Analysis of the effect of nervus vagus on gastric adenocancer development

Purposes: Failure of the autonomic nerves of the organs invites the inflammatory and tumoral process. Increased electrical potentials lead to a decrease in apoptosis and an increase in tumorogenesis. In this contect, vagal hyperactivity may cause gastric adenocarcinomas. In this study we investigated whether there was an association between a change in the histological composition of the neuroelectrical activity of the vagal nerves and the gastric tumor. Materials and Methods: Tumor cells and nerve cells with near-localized or tumor invasion were photographed in successive sections at 4x, 10x, 20x and 40x magnifications for sterotypic counts. During the course of the vagal nerve, axon density per milimeter squared, number of gastric ganglia, and neuronal densities were counted. Findings: As the tumor grade increased, the difference between the normal axon numbers was found to be significant. The difference between the degenerated axon numbers was found to be significant (P< 0.0001); Thus, it is concluded that; vagal nerve destruction may lead to tumor formation and also vagal nerve degeneration may be more in malignant tumors. VSI differences were found to be significant (P< 0.0005); more malignant tumors are likely to cause more vasoconstriction in the gastric arteries due to vagal nerve damage, which is thought to impair tumor feeding and may result in tumor necrosis. Thus, the invasion of the vagal nerves may be the criterion for malignancy, at first vagal nerve invasion has been evaluated for tumor while later as a result of denervation and vasospasm of the arteries feeding the tumor may reduce tumor size and this can be counted as an advantage. Conclusion: It is concluded that, vagal nerve injury may contribute to the progression of tumors.