The First Description of Auerbach Ganglia Injury by Acidic Blood Following Subarachnoid Hemorrhage: An Experimental Study

Introduction A significant, yet often overlooked, complication of subarachnoid hemorrhage (SAH) is the development of acidosis. Denervation atrophy is a recognized cause of neural ganglion damage following primary motor neuron damage, but the effect of tissue pH changes has not been thoroughly investigated. Aim This study investigates whether acidosis causes Auerbach ganglia damage following SAH. Methods Twenty-four hybrid rabbits were selected, and five (GI; n = 5) were used for the analysis of the Auerbach ganglia. Six animals (GII; n = 6) were allocated to the SHAM group, receiving 1 cc of saline. The remaining 13 animals (GIII; n = 13) were allocated to the study group, receiving 1 cc of autologous arterial blood injected into the cisterna magna to induce subarachnoid hemorrhage under general anesthesia. Blood pH values were recorded before the experiment, on the seventh day, and immediately before sacrifice. Animals were sacrificed after 1 week, and the degenerated neuron density of the Auerbach ganglia in 1 cm segments of the ascending colon was estimated. The pH values and degenerated Auerbach ganglia neuron densities (n/mm(3)) were compared using the Mann-Whitney U test. Results The presurgical blood pH values of all animals were 7.431 +/- 0.032. On the seventh day, pH values were 7.403 +/- 0.052 in GI; 7.395 +/- 0.024 in GII; and 7.264 +/- 0.045 in GIII. At the end of the experiment, pH values were 7.431 +/- 0.037 in GI; 7.395 +/- 0.062 in GII; and 7.330 +/- 0.035 in GIII. Degenerated neuron densities of Auerbach ganglia neurons were 13 +/- 4 in GI, 34 +/- 6 in the SHAM group, and 87 +/- 15 in GIII. The p values were: p < 0.005 for GII/GI; p < 0.0001 for GII/GIII; and p < 0.00005 for GI/GIII. Conclusion Acidosis is a potential causative factor of Auerbach ganglia degeneration following SAH, a phenomenon not previously described.

Journal

NEUROGASTROENTEROLOGY AND MOTILITY

Year

2026

Volume

38

Issue

1

ISSN

1350-1925

eISSN

1365-2982

DOI

10.1111/nmo.70214

WoS UID

WOS:001632506000001