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

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.