Key result
Experimental subarachnoid hemorrhage increases vagal axon degeneration, atrophic glomeruli, and neurogenic lung edema in rabbits.
Why the study?
To evaluate whether renal artery vasospasm-related low glomerular density or degeneration is related to neurogenic lung edema following subarachnoid hemorrhage.
Does subarachnoid hemorrhage induce neurogenic lung edema via vagal nerve degeneration and renal artery vasospasm in rabbits?
Does subarachnoid hemorrhage induce neurogenic lung edema via vagal nerve degeneration and renal artery vasospasm in rabbits?
Subarachnoid hemorrhage induces neurogenic lung edema in rabbits, potentially mediated by vagal nerve degeneration and subsequent renal artery vasospasm and glomerular atrophy.
Rabbit model links vagal degeneration and glomerular atrophy to higher NLE scores post-SAH; leaves open human relevance.
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.
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Soyalp et al. (2019) studied Subarachnoid hemorrhage and neurogenic lung edema (n=26). Injection of homologous blood into the sylvian cisterna (subarachnoid hemorrhage model) vs. Control and SHAM (saline injection) was evaluated on Degenerated vagal axon density, atrophic glomerulus density, and neurogenic lung edema (NLE) scores (p=<0.001). Experimental subarachnoid hemorrhage in rabbits significantly increased degenerated vagal axon density, atrophic glomerulus density, and neurogenic lung edema scores compared to controls (p<0.001).
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