the beam-walking test, there was a transient impairment forelimb function and a permanent impairment in hindlimb after cortical infarct both in young adult and aged rats. Galanthamine treatment did not affect the sensorimotor recovery rate. Analysis of water-maze data did not reveal significant differences in length of path, escape latency, or swim speed between sham-operated, ischemic controls and ischemic rats treated with galanthamine. In conclusion, present findings suggest that the aging brain has considerable plastic capacity to maintain functioning after focal cerebral insults restricted to the motor cortex. Galanthamine is not beneficial with respect to the histological or functional outcome in rats subjected to cortical photothrombosis.
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PMID:Effect of cholinergic medication, before and after focal photothrombotic ischemic cortical injury, on histological and functional outcome in aged and young adult rats. 1547 53

Psychotropic drugs are commonly used in the elderly, including those who may sustain ischemic attacks. Concomitant CNS medication may interfere with functional recovery. The present study evaluated the effect of risperidone, an atypical neuroleptic, and fluoxetine, a selective serotonin reuptake inhibitor, on histological and functional outcome after experimental stroke in aged rats, which might be more vulnerable to brain insults. Aged Wistar rats were treated with risperidone at a dose of 1 mg/kg (i.p., once a day), fluoxetine at a dose of 5 mg/kg (i.p., once a day), or their combination. Drug treatment was started 7 days before focal cortical photothrombosis (Rose Bengal, 20 mg/kg) and continued for 28 days thereafter. Sensorimotor recovery was assessed by a new beam-walking test and spatial learning by the Morris water-maze before cortical stroke, immediately after stroke, and at the end of follow-up. Infarct volumes were measured from nitroblue tetrazolium-stained sections at the end of follow-up. The high slip ratio for the contralateral hindlimb in ischemic rats treated with risperidone indicated sensorimotor impairment when tested 2 h after drug administration. Sensorimotor impairment was not observed, however, when the rats were tested 24 h after risperidone administration. Similarly, water-maze performance was impaired 2 h after risperidone. Fluoxetine did not affect sensorimotor or water-maze performance. Cortical infarct volumes were not different in ischemic controls and ischemic rats treated with antipsychotic drugs. The present study showed that an atypical neuroleptic, risperidone, acutely impairs behavioral performance, but does not affect histological or functional outcome in aged rats subjected to cortical photothrombosis.
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PMID:Behavioral and histological effects of chronic antipsychotic and antidepressant drug treatment in aged rats with focal ischemic brain injury. 1569 87

We investigated epileptogenesis after cortical photothrombotic stroke induced with Rose Bengal dye in adult Sprague-Dawley rats. To detect spontaneous seizures, video-electroencephalograms were recorded at 2, 4, 6, 8, and 10 months for 7-14 days (24 h/day). At the end, spatial and emotional learning and memory were assessed using the Morris water-maze and fear-conditioning test, respectively, and the brains were processed for histologic analysis. Seizures were detected in 18% of rats that received photothrombosis. The average seizure frequency was 0.39 seizures per recording day and mean seizure duration was 117 s. Over 60% of seizures occurred during the dark hours. Rats with photothrombotic lesions were impaired in the water-maze (P<0.05) but not in the fear-conditioning test as compared with controls. Histology revealed that lesion depth varied from cortical layers I to VI in photothrombotic rats with epilepsy. Epileptic rats had light mossy fiber sprouting in the inner molecular layer of the dentate gyrus both ipsilateral and contralateral to the lesion. This study extends the current understanding of epileptogenesis and functional impairment after cortical lesions induced by photothrombosis. Our observations support the hypothesis that photothrombotic stroke in rats is a useful animal model for investigating the mechanisms of post-stroke epileptogenesis.
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PMID:Epileptogenesis after cortical photothrombotic brain lesion in rats. 1762 8


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