ArticleFrontiers in cardiovascular medicine2022
Magnetic resonance analysis of deep cerebral venous vasospasm after subarachnoid hemorrhage in rabbits.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 1 citations in OpenAlex.
- Brain Lymphatic Dysfunction in Subarachnoid Hemorrhage: Pathophysiology and Clinical Implications.Biomolecules · 2026Review
- Cerebrovascular Responses in a Patient with Lundberg B Waves Following Subarachnoid Haemorrhage Assessed with a Novel Non-Invasive Brain Pulse Monitor: A Case Report.Medical devices (Auckland, N.Z.) · 2024Article
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7 authors at 1 institution in 1 country.
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Abstract
Objective: Arterial 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. Methods: Fourteen New Zealand rabbits were randomly divided into the SAH group ( Results: In 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. Conclusion: After 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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