Temporary alteration of cerebrovascular permeability to plasma protein during drug-induced seizures

Lorenzo, AV; Shirahige, I; Liang, Min; Barlow, CF

doi:10.1152/ajplegacy.1972.223.2.268

Cited by 135 publications

(31 citation statements)

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“…PKC-dependent signaling events within endothelial cells that lead to increased permeability and barrier dysfunction have been implicated in a number of human diseases, including sepsis, acute lung injury, ARDS, and diabetes (Bannerman and Goldblum, 1999;Idris et al, 2001;SiflingerBirnboim and Johnson, 2003). Electrical or chemical seizure and focal ischemia, which induce verge, also lead to increased vascular permeability (Lorenzo et al, 1972;Sperk et al, 1983). Although the data presented in this study lays the groundwork describing a novel protein involved in modulating vascular permeability, it is important to note that the model used to study verge function thus far is an immortalized brain endothelial cell line and thus may not fully replicate the function of verge in vivo.…”

Section: Discussionmentioning

confidence: 93%

Verge: A Novel Vascular Early Response Gene

et al. 2004

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Section: Discussionmentioning

confidence: 93%

Verge: A Novel Vascular Early Response Gene

et al. 2004

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“…Many observations in epilepsy patients (19)(20)(21)(22)(23)(24), confirmed by animal studies (25)(26)(27)(28), demonstrated that SE provokes transient BBB breakdown and vasogenic edema in the area of the seizure focus. It is commonly proposed that local (relative hypoxia secondary to increased ictal metabolism with an increase in local PCO 2 and lactate) and systemic (increase in blood pressure and decrease in blood pH) physiologic changes induce a vasodilatation, resulting in increased regional blood flow and BBB breakdown (25,26,29).…”

Section: Role Of the Bbb Breakdown In The Genesis Of The Lesionsmentioning

confidence: 86%

“…It is commonly proposed that local (relative hypoxia secondary to increased ictal metabolism with an increase in local PCO 2 and lactate) and systemic (increase in blood pressure and decrease in blood pH) physiologic changes induce a vasodilatation, resulting in increased regional blood flow and BBB breakdown (25,26,29).…”

Section: Role Of the Bbb Breakdown In The Genesis Of The Lesionsmentioning

confidence: 99%

Magnetic Resonance Imaging in the Study of the Lithium–Pilocarpine Model of Temporal Lobe Epilepsy in Adult Rats

et al. 2002

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Summary:Purpose: In temporal lobe epilepsy, it remains to be clarified whether hippocampal sclerosis is the cause or the consequence of epilepsy. We studied the temporal evolution of the lesions in the lithium-pilocarpine model of epilepsy in the rat with magnetic resonance imaging (MRI) to determine the progressive morphologic changes occurring before the appearance of chronic epilepsy.Methods: MRI was performed on an MR scanner operating at 4.7 T. We followed the evolution of lesions using T 2 -and T 1 -weighted sequences before and after the injection of gadolinium from 2 h to 9 weeks.Results: At 2 h after status epilepticus (SE), a blood-brain barrier breakdown could be observed only in the thalamus; it had disappeared by 6 h. At 24 h after SE, edema was present in the amygdala and the piriform and entorhinal cortices together with extensive neuronal loss; it disappeared progressively over a 5-day period. During the chronic phase, a cortical signal reappeared in all animals; this signal corresponded to gliosis, which appeared on glial fibrillary acidic protein (GFAP) immunohistochemically stained sections as hypertrophic astrocytes with thickened processes. In the hippocampus, the correlation between histopathology and T 2 -weighted signal underscored the progressive constitution of atrophy and sclerosis, starting 2 days after SE.Conclusions: These data show the reactivity of the cortex that characterizes the initial step leading to the development of epilepsy and the late gliosis that could result from the spontaneous seizures. Moreover, it appears that hippocampal sclerosis progressively worsened and could be both the cause and the consequence of epileptic activity.

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“…30 In the first (seran-polymer) model, the polymer was located in the neuropil, suggesting a leak between endothelial cells. It has been assumed that the intravenously administered albumin-bound dyes which stain the neuropil after topical application of hypertonic solutions do so by passing between endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Cerebral pathophysiology in hemorrhagic shock. Nuclide scan data, fluorescence microscopy, and anatomic correlations.

Bronshvag¹

1980

Stroke

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SUMMARY Nineteen unanesthetized sheep were given Evans blue dye or radionuclide and then were incrementally bled into hemorrhagic shock (BP less than 50/25) by withdrawal of blood orer a period of approximately one hour. Four sheep served as controls for histologic data. Static nuclide brain scans performed in 6 bled sheep demonstrated immediate uptake of the radionuclide. Fluorescence microscopic examination of brain tissue obtained at autopsy in bled sheep demonstrated dye uptake in the perirascular areas, but not in the neuropil. Electron microscopic examination of collateral cortical biopsy specimens showed swelling of perivascular astrocytic foot processes, but no endothelial abnormality. We feel that the uptake of radionuclide and dye-albumin complex by the perivascular astrocytes represents enhanced transendothelial transport rather than passage of molecules between endothelial cells. The significance of this presumably transient phenomenon is discussed.

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Temporary alteration of cerebrovascular permeability to plasma protein during drug-induced seizures

Cited by 135 publications

References 0 publications

Verge: A Novel Vascular Early Response Gene

Verge: A Novel Vascular Early Response Gene

Magnetic Resonance Imaging in the Study of the Lithium–Pilocarpine Model of Temporal Lobe Epilepsy in Adult Rats

Cerebral pathophysiology in hemorrhagic shock. Nuclide scan data, fluorescence microscopy, and anatomic correlations.

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