The Impact of Subarachnoid Hemorrhage on Regional Cerebral Blood Flow and Large-vessel Diameter in the Canine Model of Chronic Vasospasm

Bassiouni, Hischam; Schulz, Rainer; Dörge, Hilmar; Stolke, D.; Heusch, Gerd

doi:10.1016/j.jstrokecerebrovasdis.2006.10.002

Cited by 4 publications

(3 citation statements)

References 54 publications

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“…Among those, worsening of perfusion (i.e., DCI) was detected in only three studies. One study in dogs found significantly lower cerebral, cerebellar and brain stem blood flow on day 8 (CBF ~ 60-70% of baseline) compared with day 1 using the microsphere technique after cisterna magna blood injection [13]. Interestingly, large artery spasm did not correlate with CBF in this study.…”

Section: Perfusion Abnormalitiescontrasting

confidence: 74%

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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Section: Perfusion Abnormalitiescontrasting

confidence: 74%

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

et al. 2019

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“…25 There are multiple other pathways beside aVSP that lead to DCI and poor outcome (Figure). Treatments that target multiple may be needed to further improve the outcome of patients with SAH.…”

Section: Macdonald Prevention Of Angiographic Vasospasm S33mentioning

confidence: 99%

Does Prevention of Vasospasm in Subarachnoid Hemorrhage Improve Clinical Outcome? Yes

Macdonald

2013

Stroke

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“…Moreover, other studies have revealed no correlation that exists between regional CBF decrease and lumen reduction of large arteries supplying this region. 24 All of these references have addressed dissociation between macrovasculature spasms and microvasculature dysfunction. In our present model, we report evidence for vasospasms at the microvasculature level by SPECT, taken as 'snapshots' to detect cerebral perfusion of microcirculation.…”

Section: The Sah Model Establishment and Vasospasm Confirmationmentioning

confidence: 99%

Effects of Topical Administration of Nimodipine on Cerebral Blood Flow following Subarachnoid Hemorrhage in Pigs

Wang

Yin²,

Feng³

et al. 2013

Journal of Neurotrauma

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We sought to explore whether topical administration of nimodipine improves the abnormal cerebral perfusion following subarachnoid hemorrhage (SAH) in pigs. Fourteen pigs were randomly divided into three groups: sham (n=4), SAH (n=5), or SAH + nimodipine (n=5). The SAH model was established by injecting fresh autologous nonheparinized arterial blood into the suprasellae cistern. Nimodipine or saline placebo (0.04 g/mL) were administered to the operative area on the fourth day after the SAH model was established. The cerebral blood flow (CBF) was measured 60 min after topical administration of nimodipine by cranial SPECT/CT scans with 5 mCi 99mTc-ECD injected intravenously. The CCR (corticocebellar ratio) was calculated by dividing the counts/voxel of the whole cerebral hemisphere by the average count/voxel in the cerebellar region of reference and RD (relative dispersion). A predictor for impaired autoregulation of CBF was calculated by dividing standard deviation (SD) of regional perfusion by mean perfusion (RD=SD/Mean). CCR and RD were applied to describe hemisphere CBF and perfusion heterogeneity. Cerebral perfusion significantly decreased in the SAH group (CCR: 1.382±0.192, RD: 0.417±0.015) compared to sham (CCR: 1.988±0.346, RD 0.389±0.015) (p<0.05). Abnormal cerebral perfusion status, however, was not significantly improved in the nimodipine + SAH group (CCR: 1.503±0.107, RD: 0.425±0.018) compared to the SAH group (p>0.05). Topical administration of nimodipine did not significantly improve CBF following SAH. These findings were not consistent with our previous data demonstrating that the topical administration of nimodipine significantly alleviates cerebral vasospasm following SAH detected by TCD. Potential mechanisms governing these disparate outcomes require further investigation.

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The Impact of Subarachnoid Hemorrhage on Regional Cerebral Blood Flow and Large-vessel Diameter in the Canine Model of Chronic Vasospasm

Cited by 4 publications

References 54 publications

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

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

Does Prevention of Vasospasm in Subarachnoid Hemorrhage Improve Clinical Outcome? Yes

Effects of Topical Administration of Nimodipine on Cerebral Blood Flow following Subarachnoid Hemorrhage in Pigs

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