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

• Published in: Acta cirúrgica brasileira Vol. 34; no. 3
• Main Authors: Soyalp, Celaleddin, Kocak, Mehmet Nuri, Ahiskalioglu, Ali, Aksoy, Mehmet, Atalay, Canan, Aydin, Mehmet Dumlu, Cakir, Murteza, Calikoglu, Cagatay, Ozmen, Sevilay
• Format: Journal Article
• Language: English
• Published: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia 01.01.2019
• Subjects: Edema; Lung; Rabbits; Renal Artery; Subarachnoid Hemorrhage
• DOI: 10.1590/s0102-865020190030000003
• ISSN: 0102-8650

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/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.