摘要
BACKGROUND： Capillaries are the only blood supply for optic nerves, which makes the system more vulnerable to impaired blood circulation. OBJECTIVE： To observe the ultrastructural changes in the optic nerves and capillaries in rabbits following intracanalicular segment injury to the optic nerve. DESIGN, TIME AND SETTING： Comparative, observational, pathological morphology was performed at the Department of Anatomy, Weifang Medical College from September to November 2007. MATERIALS： Models of intracanalicular segment injury to the optic nerve were induced in the right eye of thirty healthy, adult rabbits by a free-falling metal cylinder. The H-7500 transmission electron microscope was provided by Hitachi, Japan. METHODS： All rabbits were randomly assigned into experimental （n = 25） and control （n = 5） groups. Optic nerve specimens were obtained from the experimental group at 0.5, 6, 12, 48, and 96 hours, respectively, following injury. Ultrastructural changes to the optic nerves and their capillaries were observed by electron microscopy. Optic nerve injury was not established in the control group, but optic nerve specimens were collected similarly to the experimental group. MAIN OUTCOME MEASURES： Ultrastructural changes in the injured optic nerves and their capillaries. RESULTS： Thirty rabbits were included in the final analysis. In the control group, cross-sections of the optic nerves exhibited varied thicknesses with regularly arranged fibers. The axons appeared to be smooth with condensed myelin sheaths and oval mitochondria. The microtubules and microfilaments were clearly seen. The lumens of the capillaries were regular with densely arranged endothelial cells and visible mitochondria. In the experimental group, 30 minutes after injury to the optic nerves, swollen axons, sparse myelin sheath, disordered microtubules and microfilaments, swollen mitochondria, and a decreased number of pinocytosis vesicles and microfilaments in endothelial cells of the capillaries were observed. At 6 hours, medullary and vacuolar degeneration in the mitochondria, and swollen endothelial cells in the capillary, were visible. At 12 hours, these changes were more obvious. At 48 hours, granular dissolution of microtubules, microfilaments, and mitochondria, as well as diffuse degeneration of mitochondria in the endothelial cells, were observed. At 96 hours, axonal disintegration, vacuolar degeneration, and dilated capillaries were observed. CONCLUSION： During early stages, the injured intracanalicular optic nerve exhibited swollen axons with vacuolar degeneration, swollen and degenerated mitochondria, decreased number of microtubules and microfilaments, and dilated capillaries with increased permeability.
BACKGROUND： Capillaries are the only blood supply for optic nerves, which makes the system more vulnerable to impaired blood circulation. OBJECTIVE： To observe the ultrastructural changes in the optic nerves and capillaries in rabbits following intracanalicular segment injury to the optic nerve. DESIGN, TIME AND SETTING： Comparative, observational, pathological morphology was performed at the Department of Anatomy, Weifang Medical College from September to November 2007. MATERIALS： Models of intracanalicular segment injury to the optic nerve were induced in the right eye of thirty healthy, adult rabbits by a free-falling metal cylinder. The H-7500 transmission electron microscope was provided by Hitachi, Japan. METHODS： All rabbits were randomly assigned into experimental （n = 25） and control （n = 5） groups. Optic nerve specimens were obtained from the experimental group at 0.5, 6, 12, 48, and 96 hours, respectively, following injury. Ultrastructural changes to the optic nerves and their capillaries were observed by electron microscopy. Optic nerve injury was not established in the control group, but optic nerve specimens were collected similarly to the experimental group. MAIN OUTCOME MEASURES： Ultrastructural changes in the injured optic nerves and their capillaries. RESULTS： Thirty rabbits were included in the final analysis. In the control group, cross-sections of the optic nerves exhibited varied thicknesses with regularly arranged fibers. The axons appeared to be smooth with condensed myelin sheaths and oval mitochondria. The microtubules and microfilaments were clearly seen. The lumens of the capillaries were regular with densely arranged endothelial cells and visible mitochondria. In the experimental group, 30 minutes after injury to the optic nerves, swollen axons, sparse myelin sheath, disordered microtubules and microfilaments, swollen mitochondria, and a decreased number of pinocytosis vesicles and microfilaments in endothelial cells of the capillaries were observed. At 6 hours, medullary and vacuolar degeneration in the mitochondria, and swollen endothelial cells in the capillary, were visible. At 12 hours, these changes were more obvious. At 48 hours, granular dissolution of microtubules, microfilaments, and mitochondria, as well as diffuse degeneration of mitochondria in the endothelial cells, were observed. At 96 hours, axonal disintegration, vacuolar degeneration, and dilated capillaries were observed. CONCLUSION： During early stages, the injured intracanalicular optic nerve exhibited swollen axons with vacuolar degeneration, swollen and degenerated mitochondria, decreased number of microtubules and microfilaments, and dilated capillaries with increased permeability.
