Experimental Model of Bilateral Carotid Artery Occlusion: a Serial Study of the Optic Nerve in the Rat.
- Author:
Myoung Hee PARK
1
;
Jung Il MOON
;
Young Bin CHOI
Author Information
1. Department of ophthalmology, St.Mary's Hospital, Korea. jimoon@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Bilateral common carotid ligation;
Chronic ischemia;
Glaucoma;
Optic nerve
- MeSH:
Animals;
Brain;
Brain Injuries;
Carotid Arteries*;
Carotid Artery, Common;
Formaldehyde;
Glaucoma;
Hemodynamics;
Humans;
Ligation;
Models, Theoretical*;
Myelin Sheath;
Nerve Fibers;
Optic Nerve Diseases;
Optic Nerve Injuries;
Optic Nerve*;
Rats*;
Vacuoles
- From:Journal of the Korean Ophthalmological Society
2002;43(12):2570-2576
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: This study was performed to examine the serial alteration of the optic nerve in chronic ischemia-induced brain injury of albino rat, which might be an experimental model of ischemia-induced optic nerve disease and vasogenic glaucoma in human. METHODS: We ligated bilateral common carotid arteries so that the brain and optic nerve had permanent ischemic injuries. Serial alteration of the optic nerve was studied on postoperative 1 day, 3 day, 5 day, 1 week, 2 week, 4 week and 9 week. After fixing the brain by perfusing formaline through the left ventiricle, we dissected the brain and optic nerve and then made specimen for Hematoxilin-Eosin (HE) stain to observe the histopathology of the optic nerve. Kluiver-Barrera (KB) stain was performed to qualify the myelin injury and optic nerve injury status. RESULTS: The HE stain specimen showed increased spaces in the nerve fiber layer and increased number of vacuoles three days after the operation. The optic neve injury became augmented with time. The KB stain showed better-defined configuration of HE stain. CONCLUSIONS: We were able to notice that optic nerve injury was induced by the bilateral common carotid ligation in this chronic ischemic experimental model, which might be an help to the studies of ischemic optic nerve disease, neurodefensive mechanism, and the hemodynamic mechanism of glaucoma in human.
