{"title":"后交通动脉痉挛对蛛网膜下腔出血后动眼神经根轴突变性的预测作用:实验研究","authors":"M. Zeynal, M. Şahin","doi":"10.56766/ntms.1277530","DOIUrl":null,"url":null,"abstract":"Background: The oculomotor nerve root's medial aspect in the cisternal space is closely associated with the posterior communicating artery and receives blood supply from it. This study investigates whether ischemic damage to oculomotor nerve roots results from posterior communicating artery spasm in subarachnoid hemorrhages. \nMethods: A total of 18 rabbits participated in this study. Baseline pupil diameters were measured using sunlight and ocular tomography. Rabbits were divided into control (GI, n=5), SHAM (GII, n=5; 0.75 cc serum physiologic injection), and subarachnoid hemorrhage-induced groups (GIII, n=8; 0.75 cc autolog blood injection). Pupil diameters were re-measured after the experiment and daily for three weeks. The animals were observed for one week before euthanasia. The posterior communicating artery vasospasm index (VSI) was determined using the wall surface/lumen surface ratio. Stereological methods were employed to examine the normal and degenerated axon densities of the oculomotor nerves. The Kruskal-Wallis and Mann-Whitney U tests were used to evaluate degenerated axon density (n/mm2) and VSI values. A p-value of less than 0.005 was considered significant. \nResults: Degenerated axon numbers (n/mm2) and VSI values of the posterior communicating artery were as follows: 3±1/0.936±0.212 in GI; 18±4/1.578±0.235 in GII; and 212±34/2.515±0.347 in GIII. The p-values were p","PeriodicalId":371755,"journal":{"name":"New Trends in Medicine Sciences","volume":"110 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Predictive Role of Posterior Communicating Artery Spasm on Axonal Degeneration in Oculomotor Nerve Root Following Subarachnoid Hemorrhage: Experimental Study\",\"authors\":\"M. Zeynal, M. Şahin\",\"doi\":\"10.56766/ntms.1277530\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Background: The oculomotor nerve root's medial aspect in the cisternal space is closely associated with the posterior communicating artery and receives blood supply from it. This study investigates whether ischemic damage to oculomotor nerve roots results from posterior communicating artery spasm in subarachnoid hemorrhages. \\nMethods: A total of 18 rabbits participated in this study. Baseline pupil diameters were measured using sunlight and ocular tomography. Rabbits were divided into control (GI, n=5), SHAM (GII, n=5; 0.75 cc serum physiologic injection), and subarachnoid hemorrhage-induced groups (GIII, n=8; 0.75 cc autolog blood injection). Pupil diameters were re-measured after the experiment and daily for three weeks. The animals were observed for one week before euthanasia. The posterior communicating artery vasospasm index (VSI) was determined using the wall surface/lumen surface ratio. Stereological methods were employed to examine the normal and degenerated axon densities of the oculomotor nerves. The Kruskal-Wallis and Mann-Whitney U tests were used to evaluate degenerated axon density (n/mm2) and VSI values. A p-value of less than 0.005 was considered significant. \\nResults: Degenerated axon numbers (n/mm2) and VSI values of the posterior communicating artery were as follows: 3±1/0.936±0.212 in GI; 18±4/1.578±0.235 in GII; and 212±34/2.515±0.347 in GIII. The p-values were p\",\"PeriodicalId\":371755,\"journal\":{\"name\":\"New Trends in Medicine Sciences\",\"volume\":\"110 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"New Trends in Medicine Sciences\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.56766/ntms.1277530\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"New Trends in Medicine Sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.56766/ntms.1277530","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Predictive Role of Posterior Communicating Artery Spasm on Axonal Degeneration in Oculomotor Nerve Root Following Subarachnoid Hemorrhage: Experimental Study
Background: The oculomotor nerve root's medial aspect in the cisternal space is closely associated with the posterior communicating artery and receives blood supply from it. This study investigates whether ischemic damage to oculomotor nerve roots results from posterior communicating artery spasm in subarachnoid hemorrhages.
Methods: A total of 18 rabbits participated in this study. Baseline pupil diameters were measured using sunlight and ocular tomography. Rabbits were divided into control (GI, n=5), SHAM (GII, n=5; 0.75 cc serum physiologic injection), and subarachnoid hemorrhage-induced groups (GIII, n=8; 0.75 cc autolog blood injection). Pupil diameters were re-measured after the experiment and daily for three weeks. The animals were observed for one week before euthanasia. The posterior communicating artery vasospasm index (VSI) was determined using the wall surface/lumen surface ratio. Stereological methods were employed to examine the normal and degenerated axon densities of the oculomotor nerves. The Kruskal-Wallis and Mann-Whitney U tests were used to evaluate degenerated axon density (n/mm2) and VSI values. A p-value of less than 0.005 was considered significant.
Results: Degenerated axon numbers (n/mm2) and VSI values of the posterior communicating artery were as follows: 3±1/0.936±0.212 in GI; 18±4/1.578±0.235 in GII; and 212±34/2.515±0.347 in GIII. The p-values were p