Malignant Infarction in Cats After Prolonged Middle Cerebral Artery Occlusion

Toyota, Shingo; Graf, Rudolf; Valentino, Mario; Yoshimine, Toshiki; Heiss, Wolf‐Dieter

doi:10.1161/01.str.0000015557.18508.dd

Cited by 22 publications

(15 citation statements)

References 63 publications

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“…We have shown in transient 3 h focal ischemia in cats that vasogenic edema formation and brain swelling play a crucial role in secondary, delayed CBF reduction and glutamate elevation after reperfusion, resulting in infarct growth and potentially in a space-occupying, malignant course with transition from focal into global ischemia (Taguchi et al, 1996;Toyota et al, 2002Toyota et al, , 2003. Similar exacerbation has been observed after 2.5 h focal ischemia in rats and was attributed to blood-brain barrier damage and resulting edema formation (Neumann-Haefelin et al, 2000).…”

Section: Biphasic Appearance Of Depolarizations and Malignant Course mentioning

confidence: 56%

Peri-Infarct Depolarizations Reveal Penumbra-Like Conditions in Striatum

Umegaki¹,

Sanada²,

Waerzeggers³

et al. 2005

J. Neurosci.

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Spreading depression-like peri-infarct depolarizations not only characterize but also worsen penumbra conditions in cortical border zones of experimental focal ischemia. We intended to investigate the relevance of ischemic depolarization in subcortical regions of ischemic territories.Calomel We conclude that in focal ischemia, transient peri-infarct depolarizations emerge not only in cortical but also in striatal gray matter, thereby demonstrating the existence of subcortical zones of ischemic penumbra. The generation of these ischemic depolarizations is a multifocal process possibly linked to brain swelling and intracranial pressure rise in the later course of focal ischemia, and therefore a relevant correlate of progressively worsening conditions.

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Section: Biphasic Appearance Of Depolarizations and Malignant Course mentioning

confidence: 56%

Peri-Infarct Depolarizations Reveal Penumbra-Like Conditions in Striatum

Umegaki¹,

Sanada²,

Waerzeggers³

et al. 2005

J. Neurosci.

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“…In cats, distal or proximal MCAo of similar occlusion times produces large hemispheric infarctions, progressive edema, and death. 85,86 In humans, malignant infarction is associated with diminished local collateral flow and a reduced region of penumbra. 87,88 Similarly in rats, laser Doppler flow measurements suggest that suture occlusion of the MCAo also results in reduced local collateral flow, compared with other stroke models.…”

Section: Modeling Malignant Infarctionmentioning

confidence: 99%

Rodent models of focal stroke: Size, mechanism, and purpose

2005

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Summary: Rodent stroke models provide the experimental backbone for the in vivo determination of the mechanisms of cell death and neural repair, and for the initial testing of neuroprotective compounds. Less than 10 rodent models of focal stroke are routinely used in experimental study. These vary widely in their ability to model the human disease, and in their application to the study of cell death or neural repair. Many rodent focal stroke models produce large infarcts that more closely resemble malignant and fatal human infarction than the average sized human stroke. This review focuses on the mechanisms of ischemic damage in rat and mouse stroke models, the relative size of stroke generated in each model, and the purpose with which focal stroke models are applied to the study of ischemic cell death and to neural repair after stroke.

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“…Second, there is no accepted model of the malignant MCA syndrome in NHP or cat. A non-survival model of MCA ischemia/reperfusion (3/6 h) has been described in the cat [66, 67], and several models of stroke have been described in NHP [68–73], including two with potentially high mortality in baboons [68, 74], depending on timing of reperfusion. Meaningful implementation of this recommendation in the spirit of STAIR would require developing an ethically acceptable, high mortality model of the malignant MCA syndrome in cat or NHP.…”

Section: Stroke Therapy Academic Industry Roundtablementioning

confidence: 99%

Glibenclamide in Cerebral Ischemia and Stroke

et al. 2013

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The sulfonylurea receptor 1 (Sur1)–transient receptor potential 4 (Trpm4) channel is an important molecular element in focal cerebral ischemia. The channel is upregulated in all cells of the neurovascular unit following ischemia, and is linked to microvascular dysfunction that manifests as edema formation and secondary hemorrhage, which cause brain swelling. Activation of the channel is a major molecular mechanism of cytotoxic edema and “accidental necrotic cell death.” Blockade of Sur1 using glibenclamide has been studied in different types of rat models of stroke: (i) in conventional non-lethal models (thromboembolic, 1–2 h temporary, or permanent middle cerebral artery occlusion), glibenclamide reduces brain swelling and infarct volume and improves neurological function; (ii) in lethal models of malignant cerebral edema, glibenclamide reduces edema, brain swelling, and mortality; (iii) in models with rtPA, glibenclamide reduces swelling, hemorrhagic transformation, and death. Retrospective studies of diabetic patients who present with stroke have shown that those whose diabetes is managed with a sulfonylurea drug and who are maintained on the sulfonylurea drug during hospitalization for stroke have better outcomes at discharge and are less likely to suffer hemorrhagic transformation. Here, we provide a comprehensive review of the basic science, preclinical experiments, and retrospective clinical studies on glibenclamide in focal cerebral ischemia and stroke. We also compare the preclinical work in stroke models to the updated recommendations of the Stroke Therapy Academic Industry Roundtable (STAIR). The findings reviewed here provide a strong foundation for a translational research program to study glibenclamide in patients with ischemic stroke.

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Malignant Infarction in Cats After Prolonged Middle Cerebral Artery Occlusion

Cited by 22 publications

References 63 publications

Peri-Infarct Depolarizations Reveal Penumbra-Like Conditions in Striatum

Peri-Infarct Depolarizations Reveal Penumbra-Like Conditions in Striatum

Rodent models of focal stroke: Size, mechanism, and purpose

Glibenclamide in Cerebral Ischemia and Stroke

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