ArticleFrontiers in neuroscience2026
Dysregulated sympathovagal interplay contributes to gastric mucosal injury following subarachnoid hemorrhage.
Article in Frontiers in neuroscience, 2026. 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
Background: The neural mechanisms underlying brain injury-induced gastric mucosal injury remain poorly defined, with conflicting evidence regarding vagal versus sympathetic dominance. This study aimed to characterize the temporal profile of gastric injury and autonomic nervous activity following subarachnoid hemorrhage (SAH), and to clarify the role of autonomic regulation in SAH-associated gastric pathogenesis. Methods: SAH was induced in rats by internal carotid artery puncture. Gastric mucosal injury was assessed macroscopically and histopathologically from 6 to 72 h post-SAH. Autonomic activity was evaluated through simultaneous electroneurogram recordings of gastric vagal and sympathetic nerve and measurement of tissue acetylcholine (ACh) and norepinephrine (NE) levels. Functional roles were probed via selective surgical and pharmacological interventions. Results: SAH induced gastric mucosal erosions/ulcerations within 6 h, peaking at 24 h. This injury was accompanied by elevated tissue levels of ACh (15.90 ± 6.00 vs. 7.86 ± 1.87 ng/mg; Conclusion: SAH-induced gastric mucosal injury involves dysregulated sympathovagal interplay, with the vagal pathway potentially playing a predominant role. Further studies are needed to elucidate the mechanisms linking SAH to autonomic dysregulation and consequent gastric mucosal injury.
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