A new described mechanisms of intestinal glandular atrophy induced by vagal nerve/Auerbach network degeneration following subarachnoid hemorrhage: The first experimental study

•Pathogenesis of neurogenic stress gastric ulceration has not been well investigated.•Vagal pathway injury may cause indirect sympathetic overactivity.•SAH induced vagal ischemia result in stress ulcer and intestinal atrophy. Stress ulcers is a trouble complication of subarachnoid hemorrhage (SAH). Although gastrointestinal ulcerations may be attributed to increased HCL secretion in SAH; the exact mechanism of that complication has not been investigated definitively. We studied if vagal network degeneration may cause intestinal atrophy following SAH. Study was conducted on 25 rabbits, with 5 control group (Group-A), 5 SHAM group (Group-B), and 15 SAH group via injection of autologue blood to cisterna magna. Seven animals followed for seven days (Early Decapitated-Group-C) and eight animals followed 21 days (Late Decapitated-Group-D). The vagal nodosal ganglia (NGs), Auerbach plexuses and goblet cells of duodenums were examined by current stereological methods and compared statistically. The mean numbers of degenerated axon density/mm2 of gastric branches of vagal nerves was 8 ± 2, 34 ± 11, 189 ± 49 and 322 ± 81 in the Group A, B, C, and D respectively. The mean numbers of degenerated neuron density/mm3 of NGs was 5 ± 2, 54 ± 7, 691 ± 87 and 2930 ± 410 in the Group A, B, C, and D respectively. The mean numbers of degenerated Auerbach neurons 2 ± 1, 4 ± 1, 12 ± 3 and 27 ± 5/mm3 in the Group A, B, C, and D respectively. The mean numbers of degenerated goblet cells/mm3 were 4.3 ± 1.02, 11.5 ± 0.26, 143 ± 26 and 937 ± 65 Group A, B, C, and D respectively. Statistical analysis showed that vagal network ischemia could cause intestinal bleeding and so atrophy in SAH progression. Statistical analyses of groups were; Group-D/Group-A