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

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 < 0.001, Group-D/Group-B < 0.005, Group-C/Group-A < 0.005. Undiscovered effect of ischemic vagal network injuries should be regarded as a major cause of stress ulcerations following SAH which has not been mentioned in the literature.