New Determinants for Casual Peripheral Mechanism of Neurogenic Lung Edema in Subarachnoid Hemorrhage Due To Ischemic Degeneration of Vagal Nerve, Kidney and Lung Circuitry. Experimental Study

Abstract

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/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.