An improved version of embolic model of brain ischemic injury in the rat

Wang, Chen Xu; Yang, Tao; Shuaib, Ashfaq

doi:10.1016/s0165-0270(01)00408-3

Cited by 61 publications

(55 citation statements)

References 14 publications

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“…Focal cerebral ischemia was induced by embolization of a preformed clot in the middle cerebral artery, as described. 11 Body temperature was maintained at 37°CϮ0.5 with a heating pad for the duration of surgery. Glycemia, arterial blood pressure, and blood gases were also monitored during surgery.…”

Section: Methodsmentioning

confidence: 99%

Protective Effect of High-Density Lipoprotein-Based Therapy in a Model of Embolic Stroke

Lapergue

Moreno²,

Dang³

et al. 2010

Stroke

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Background and Purpose-High-density lipoprotein (HDL) levels are inversely associated with stroke incidence, suggesting a protective effect. Using a rat model, we tested the hypothesis that HDL exerts direct vasculo-/ neuroprotective effects when administered during the acute phase of embolic stroke. Methods-After embolic occlusion, Sprague-Dawley rats were randomly treated intravenously with purified HDL versus saline immediately (2, 10 mg/kg) or 3 or 5 hours (10 mg/kg) after stroke. The effects of HDL were assessed blindly 24 hours later by evaluating neurological deficit score and measuring the infarct volume and blood-brain barrier breakdown. Protease activities and neutrophil infiltration were also evaluated. Results-HDL injection immediately after stroke (10 mg/kg) reduced by 68% the mortality at 24 hours (Pϭ0.015). HDL administration immediately or at 3 or 5 hours after stroke also reduced cerebral infarct volume by 74%, 68%, and 70.7%, respectively (Pϭ0.0003, Pϭ0.011, and Pϭ0.019; nϭ17 per group). The neurological deficit at 24 hours in the HDL-treated group was decreased versus the saline-treated group (Pϭ0.015). Ischemia-induced blood-brain barrier breakdown was significantly reduced in HDL-treated rats versus controls (Pϭ0.0045). Neuroprotective effects of HDL were associated with decreased neutrophil recruitment in the infarct area (Pϭ0.0027) accompanied by reduced matrix metalloproteinase gelatinase activity. Immunostaining showed that HDL was associated with endothelial and glial cells, and also that intercellular adhesion molecule-1 expression was decreased in vessels within the infarct area. Conclusions-Administration of HDL is neuroprotective when performed up to 5 hours after experimental stroke.This effect may be attributed to the ability of HDL to protect the blood-brain barrier and limit neutrophil recruitment. (Stroke. 2010;41:1536-1542.)

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Section: Methodsmentioning

confidence: 99%

Protective Effect of High-Density Lipoprotein-Based Therapy in a Model of Embolic Stroke

Lapergue

Moreno²,

Dang³

et al. 2010

Stroke

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“…eMCAO was induced by injection of a preformed clot at the origin of MCA as already described. 12 Continuous laser Doppler flowmetry (VMS, Moor Instrument) was used to monitor regional cerebral perfusion to ensure the adequacy of MCA occlusion (perfusion decreased to <20% of preischemic baselines). Animals were assigned to 1 of 4 groups (n=12 per group, except for the tPA-treated group, n=24): control (saline treatment only), tPA alone (10 mg/kg), HDLs alone (10 mg/kg intravenous, jugular vein) (Figure IV in online-only Data Supplement), and tPA plus HDLs.…”

Section: Animal Procedures and Experimental Designmentioning

confidence: 99%

High-density Lipoprotein–based Therapy Reduces the Hemorrhagic Complications Associated With Tissue Plasminogen Activator Treatment in Experimental Stroke

Lapergue

Dang

Desilles

et al. 2013

Stroke

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Background and Purpose-We have previously reported that intravenous injection of high-density lipoproteins (HDLs) was neuroprotective in an embolic stroke model. We hypothesized that HDL vasculoprotective actions on the bloodbrain barrier (BBB) may decrease hemorrhagic transformation-associated with tissue plasminogen activator (tPA) administration in acute stroke. Methods-We used tPA alone or in combination with HDLs in vivo in 2 models of focal middle cerebral artery occlusion (MCAO) (embolic and 4-hour monofilament MCAO) and in vitro in a model of BBB. Sprague-Dawley rats were submitted to MCAO, n=12 per group. The rats were then randomly injected with tPA (10 mg/kg) or saline with or without human plasma purified-HDL (10 mg/kg). The therapeutic effects of HDL and BBB integrity were assessed blindly 24 hours later. The integrity of the BBB was also tested using an in vitro model of human cerebral endothelial cells under oxygen-glucose deprivation. Results-tPA-treated groups had significantly higher mortality and rate of hemorrhagic transformation at 24 hours in both MCAO models.

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“…Among the stroke patients, 85 -90% of the cases are ischaemic stroke with a predominant (75-80%) cause of cerebral arterial thrombosis, and majorities of ischaemic episodes occur as a result of occlusion of the middle cerebral artery or its branches [3,4].…”

mentioning

confidence: 99%

“…This model mimics human stroke and is more relevant to the pathophysiological situation in patients. Furthermore, different lesion sizes could be generated in this model by injection of various volumes of clot into the middle cerebral artery [3]. Therefore, we investigated whether a combination of thiazolidinediones with the lowest effective dose of MK-801 (0.1 mg/kg), which has been reported to be free of side effects [6], may provide more neuroprotection during the embolic model of stroke in rats.…”

mentioning

confidence: 99%

Combination Therapy of Rosiglitazone, a Peroxisome Proliferator‐Activated Receptor‐γ Ligand, and NMDA Receptor Antagonist (MK‐801) on Experimental Embolic Stroke in Rats

Allahtavakoli

Shabanzadeh

Roohbakhsh

et al. 2007

Basic Clin Pharma Tox

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Peroxisome proliferator-activated receptor-γ (PPAR-γ ) agonists have been found to have potent anti-inflammatory actions and suggested as potential therapies for brain ischaemia. Glutamate is the most common excitatory neurotransmitter in the central nervous system and is released excessively during ischaemia. Stroke therapy will require combinations of drug classes, because no single drug class has yet been proven efficacious in human beings. The present study was conducted to assess whether N-methyl-d -aspartate (NMDA) receptor antagonist (MK-801) treatment can improve recovery from ischaemic brain injury and whether rosiglitazone, a PPAR-γ ligand, can increase its neuroprotective effect in an embolic model of stroke. Stroke was induced in rats by embolizing a preformed clot into the middle cerebral artery. Rosiglitazone (0.1 mg/kg, intraperitoneally) and MK-801 (0.1 mg/kg, intravenously) were injected immediately after embolization. Forty-eight hours later, the brains were removed, sectioned and stained with triphenyltetrazolum chloride and analysed by a commercial image processing software programme. Rosiglitazone and MK-801 alone or in combination decreased infarct volume by 49.16%, 50.26% and 81.32%, respectively (P < 0.001). Moreover, the combination therapy significantly decreased the infarct volume when compared to any drug used alone (P < 0.05). MK-801 reduced the brain oedema by 68% compared to the control group (P < 0.05), but rosiglitazone or combination did not show any significant effect. The drugs alone or in combination also demonstrated improved neurological function, but combination therapy was more effective on neurological deficits improving. Our data show that the combination of MK-801 and rosiglitazone is more neuroprotective in thromboembolic stroke than given alone; this effect perhaps represents a possible additive effect in the brain infarction.

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An improved version of embolic model of brain ischemic injury in the rat

Cited by 61 publications

References 14 publications

Protective Effect of High-Density Lipoprotein-Based Therapy in a Model of Embolic Stroke

Protective Effect of High-Density Lipoprotein-Based Therapy in a Model of Embolic Stroke

High-density Lipoprotein–based Therapy Reduces the Hemorrhagic Complications Associated With Tissue Plasminogen Activator Treatment in Experimental Stroke

Combination Therapy of Rosiglitazone, a Peroxisome Proliferator‐Activated Receptor‐γ Ligand, and NMDA Receptor Antagonist (MK‐801) on Experimental Embolic Stroke in Rats

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