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J Res Clin Med. 2020;8: 24.
doi: 10.34172/jrcm.2020.024
  Abstract View: 936
  PDF Download: 604

Original Article

The role of vagal ischemia on the destiny of Peyer’s patches: first experimental study

Sevilay Ozmen 1* ORCID logo, Onur Ceylan 1, Mehmet Dumlu Aydin 2, Erdem Karadeniz 3, Nazan Aydin 4, Elif Oral Ahiskalioglu 5, Tuba Demirci 6, Ismail Malkoc 7, Elif Demirci 1

1 Ataturk University, Medical Faculty, Department of Pathology, Erzurum, Turkey
2 Ataturk University, Medical Faculty, Department of Neurosurgery, Erzurum, Turkey
3 Ataturk University, Medical Faculty, Department of General Surgery, Erzurum, Turkey
4 Uskudar University, Department of Psychology, Humanities and Social Sciences Faculty, Istanbul, Turkey
5 Ataturk University, Medical Faculty Anesthesiology and Reanimation, Department of, Erzurum, Turkey
6 Ataturk University, Medical Faculty, Department of Histology, Erzurum, Turkey
7 Duzce University, Medical Faculty, Department of Anatomy, Erzurum, Turkey
*Corresponding Author: *Corresponding Author: Sevilay Ozmen MD, Ataturk University, Medical Faculty, Department of Pathology Erzurum Turkey, Phone +90 5337254072 Email: , Email: ertekozmen@gmail.com

Abstract

Introduction: The vagal network has a major potential role in the immune-life of Peyer’s patches, but there is no satisfying information if vagal ischemia causes Peyer’s patches (PP) disruption following subarachnoid hemorrhage (SAH).

Methods: Twenty-two rabbits were used as control (GI, n=5), “sham” (GII, n=5), and SAH (GIII, n=12) groups in this experiment. 0.5 cc saline for GII and 0.5 cc autologous blood for GIII was injected into cisterna magna of the rabbits. Four weeks later, they were euthanized. Their brains, vagal nerves, nodose ganglia, Peyer’s patches, and intestines were examined, using stereological methods. The Peyer’s patches volumes (PPVs)/intestine volume per cubic millimeter was accepted as PP injury score based on a total of 10 points.

Results: The mean degenerated neuron densities of the nodose ganglia and degenerated axon densities of vagal nerves were 5±2/mm3 and 6±2/mm2 in the GI, 13±4/mm3 and 89±16/mm2 in the GII and 321±83/mm3 and 293±88/mm2 in GIII. The mean PPVs and PP score were 8±1×106 µm3 /mm3 and 0-3 in the GI, 10±3×106 µm3 /mm3 and 4-7 in the GII, and 21±5×106 µm3 /mm3 and 8-10 in GIII. P<0.0001 in PPV/PP score/degenerated axon densities of vagal nerves; P<0.0005 in PPV/PP score/degenerated neuron densities of the nodose ganglia between GI/GIII; P<0.001 in (PPV/PP score)/degenerated axon densities of vagal nerves; P<0.005 in PPV/PP score/degenerated neuron densities of the nodose ganglia between GII/GIII; and P>0.05 in GI/GII were noted.

Conclusion: Vagal ischemia/insult may be responsible for PP denervation, and injury-induced dangerous intestinal immunodeficiency following SAH.

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Submitted: 01 May 2020
Accepted: 05 Jun 2020
ePublished: 24 Jun 2020
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