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Background: Although posttraumatic mesenteric artery ischemia is attributed to various etiologies, sacral parasympathetic network/mesenteric artery relations have not been studied so far. The primary objective of this study is to elucidate whether there is a relationship between Onuf's nucleus ischemia and mesenteric artery vasospasm following subarachnoid hemorrhage (SAH)., Methods: This study was conducted on 22 rabbits. The animals were grouped as follows: 5 of animals control, 5 SHAM which saline was given, and 12 animals study group that was homologous blood injected into the spinal subarachnoid space at the Lı level. Neurodegeneration in Onuf's nucleus, axonal degeneration of S2 roots, and mesenteric arteries vasospasm indexes (VSI; Wall surface/Lumen surface), brachias of mesentery arteries in various tissues and ischemic mucosal changes of intestines of all animals were determined histopathologically. Important degenerative changes were detected in axons in S2 roots and Onuf's nucleus in severe mesenteric artery vasospasm observed., Results: The mean degenerated neuron density of Onuf's nucleus (n/mm 3 ), degenerated axon density in S2 roots (n/mm 2 ), and VSI values of mesenteric arteries of control, SHAM, and study groups were estimated as 5.00 ± 1.58, 4.00 ± 1.58, 1.76 ± 0.13; 18.29 ± 4.31, 11.00 ± 2.24, 2.23 ± 0.20; and 135.21 ± 30.75, 117.33 ± 22.11, 2.81 ± 0.44, respectively. Statistical analyses between the VSI values, mucosal ischemic changes degenerated neurons in Onuf's nucleus, and axons in S2 levels were meaningful (p < 0.005)., Conclusion: We interestingly noticed that Onuf's nucleus-S2 roots complex degeneration plays an important role in mesenteric artery vasospasm and the development of intestinal ischemic mucosal changes following SAH which has not been extensively mentioned in the literature., (Copyright © 2019. Published by Elsevier Taiwan LLC.)

Purpose: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage., Methods: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded., Results: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001)., Conclusion: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.