Soyalp, CelaleddinKocak, Mehmet NuriAhiskalioglu, AliAksoy, MehmetAtalay, CananAydin, Mehmet DumluOzmen, Sevilay2025-05-102025-05-1020190102-86501678-267410.1590/s0102-8650201900300000032-s2.0-85063249782https://doi.org/10.1590/s0102-865020190030000003https://hdl.handle.net/20.500.14720/15793Ahiskalioglu, Ali/0000-0002-8467-8171; Calikoglu, Cagatay/0000-0002-8569-494X; Aksoy, Mehmet/0000-0003-0867-8660Purpose: 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/mm(2)), atrophic glomerulus density (n/mm(3)) 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.eninfo:eu-repo/semantics/openAccessSubarachnoid HemorrhageRenal ArteryLungEdemaRabbitsNew Determinants for Casual Peripheral Mechanism of Neurogenic Lung Edema in Subarachnoid Hemorrhage Due To Ischemic Degeneration of Vagal Nerve, Kidney and Lung Circuitry. Experimental StudyArticle343Q4Q230892389WOS:000461476800002