Dysregulated sympathovagal interplay contributes to gastric mucosal injury following subarachnoid hemorrhage

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; p = 0.020) and NE (436.76 ± 131.97 vs. 223.66 ± 53.67 pg./mg; p = 0.009) at 24 h. By 72 h, autonomic nerve activity was amplified (e.g., vagal positive peak amplitude: 150.50 μV [84.50–360.25] vs. 101.19 μV [47.58–123.45]; p = 0.043; sympathetic peak-to-peak amplitude: 267.14 μV [150.50–492.00] vs. 131.00 μV [117.50–149.00]; p = 0.023). Both surgical vagotomy and sympathectomy attenuated the injury, reducing the total histopathological score (0.90 [0.60–1.45] and 0.88 [0.58–1.09] vs. 2.15 [1.65–3.77]; p = 0.022 and 0.003). Crucially, vagotomy demonstrated superior efficacy: it normalized the macroscopic erosion index (0.00 [0.00–0.00] vs. 13.00 [0.00–16.00]; p = 0.038) and significantly reduced tissue levels of both ACh (8.82 ± 1.72 vs. 15.90 ± 6.00 ng/mg; p = 0.033) and NE (177.94 ± 37.45 vs. 436.76 ± 131.97 pg./mg; p = 0.004), whereas sympathectomy primarily reduced NE ( p = 0.015). 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.