A novel swine model of subarachnoid hemorrhage-induced cerebral vasospasm

Zibly, Zion; Fein, Lory; Sharma, Mayur; Assaf, Yaniv; Wohl, Anton; Harnof, Sagi

doi:10.4103/neuroindia.ni_357_16

Cited by 5 publications

(2 citation statements)

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“…The underlying mechanisms leading to CV remain poorly understood and have therefore been a prime focus of preclinical studies. The majority have used rodent models, but primate, swine, and dog models have also been employed (85).…”

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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Section: Subarachnoid Hemorrhagementioning

confidence: 99%

Translational Genomics in Neurocritical Care: a Review

2020

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“…As it is difficult to carry out in vivo experimental studies on cerebral vasospasm and pathological changes in brain tissue after SAH, and as the materials provided by clinical autopsy are extremely limited, animal models have become one of the primary means of studying cerebral vasospasm ( 19 ). In the present study, ultrasound-guided double injections of blood into cisterna magna were used to make the SAH model in rabbits.…”

Section: Introductionmentioning

confidence: 99%

Magnetic resonance analysis of deep cerebral venous vasospasm after subarachnoid hemorrhage in rabbits

Zhang

Fang

Zhu³

et al. 2022

Front. Cardiovasc. Med.

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ObjectiveArterial spasm is proved to be an inducer of cerebral ischemia and cerebral infarction, while when a venous spasm occurs, cerebral edema is seen to be caused by a disturbance in cerebral blood flow. However, it is unclear and unproven whether venous spasm occurs after subarachnoid hemorrhage (SAH). To provide the theoretical basis for treating cerebral vasospasm after SAH, magnetic resonance imaging (MRI) was employed to observe the changes in the diameter of deep cerebral veins in rabbits after SAH.MethodsFourteen New Zealand rabbits were randomly divided into the SAH group (n = 10) and the normal saline group (NS group, n = 4). Specifically, the SAH models were established by the ultrasound-guided double injections of blood into cisterna magna. Moreover, the MRI was performed to observe the changes in the diameter of deep cerebral veins (internal cerebral vein, basilar vein, and great cerebral vein) and basilar artery before modeling (0 d) and 1, 3, 5, 7, 9, and 11 d after modeling.ResultsIn the SAH group, the diameter of the basilar artery showed no evident change on the 1st d. However, it became narrower obviously on the 3rd d and 5th d, and the stenosis degree was more than 30%. The diameter gradually relieved from 7th to 9th d, and finally returned to normal on the 11th d. Moreover, the diameter of the internal cerebral vein significantly narrowed on the 1st d, the stenosis degree of which was 19%; the stenosis then relieved slightly on the 3rd d (13%), reached the peak (34%) on the 5th d, and gradually relieved from 7th d to 11th d. Moreover, the stenosis degree of the basilar vein was 18% on the 1st d, 24% on the 3rd d, and reached the peak (34%) on the 5th d.ConclusionAfter SAH in rabbits, the cerebral vasospasm was seen to occur in the basilar artery, and likewise, spasmodic changes took place in the deep cerebral vein. Furthermore, the time regularity of spasmodic changes between the cerebral vein and basilar artery was of significant difference, indicating that the venous vasospasm resulted in active contraction.

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Delayed Cerebral Ischemia After Subarachnoid Hemorrhage: Experimental-Clinical Disconnect and the Unmet Need

et al. 2019

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Background-Delayed cerebral ischemia (DCI) is among the most dreaded complications following aneurysmal subarachnoid hemorrhage (SAH). Despite advances in neurocritical care, DCI remains a significant cause of morbidity and mortality, prolonged intensive care unit and hospital stay, and high healthcare costs. Large artery vasospasm has classically been thought to lead to DCI. However, recent failure of clinical trials targeting vasospasm to improve outcomes has underscored the disconnect between large artery vasospasm and DCI. Therefore, interest has shifted onto other potential mechanisms such as microvascular dysfunction and spreading depolarizations. Animal models can be instrumental in dissecting pathophysiology, but clinical relevance can be difficult to establish.Methods-Here, we performed a systematic review of the literature on animal models of SAH, focusing specifically on DCI and neurological deficits.Results-We find that dog, rabbit and rodent models do not consistently lead to DCI, although some degree of delayed vascular dysfunction is common. Primate models reliably recapitulate delayed neurological deficits and ischemic brain injury; however, ethical issues and cost limit their translational utility.Conclusions-To facilitate translation, clinically relevant animal models that reproduce the pathophysiology and cardinal features of DCI after SAH are urgently needed.

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A novel swine model of subarachnoid hemorrhage-induced cerebral vasospasm

Cited by 5 publications

References 1 publication

Translational Genomics in Neurocritical Care: a Review

Translational Genomics in Neurocritical Care: a Review

Magnetic resonance analysis of deep cerebral venous vasospasm after subarachnoid hemorrhage in rabbits

Delayed Cerebral Ischemia After Subarachnoid Hemorrhage: Experimental-Clinical Disconnect and the Unmet Need

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