Academic literature on the topic 'Stroke; animal models; middle cerebral artery occlusion'
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Journal articles on the topic "Stroke; animal models; middle cerebral artery occlusion"
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Golubev, A. M. "Models of Ischemic Stroke (Review)." General Reanimatology 16, no. 1 (March 2, 2020): 59–72. http://dx.doi.org/10.15360/1813-9779-2020-1-59-72.
Full textAbstract:
The incidence of ischemic stroke remains high in many countries, despite a declining trend in the incidence of brain circulation disorders. Limited knowledge of the pathogenesis, diagnosis, clinical presentation, and treatment of this life-threatening disease can be complemented by modelling of ischemic stroke on animals, particularly, in rodents (rats, mice).The aim of review: to provide a rationale for choosing an optimal model of human ischemic stroke.Among more than 300 primary literature sources from various databases (Scopus, Web of science, RSCI, etc.), 84 sources were selected for evaluation, of which 72 were published in the recent years (2015–2019). The criteria for exclusion of sources were low relevance and outdated data.The review examined six experimental models of acute cerebrovascular events including middle cerebral artery occlusion, embolic stroke model; phototrombosis; models using thrombin, endothelin-1 and electrocoagulation of the middle cerebral artery.The review outlines the factors influencing reliability and reproducibility of research results, related to adherence to the rules of animal accommodation and acclimatization, nutrition and care, selection of anesthesia and pain relief methods, compliance with aseptic techniques, monitoring of basic physiological parameters at all stages of the ischemic stroke modeling experiment, with humane withdrawal of animals from the experiment.It was concluded that the model of ischemic stroke, based on the occlusion of the middle cerebral artery, is most promising as being the closest to features of human ischemic stroke and enabling to obtain reproducible results in the experiment.
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Liu, Fudong, and Louise D. McCullough. "Middle Cerebral Artery Occlusion Model in Rodents: Methods and Potential Pitfalls." Journal of Biomedicine and Biotechnology 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/464701.
Full textAbstract:
A variety of animal models have been developed for modeling ischemic stroke. The middle cerebral artery occlusion (MCAO) model has been utilized extensively, especially in rodents. While the MCAO model provides stroke researchers with an excellent platform to investigate the disease, controversial or even paradoxical results are occasionally seen in the literature utilizing this model. Various factors exert important effects on the outcome in this stroke model, including the age and sex of the animal examined. This paper discusses emerging information on the effects of age and sex on ischemic outcomes after MCAO, with an emphasis on mouse models of stroke.
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Percie du Sert, Nathalie, Alessio Alfieri, Stuart M. Allan, Hilary VO Carswell, Graeme A. Deuchar, Tracy D. Farr, Paul Flecknell, et al. "The IMPROVE Guidelines (Ischaemia Models: Procedural Refinements Of in Vivo Experiments)." Journal of Cerebral Blood Flow & Metabolism 37, no. 11 (August 11, 2017): 3488–517. http://dx.doi.org/10.1177/0271678x17709185.
Full textAbstract:
Most in vivo models of ischaemic stroke target the middle cerebral artery and a spectrum of stroke severities, from mild to substantial, can be achieved. This review describes opportunities to improve the in vivo modelling of ischaemic stroke and animal welfare. It provides a number of recommendations to minimise the level of severity in the most common rodent models of middle cerebral artery occlusion, while sustaining or improving the scientific outcomes. The recommendations cover basic requirements pre-surgery, selecting the most appropriate anaesthetic and analgesic regimen, as well as intraoperative and post-operative care. The aim is to provide support for researchers and animal care staff to refine their procedures and practices, and implement small incremental changes to improve the welfare of the animals used and to answer the scientific question under investigation. All recommendations are recapitulated in a summary poster (see supplementary information).
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Mauler, Frank, and Ervin Horváth. "Neuroprotective Efficacy of Repinotan HCl, a 5-HT1A Receptor Agonist, in Animal Models of Stroke and Traumatic Brain Injury." Journal of Cerebral Blood Flow & Metabolism 25, no. 4 (January 26, 2005): 451–59. http://dx.doi.org/10.1038/sj.jcbfm.9600038.
Full textAbstract:
Repinotan is a highly potent 5-HT1A receptor agonist with strong neuroprotective efficacy in animal models of middle cerebral artery occlusion and traumatic brain injury. In this study, we characterized the time window for neuroprotective effects of repinotan in animal models. In the permanent middle cerebral artery occlusion model, repinotan showed neuroprotective efficacy when administered as a triple bolus injection (0.3–100 μg/kg) or an intravenous infusion (0.3–100 μg/kg per hour). A 73% reduction in infarct volume was observed with a 3 μg/kg intravenous bolus, and a 65% reduction was observed with a 3 and 10 μg/kg per hour intravenous infusion. When delayed until 5 hours after occlusion, repinotan (10 μg/kg per hour) reduced infarct volume by 43%. In the transient middle cerebral artery occlusion model, repinotan (10 μg/kg per hour) administered immediately after occlusion reduced infarct volume by 97%, and a delay to 5 hours reduced infarct volume by 81%. In the acute subdural hematoma model, repinotan (3 and 10 μg/kg per hour) reduced infarct volume by 65%. In this model, repinotan (3 μg/kg per hour) administered 5 hours after occlusion reduced infarct volume by 54%. The favorable neuroprotective efficacy, broad dose–response curve, and prolonged therapeutic window observed in all models strongly suggest that repinotan is a promising candidate for treating acute ischemic stroke in humans.
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Ramli, Yetty, Ahmad S. Alwahdy, Mohammad Kurniawan, Berry Juliandi, Puspita E. Wuyung, and Yayi D. B. Susanto. "Permanent flame-blunted monofilament of middle cerebral artery occlusion technique for ischemia stroke induction in animal models." Medical Journal of Indonesia 26, no. 3 (November 27, 2017): 183–9. http://dx.doi.org/10.13181/mji.v26i3.1645.
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Background: Rat is the most frequently used animal for ischemic stroke studies. Recently, middle cerebral artery occlusion (MCAO) by introducing various types of surgical monofilament intraluminally has been widely used, with their advantages and disadvantages. For permanent occlusion, problems with mortality in rats are higher than transient. In this study, we used permanent occlusion using modified monofilament by flaming on its tip which may reduce mortality rate, so that chronic phase of stroke can be learned extensively.Methods: Three male Sprague-Dawley rats underwent permanent MCAO. The flame-blunted monofilament was introduced through common carotid artery. Hematoxylin eosin histopathology confirmation and functional assessment post-stroke induction were then evaluated.Results: Evaluation was conducted on 3 rats in different time post-stroke induction (48 hours, 72 hours, and 3 weeks). Using histopathological examination, the infarction was proved in all 3 rats showing red neurons, perivascular edema and neutrophil spongiosis, in infarct and peri-infarct area. The changes in histopathology showed spongiosis were more dominant in 3 week-post-MCAO rats. On the other hand, red neurons and perivascular edema were less compared to 48 and 72-hour-post-MCAO rats.Conclusion: Flame–blunted monofilament showed its efficacy in producing infarct area. The advantages of this technique are easy to perform with simple and less expensive modification of the monofilament. Conducting successful permanent occlusion with less mortality rate will give chances to do further research on stroke in chronic phase and its effect on novel treatment.
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Boltze, Johannes, Annette Förschler, Björn Nitzsche, Daniela Waldmin, Anke Hoffmann, Christiane M. Boltze, Antje Y. Dreyer, et al. "Permanent Middle Cerebral Artery Occlusion in Sheep: A Novel Large Animal Model of Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 28, no. 12 (August 13, 2008): 1951–64. http://dx.doi.org/10.1038/jcbfm.2008.89.
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As effective stroke treatment by thrombolysis is bound to a narrow time window excluding most patients, numerous experimental treatment strategies have been developed to gain new options for stroke treatment. However, all approaches using neuroprotective agents that have been successfully evaluated in rodents have subsequently failed in clinical trials. Existing large animal models are of significant scientific value, but sometimes limited by ethical drawbacks and mostly do not allow for long-term observation. In this study, we are introducing a simple, but reliable stroke model using permanent middle cerebral artery occlusion in sheep. This model allows for control of ischemic lesion size and subsequent neurofunctional impact, and it is monitored by behavioral phenotyping, magnetic resonance imaging, and positron emission tomography. Neuropathologic and (immuno)-histologic investigations showed typical ischemic lesion patterns whereas commercially available antibodies against vascular, neuronal, astroglial, and microglial antigens were feasible for ovine brain specimens. Based on absent mortality in this study and uncomplicated species-appropriate housing, long-term studies can be realized with comparatively low expenditures. This model could be used as an alternative to existing large animal models, especially for longitudinal analyses of the safety and therapeutic impact of novel therapies in the field of translational stroke research.
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Leon, Rachel L., Xinlan Li, Jason D. Huber, and Charles L. Rosen. "Worsened Outcome from Middle Cerebral Artery Occlusion in Aged Rats Receiving 17β-Estradiol." Endocrinology 153, no. 7 (May 11, 2012): 3386–93. http://dx.doi.org/10.1210/en.2011-1859.
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Although estrogens are neuroprotective in young adult animal models of stroke, clinical trials demonstrate that estrogens increase the incidence and severity of stroke in aged women. We have previously shown that experimental stroke pathophysiology differs between young adult and aged rats. The aim of this study was to determine the effects of 17β-estradiol after middle cerebral artery occlusion and reperfusion in young adult and aged female rats. Focal embolic stroke was performed by middle cerebral artery occlusion with fibrin clot followed by reperfusion with iv human recombinant tissue plasminogen activator. Histological and functional outcomes were measured at 24 h after middle cerebral artery occlusion with fibrin clot. Aged rats treated with 17β-estradiol had significantly increased infarct volumes compared with placebo-treated aged rats. Young adult rats treated with 17β-estradiol had significantly decreased infarct volumes and improved functional outcome compared with ovariectomized young adult rats. Our results suggest that 17β-estradiol may act in an age-dependent manner in the postischemic rat brain. In young adult rats, it is neuroprotective; chronic treatment with 17β-estradiol during aging leads to worsened ischemic brain injury in aged female rats.
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Krueger, Martin, Wolfgang Härtig, Clara Frydrychowicz, Wolf C. Mueller, Andreas Reichenbach, Ingo Bechmann, and Dominik Michalski. "Stroke-induced blood–brain barrier breakdown along the vascular tree – No preferential affection of arteries in different animal models and in humans." Journal of Cerebral Blood Flow & Metabolism 37, no. 7 (October 1, 2016): 2539–54. http://dx.doi.org/10.1177/0271678x16670922.
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Stroke-induced blood–brain barrier breakdown promotes complications like cerebral edema and hemorrhagic transformation, especially in association with therapeutical recanalization of occluded vessels. As arteries, capillaries and veins display distinct functional and morphological characteristics, we here investigated patterns of blood–brain barrier breakdown for each segment of the vascular tree in rodent models of embolic, permanent, and transient middle cerebral artery occlusion, added by analyses of human stroke tissue. Twenty-four hours after ischemia induction, loss of blood–brain barrier function towards FITC-albumin was equally observed for arteries, capillaries, and veins in rodent brains. Noteworthy, veins showed highest ratios of leaky vessels, whereas capillaries exhibited the most and arteries the least widespread perivascular tracer extravasation. In contrast, human autoptic stroke tissue exhibited pronounced extravasations of albumin around arteries and veins, while the pericapillary immunoreactivity appeared only faint. Although electron microscopy revealed comparable alterations of the arterial and capillary endothelium throughout the applied animal models, structural loss of arterial smooth muscle cells was only observed in the translationally relevant model of embolic middle cerebral artery occlusion. In light of the so far available concepts of stroke treatment, the consideration of a differential vascular pathophysiology along the cerebral vasculature is likely to allow development of novel effective treatment strategies.
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Brown, Aliza, Sean Woods, Robert Skinner, Jeff Hatton, John Lowery, Paula Roberson, Leah Hennings, and William C. Culp. "Neurological Assessment Scores in Rabbit Embolic Stroke Models." Open Neurology Journal 7, no. 1 (October 31, 2013): 38–43. http://dx.doi.org/10.2174/1874205x01307010038.
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Background: Neurological outcomes and behavioral assessments are widely used in animal models of stroke, but assessments in rabbit models are not fully validated. The wryneck model of neurological assessment scores (NAS) was compared to percent infarct volume (%IV) values (infarct volume is a proven clinical indicator of stroke severity) and arterial occlusion localization in three rabbit angiographic stroke models. Hypothesis: NAS values will correlate with percent infarct volume values. Methods: Anesthetized New Zealand White rabbits (N=131, 4-5 kg) received internal carotid artery emboli by angiographic catheter introduced into the femoral artery and occlusions were characterized. Rabbits were evaluated at 24 hours post embolism using the NAS test of 0 (normal) to 10 (death). Deficit criteria included neck twist, righting reflex, extension reflex in hind paw and forepaw, and posture. Brain sections stained with triphenyltetrazolium chloride (TTC) were analyzed for %IV. Volume of the infarct was measured and calculated as a percent of the total brain volume. Results: The aggregate correlation for NAS values vs. %IV values was R=0.61, p<0.0001, a strong positive relationship, while correlations of the NAS components ranged from R=0.28-0.46. Occlusionsof the posterior cerebral artery vs. the middle cerebral artery alone produced significantly greater deficit scores at p<0.0001. Conclusions: These positive results validate the NAS system in the rabbit angiographic embolic stroke model.
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Rewell, Sarah SJ, John A. Fernandez, Susan F. Cox, Neil J. Spratt, Lisa Hogan, Elena Aleksoska, Leena van Raay, Gabriel T. Liberatore, Peter E. Batchelor, and David W. Howells. "Inducing Stroke in Aged, Hypertensive, Diabetic Rats." Journal of Cerebral Blood Flow & Metabolism 30, no. 4 (January 13, 2010): 729–33. http://dx.doi.org/10.1038/jcbfm.2009.273.
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Animal models of ischemic stroke often neglect comorbidities common in patients. This study shows the feasibility of inducing stroke by 2 h of thread occlusion of the middle cerebral artery in aged (56 week old) spontaneously hypertensive rats (SHRs) with both acute (2 weeks) and chronic (36 weeks) diabetes. After modifying the streptozotocin dosing regimen to ensure that old SHRs survived the induction of diabetes, few died after induction of stroke. Induction of stroke is feasible in rats with multiple comorbidities. Inclusion of such comorbid animals may improve translation from the research laboratory to the clinic.
Dissertations / Theses on the topic "Stroke; animal models; middle cerebral artery occlusion"
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Gharbawie, Omar A., and University of Lethbridge Faculty of Arts and Science. "Modeling middle cerebral artery stroke in rats : an examination of the skilled reaching impairments." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2006, 2006. http://hdl.handle.net/10133/388.
Full textAbstract:
Middle cerebral artery (MCA) stroke can produce chronic incapacitating motor
impairments. Understanding the neural basis of the motor syndromes is complicated by
the diversity of neural structures damaged but the problem can be addressed in laboratory
rats by inducing selective infarcts. Nevertheless, the motor syndromes that ensue from
stroke in rats remain poorly understood and undermine its potential as a model for
clinical stroke. The objective of the present thesis was to document the skilled reaching
impairments from neocortical and subcortical MCA infarcts in rats. In addition, the
integrity of the motor system components spared by the infarct was assessed
neurophysiologically and neuroanatomically. Characteristic reaching impairments
emerged from each infarct but there were also some overlapping features that might be
explained by neural dysfunction extending beyond the boundaries of the infarct. The
present studies showed that the laboratory rat is an ideal animal model for studying
stroke, which should be of interest to both clinical and research scientists studying stroke.xiii, 345 leaves : ill. ; 29 cm. + 1 CD-ROM
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Wells, Adam James. "A surgical model of middle cerebral artery occlusive stroke in the sheep." Thesis, 2014. http://hdl.handle.net/2440/91277.
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Background: Stroke is an acute neurological injury secondary to vascular pathology, and is the second biggest killer of Australians and the leading cause of adult disability. The rationale of current therapy for occlusive stroke is rapid reperfusion of the ischaemic brain to limit the size of the injury. However, there are no standard neuroprotective therapies that have proven to be beneficial in clinical stroke, despite in excess of 1000 novel drugs showing promise in preclinical rodent studies. The consistent failure of clinical translation in rodent models suggests that they are perhaps not the best choice to simulate the intracranial pathophysiological changes that occur following human cerebral ischaemia, and that a better representative animal model with similar neuroanatomical features is required. Small ruminants such as the sheep have proven to be valuable in traumatic brain injury models, and a surgical model of permanent middle cerebral artery occlusion (MCAO) has recently been developed in the sheep. However, the existing model has a number of shortcomings and is in need of further characterisation before its widespread use in preclinical testing. The aim of this study was therefore to characterise the pathophysiological and radiological response to both temporary and permanent MCAO using a sheep model. Methods: Several different studies were performed. In the first to determine the feasibility of the project, 18 adult male and female Merino sheep were randomised to sham surgery (n=6), permanent MCAO (n=6) or 2 h temporary MCAO (n=6), and animals had intracranial pressure (ICP) and regional brain tissue oxygen (PbtO₂) monitored for 4 h. 6 further animals had magnetic resonance imaging (MRI) after permanent (n=3) or temporary (n=3) MCAO. In the second study, 10 adult Merino sheep were randomised to sham surgery (n=5) or temporary MCAO (n=5), with continuous monitoring of PbtO₂ to determine the relationship between duration of temporary MCAO and the development of regional hypoxia. In the third study, 28 adult female Merino sheep were randomised to sham surgery (n=6), permanent MCAO (n=10) or temporary MCAO (n=12), and monitored for 24 h under light general anaesthesia. MRI was performed in 12 animals (permanent MCAO n=6, temporary MCAO n=6). Stroke volume was calculated after staining fresh brains with 2,3,5-triphenyltetrazolium chloride (TTC). Results: The first study demonstrated the feasibility of performing surgical MCAO, with significantly larger ischaemic lesion areas on histology and MRI following permanent versus temporary occlusion. The second study demonstrated that PbtO₂ fell from a mean baseline of 45.0 +/- 14.1mmHg to a predefined hypoxic threshold of 15mmHg after 42.4 +/- 11.2 minutes of temporary MCAO, at a rate of 1.3mmHg/min. The third study showed a significantly elevated ICP, infarct volumes of 27.4 +/- 6.4%, evidence of space occupying cerebral oedema on MRI and a 30% mortality rate following permanent MCAO monitored for 24 h. Conclusions: A surgical model of temporary and permanent proximal MCAO stroke has been developed in the sheep. The response of the sheep brain to cerebral ischaemia shares many features with the human brain, particularly following permanent proximal occlusion and the development of space occupying cerebral oedema. The sheep as a representative model of human occlusive stroke appears highly promising for use in preclinical testing, for drugs that demonstrate efficacy in the sheep model may be more likely to successfully translate to clinical stroke.Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2014
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Che-Chuan, Wang, and 王哲川. "Therapeutic evaluation of agmatine in middle cerebral artery occlusion induced stroke animal model : the rule of aquaporin 4." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/01789995492031301378.
Full textAbstract:
碩士南台科技大學
生物科技系
97
Cerebral edema contributes to morbidity and mortality in stroke. The regulation of water balance in the brain is crucial. A disruption in this equilibrium causes an increase in brain water content that significantly contributes to the pathophysiology of traumatic brain injury, hydrocephalus, and a variety of neurological disorders. The discovery of the aquaporin (AQP) family of membrane water channels has provided important new insights into the physiology and pathology of brain water homeostasis. A number of recent studies are described in the review that demonstrated the important role of AQP4 in brain water balance and cerebral edema. Agmatine is an endogenous clonidine-displacing substance, an agonist for the α-2-adrenergic and imidazoline receptors, and an antagonist at N-methyl-D-aspartate (NMDA) receptors. In the present study, we examined alterations in glial and neuronal cell responses to the reported neuroprotective action of agmatine against cerebral ischemia. Rats were randomly divided into three groups: sham operation group, middle cerebral artery occlusion (MCAo) with saline treatment group, and MCAo with agmatine (100 mg/kg body weight) treatment group. Adult Sprague-Dawley rats were given intraperitoneal injection of agmatine or saline immediately after 90 min occlusion of the middle cerebral artery. In all animals, regional cerebral blood flow (rCBF) were measured by laser-Doppler flowmetery with flexible probe fixed on the skull starting before onset of ischemia until 2 hours after reperfusion. Implanting an intracranial microdialysis probe was assessed the markers of cerebral ischemia and cellular injury (including glycerol, glutamate and lactate/pyruvate ratio) in brain. Focal cerebral ischemia (for 90 minutes) was induced by MCAo by introducing a 4-0 monofilament nylon suture, whose tip have been rounded by heating near a flame and coated with poly-L-lysine, were introduced from the carotid bifurcation into the internal carotid artery until a mild resistance were felt (18 to 19 mm), thereby occluding the origin of the MCA. We used immunohistochemistry and immunofluorescence staining to determine the levels of AQP-4, and iNOS at different time points (1hr, 3hrs, 48hr, and 72hours) after transient MCAo. Brain swelling were quantitated in dry/ wet ratio at the level of the ipsilateral hemisphere. The maximum grip angle in an inclined plane was measured to determine motor performance whereas the percent of maximal possible effect was used to measure blockade of proprioception. The triphenyltetrazolium chloride (TTC) staining procedures were used for cerebral infarction assay. Our results revealed that, after the onset of MCAo, the neuronal ischemia/ damage markers were all significantly increased. Similarly, the protein expression of iNOS and AQP-4, were all significantly elevated in the cortex, hippocampus, and striatum of rat brain after at 3days after reperfusion, and result in neuronal apoptosis, gliosis and locomotor dysfuction. Systemic treatment with agmatine significantly enhanced survival of glial cells at 3 days after reperfusion of the MCA, and the preservation of these glial cells in the ischemic brain corresponded with a markedly reduced area of infarction as well as increased neuronal survival. The ischemia-induced locomotor and proprioception deficits were partially ameliorated in agmatine-treated animals evaluated at 3 days after the reperfusion of the MCA. Immunohistological assays further demonstrated that agmatine treatment significantly reduced the overexpression of the iNOS and AQP-4 of the ischemic brains. These results suggest that agmatine may cause attenuation of cerebral infarction as well as motor deficits by enhancing glial cell and neuronal survival.
Book chapters on the topic "Stroke; animal models; middle cerebral artery occlusion"
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Cam, Ertugrul, Ertugrul Kilic, Burak Yulug, and Marie-Françoise Ritz. "Occlusion of the Middle Cerebral Artery in Rats." In New Animal Models of Human Neurological Diseases, 52–65. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000117723.
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Orsu, Prabhakar, and Y. Srihari. "Experimental Animal Models of Cerebral Ischemic Reperfusion Injury." In Preclinical Animal Modeling in Medicine. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.97592.
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Restitution of blood flow in the ischemic region helps liberate cells from mortification in any tissue or organ. Reperfusion post cerebral ischemia worsen the condition and lead to “cerebral reperfusion injury”. In cerebral reperfusion injury, significant changes observed are infarct size, behavioural deficits, hematoma formation, inflammatory mediators, and oxidative stress markers representing the extent of brain injury. Experimental In vivo models mimicking pathological and neurological processes are key tools in researching cerebral reperfusion injury and potential therapeutic agents’ development. This review explains currently used In vivo models like middle cerebral artery occlusion model, emboli stroke model, two-vessel occlusion model of forebrain ischemia, four-vessel occlusion model of forebrain ischemia, photochemical stroke model, collagenase induced brain haemorrhage model, autologous whole blood induced haemorrhage model. This review provides contemplative facts to setup authentic and relevant animal models to study cerebral reperfusion injury.
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Wang-Fischer, Yanlin, and Lee Koetzner. "Surgery Procedure for Distal Middle Cerebral Artery Occlusion Model." In Manual of Stroke Models in Rats, 99–106. CRC Press, 2008. http://dx.doi.org/10.1201/9781420009521-12.
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Wang-Fischer, Yanlin, and Lee Koetzner. "Surgery Procedure for Distal Middle Cerebral Artery Occlusion Model." In Manual of Stroke Models in Rats, 99–105. CRC Press, 2008. http://dx.doi.org/10.1201/9781420009521.ch12.
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Gupta, Sangeetha, and Uma Sharma. "Intraluminal filament induced middle cerebral artery occlusion model of transient focal cerebral ischemia in rats." In Handbook of Animal Models in Neurological Disorders, 613–29. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-323-89833-1.00052-5.
Full textConference papers on the topic "Stroke; animal models; middle cerebral artery occlusion"
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Hirschberg, M., A. Manoutchei, B. Klemens, and B. Hofferberth. "CEREBRAL THROMBOLYSIS WITH INTRAVENOUSLY ADMINISTERED RECOMBINANT LOW- MOLECULAR-WEIGHT-UROKINASE AND RECOMBINANT PRO-UROKINASE IN A DOG MODEL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643571.
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There is increasing evidence that recombinant prourokinase (rec-pro-UK) is a proenzyme which in vivo systems may induce activation of the fibrinolytic system with a better thrombus selectivity than that obtained with active urokinase.In order to study the effects of rec-pro-UK and low-molecular-weight-urokinase (LMW-UK) on acute stroke, a thrombus was induced in the middle cerebral artery (MCA) of anesthetized mongrel dogs (n=12). Occlusion of the vessel was confirmed by angiography. Following a 1 hour period of MCA occlusion, in six animals LMW-UK was administered intravenously at a dose of 4000 lU/kg/min. Angiographically confirmed thrombolysis occurred after 30 minutes. Thrombolysis by LMW-UK was accompanied by bleeding from all surgical wounds and consumption of plasminogen, alpha-2-antiplasmin and fibrinogen. Rec-pro-UK was administered to six other dogs in a LMW-UK-equivalent dosis. Thrombolysis was achieved after 30 minutes in all six cases without inducing a systemic lytic state. Neither in the LMW-UK-group nor in the group treated with rec-pro-UK intracerebral bleeding complications were observed on post mortem examination.Our findings indicate that intravenous administration of rec-pro-UK - because of the lack of systemic side-effects - may be a safe way of rapid thrombolysis of occluded cerebral arteries in acute stroke.