Experimental Subarachnoid Hemorrhage: Subarachnoid Blood Volume, Mortality Rate, Neuronal Death, Cerebral Blood Flow, and Perfusion Pressure in Three Different Rat Models

Prunell, Giselle; Mathiesen, Tiit; Diemer, Nils Henrik; Svendgaard, Niels-Aage

doi:10.1097/00006123-200301000-00022

Cited by 131 publications

(141 citation statements)

References 47 publications

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“…In line with earlier studies that employed this endovascular perforation model [3,4,5], we observed high acute mortality (43%) that matches mortality rates of about 40% after clinical aneurysmal SAH [13,14]. Previous studies with this model have primarily focused on the first 24 h after SAH [5].…”

Section: Discussionsupporting

confidence: 88%

“…A frequently applied model that closely resembles the clinical pathology, involves perforation of the bifurcation of the internal carotid artery into the middle cerebral artery and anterior cerebral artery with an endovascular filament [3]. The arterial rupture leads to immediate extravasation of intracranial blood and acute elevation of intracranial pressure, resulting in significant reduction in cerebral perfusion within the first minutes [3,4,5,6]. In the following hours, intracranial pressure largely recovers, and perfusion is partially restored [6].…”

Section: Introductionmentioning

confidence: 99%

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Progression of Brain Lesions in Relation to Hyperperfusion from Subacute to Chronic Stages after Experimental Subarachnoid Hemorrhage: A Multiparametric MRI Study

et al. 2013

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Background: The pathogenesis of delayed cerebral injury after aneurysmal subarachnoid hemorrhage (SAH) is largely unresolved. In particular, the progression and interplay of tissue and perfusion changes, which can significantly affect the outcome, remain unclear. Only a few studies have assessed pathophysiological developments between subacute and chronic time points after SAH, which may be ideally studied with noninvasive methods in standardized animal models. Therefore, our objective was to characterize the pattern and correlation of brain perfusion and lesion status with serial multiparametric magnetic resonance imaging (MRI) from subacute to chronical after experimental SAH in rats. Methods: SAH was induced by endovascular puncture of the intracranial bifurcation of the right internal carotid artery in adult male Wistar rats (n = 30). Diffusion-, T2-, perfusion- and contrast-enhanced T1-weighted MRI were performed on a 4.7-tesla animal MR system to measure cytotoxic and vasogenic edema, hemodynamic parameters and blood-brain barrier permeability, respectively, at days 2 and 7 after SAH. The neurological status was repeatedly monitored with different behavioral testsbetween days -1 and 7 after SAH. Lesioned tissue - identified by edema-associated T2 prolongation - and unaffected tissue were outlined on multislice images and further characterized based on tissue and perfusion indices. Correlation analyses were performed to evaluate relationships between different MRI-based parameters and between MRI-based parameters and neurological scores. Results: Similar to clinical SAH and previous studies in this experimental SAH model, mortality up to day 2 was high (43%). In surviving animals, neurological function was significantly impaired subacutely, and tissue damage (characterized by T2 prolongation and diffusion reduction) and blood-brain barrier leakage (characterized by contrast agent extravasation) were apparent in ipsilateral cortical and subcortical tissue as well as in contralateral cortical tissue. Notably, ipsilateral cortical areas revealed increased cerebral blood flow and volume. Animals that subsequently died between days 2 and 7 after SAH had markedly elevated ipsilateral perfusion levels at day 2. After a week, neurological function had improved in surviving animals, and brain edema was partially resolved, while blood-brain barrier permeability and hyperperfusion persisted. The degree of brain damage correlated significantly with the level of perfusion elevation (r = 0.78 and 0.85 at days 2 and 7, respectively; p < 0.05). Furthermore, chronic (day 7 after SAH) blood-brain barrier permeability and vasogenic edema formation were associated with subacute (day 2 after SAH) hyperperfusion (r = 0.53 and 0.66, respectively; p < 0.05). Conclusion: Our imaging findings indicate that SAH-induced brain injury at later stages is associated with progressive changes in tissue perfusion and that chronic hyperperfusion may contribute or point to delayed cerebral damage. Furthermore, multiparametric MRI may significan...

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Progression of Brain Lesions in Relation to Hyperperfusion from Subacute to Chronic Stages after Experimental Subarachnoid Hemorrhage: A Multiparametric MRI Study

et al. 2013

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“…In previous reports we showed that the endovascular perforation of the internal cerebral artery and the injection of blood into the prechiasmatic cistern were suitable means of studying the pathophysiology of SAH. 49,50 To characterize these models further, we used them to induce SAH in the present study.…”

mentioning

confidence: 99%

Delayed cell death related to acute cerebral blood flow changes following subarachnoid hemorrhage in the rat brain

Prunell

Svendgaard²,

Alkass³

et al. 2005

Journal of Neurosurgery

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100

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“…22 After injection of blood into the cisterna magna, neurological function usually remains intact, and the mortality rate is surprisingly lower than that in humans. 26 The filament SAH model better mimics the pathophysiological events after aneurysms rupture an intracranial vessel, with a mortality rate similar to that seen in humans (~ 40-50%). The endovascular perforation of the ICA results in a prompt, very reproducible elevation of ICP and acute vasospasm, 4 which is detectable for up to 72 hours after SAH.…”

Section: Discussionmentioning

confidence: 94%

Brain edema formation and neurological impairment after subarachnoid hemorrhage in rats

Thal¹,

Sporer²,

Kłopotowski

et al. 2009

JNS

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Experimental Subarachnoid Hemorrhage: Subarachnoid Blood Volume, Mortality Rate, Neuronal Death, Cerebral Blood Flow, and Perfusion Pressure in Three Different Rat Models

Cited by 131 publications

References 47 publications

Progression of Brain Lesions in Relation to Hyperperfusion from Subacute to Chronic Stages after Experimental Subarachnoid Hemorrhage: A Multiparametric MRI Study

Progression of Brain Lesions in Relation to Hyperperfusion from Subacute to Chronic Stages after Experimental Subarachnoid Hemorrhage: A Multiparametric MRI Study

Delayed cell death related to acute cerebral blood flow changes following subarachnoid hemorrhage in the rat brain

Brain edema formation and neurological impairment after subarachnoid hemorrhage in rats

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