ArticleFrontiers in neurology2025
Association between cerebrospinal fluid acidosis and cerebral vasospasm and vacuolation following subarachnoid hemorrhage in a rabbit model.
Article in Frontiers in neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Subarachnoid hemorrhage (SAH) is a life-threatening neurological emergency often complicated by delayed cerebral vasospasm, a major cause of morbidity and mortality. Clinical observations indicate that cerebrospinal fluid (CSF) acidosis can develop after aneurysmal SAH and may be associated with delayed cerebral ischaemia. Methods: We examined the relationship between CSF acidosis, vasospasm severity, and vacuolation in a rabbit model of SAH. Twenty-four hybrid rabbits were randomized into control ( Results: CSF pH was significantly lower in the SAH group than in control or sham-controlled animals (overall mean 7.22 ± 0.03 vs. 7.35 ± 0.02 and 7.31 ± 0.01; Discussion: CSF acidosis, vacuolation, and vasospasm severity appear to be interconnected factors in the pathophysiology of SAH. CSF acidosis may contribute to vacuolation and, when profound, to vasospasm severity. However, vacuolation and vasospasm represent distinct pathological processes.
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