A light-microscopic study of an early phase of paraplegia induced by ischemia and reperfusion in dogs
2003
Sulla, I.,University of Veterinary Medicine, Kosice (Slovak Republic)
Several aspects of pathophysiologic mechanisms involved in the development of paraplegia induced by ischemia and reperfusion are only poorly understood and their histologic manifestation still remains incompletely documented. This inspired the authors to study light-microscopic changes of spinal cord neurons caused by a temporary high thoracic aorta occlusion and reperfusion. Nine adult mongrel dogs, weighing eighteen to twenty-five kilograms, were used in the study. Three animals served as sham controls, in six the thoracic aorta was constricted by a tourniquet applied on the vessel through a thoracotomy for thirty minutes, which was followed by thirty minutes of survival. The procedures were performed in general anaesthesia induced by pentobarbital (30 mg/kg i.v.), maintained with mixture of 1-2% halothane with oxygen. Experiments were finished by perfusion (3000 cc of saline) and fixation (3000 cc of 10% neutral formaldehyde) of all animals, then 30 microm thic sections from L3-S1 spinal cord segments were processed by the Nauta staining method. Light-microscopic changes in experimental animals were characterized by distinct argyrophilia of neurons in all but three superficial dorsal horn layers, of interneurons in zona intermedia, and motoneurons in ventral horn layers. Since normal neural cells are Nauta-negative, their silver impregnation after thirty minutes of ischemia, folloved by thirty of reperfusion, can be considered a histopatologic manifestation of an early phase of neuronal damage, leading, without treatment, to cell death and irreversible paraplegia.
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