A new percutaneous model of Subarachnoid Haemorrhage in rats

Muñoz-Sánchez, M.Á.; Egea-Guerrero, Juan José; Revuelto-Rey, J.; Moreno-Valladares, Manuel; Murillo-Cabezas, Francisco

doi:10.1016/j.jneumeth.2012.08.010

Cited by 10 publications

(3 citation statements)

References 36 publications

(73 reference statements)

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“…However, this is far from the ideal injection, which would occur at physiologic MABP. Furthermore, researchers often hold the rodent upside down following injection into the cisterna magna to facilitate blood distribution (Ram et al, 1991 ; Lin et al, 2003 ; Lee et al, 2008 ; Takata et al, 2008 ; Güresir et al, 2010 , 2012 ; Cai J. et al, 2012 ; Munoz-Sanchez et al, 2012a ). This step will falsely elevate the measured ICP.…”

Section: Pathophysiology Of Rodent Models Of Sahmentioning

confidence: 99%

“…Rodent models of SAH exhibit a wide range of mortality (Table 6 ). Cisterna magna single injection models produce 0–16% mortality (Delgado et al, 1985 ; Solomon et al, 1985 ; Ram et al, 1991 ; Glenn et al, 2002 ; Gules et al, 2002 ; Lin et al, 2003 ; Prunell et al, 2003 ; Turowski et al, 2007 ; Munoz-Sanchez et al, 2012a ; Boyko et al, 2013 ), while cisterna magna double injection models exhibit a greater range of 0–43% rate within the first few days (Glenn et al, 2002 ; Gules et al, 2002 ; Weidauer et al, 2006 ; Lee et al, 2008 , 2009 ; Cai J. et al, 2012 ). At a later time point of 9 d following hemorrhage, mortality was as high as 53% in one double injection model (Vatter et al, 2006 ).…”

Section: Mortality and Functional Outcomes In Rodent Models Of Sahmentioning

confidence: 99%

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A Comparison of Pathophysiology in Humans and Rodent Models of Subarachnoid Hemorrhage

Leclerc

Garcia

Diller

et al. 2018

Front. Mol. Neurosci.

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Non-traumatic subarachnoid hemorrhage (SAH) affects an estimated 30,000 people each year in the United States, with an overall mortality of ~30%. Most cases of SAH result from a ruptured intracranial aneurysm, require long hospital stays, and result in significant disability and high fatality. Early brain injury (EBI) and delayed cerebral vasospasm (CV) have been implicated as leading causes of morbidity and mortality in these patients, necessitating intense focus on developing preclinical animal models that replicate clinical SAH complete with delayed CV. Despite the variety of animal models currently available, translation of findings from rodent models to clinical trials has proven especially difficult. While the explanation for this lack of translation is unclear, possibilities include the lack of standardized practices and poor replication of human pathophysiology, such as delayed cerebral vasospasm and ischemia, in rodent models of SAH. In this review, we summarize the different approaches to simulating SAH in rodents, in particular elucidating the key pathophysiology of the various methods and models. Ultimately, we suggest the development of standardized model of rodent SAH that better replicates human pathophysiology for moving forward with translational research.

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Section: Pathophysiology Of Rodent Models Of Sahmentioning

confidence: 99%

Section: Mortality and Functional Outcomes In Rodent Models Of Sahmentioning

confidence: 99%

A Comparison of Pathophysiology in Humans and Rodent Models of Subarachnoid Hemorrhage

Leclerc

Garcia

Diller

et al. 2018

Front. Mol. Neurosci.

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show abstract

“…Variations in some parameters of the first method, including injected blood volume, CSF removal prior to injection to prevent egress of blood into the spinal canal, and replenishing intravascular volume to keep cerebral perfusion pressure constant through maintenance of mean arterial pressure, as well as the rapidity of injection have raised questions about comparability and biofidelity of the results (88)(89)(90)(91). The latter model appears to remove some of the mentioned confounding factors, as the hemorrhage occurs at physiologic mean arterial pressure (MAP) and intracranial pressure (ICP), but is limited by variable puncture site and ultimate hemorrhage volume.…”

Section: Subarachnoid Hemorrhagementioning

confidence: 99%

Translational Genomics in Neurocritical Care: a Review

2020

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Translational genomics represents a broad field of study that combines genome and transcriptome-wide studies in humans and model systems to refine our understanding of human biology and ultimately identify new ways to treat and prevent disease. The approaches to translational genomics can be broadly grouped into two methodologies, forward and reverse genomic translation. Traditional (forward) genomic translation begins with model systems and aims at using unbiased genetic associations in these models to derive insight into biological mechanisms that may also be relevant in human disease. Reverse genomic translation begins with observations made through human genomic studies and refines these observations through follow-up studies using model systems. The ultimate goal of these approaches is to clarify intervenable processes as targets for therapeutic development. In this review, we describe some of the approaches being taken to apply translational genomics to the study of diseases commonly encountered in the neurocritical care setting, including hemorrhagic and ischemic stroke, traumatic brain injury, subarachnoid hemorrhage, and status epilepticus, utilizing both forward and reverse genomic translational techniques. Further, we highlight approaches in the field that could be applied in neurocritical care to improve our ability to identify new treatment modalities as well as to provide important information to patients about risk and prognosis.

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