It is well known that neuronal death, clinically manifested as paresis or plegia, is the end result of many pathological events affecting the central nervous system. However, several aspects of pathophysiological mechanisms involved in the development of tetra- or paraplegia caused by spinal cord traumatic or ischemic damage are only insufficiently understood and their histopathological manifestations remain poorly documented. That is why the authors decided to report on light-microscopic changes observed in 30 μm thick spinal cord sections cut from L3-S1 segments processed by the Nauta staining method in a group of 6 dogs with ischemic paraplegia induced by 30 min of a high thoracic aorta occlusion, and in a different group of 6 dogs with traumatic paraplegia induced by 5 min spinal cord compression with 200 g metallic rod. Both experimental groups (ischemic and compression) of spinal cord injuries (SCI) comprised the same number of mongrel dogs of both sexes, weighing 18-25 kg. In addition, each of the experimental groups had 3 normal dogs that served as controls. All experimental procedures were accomplished under general anaesthesia induced by pentobarbital and maintained by a mixture of halothane and oxygen. Following the 72 hour survival period, all 18 animals were euthanized by transcardial perfusion with 3,000 ml of saline and fixed by 3,000 ml of 10 % neutral formaldehyde during deep pentobarbital anaesthesia. The histopathological manifestation of neural tissue damage caused by ischemia or compression was similar. The light-microscopic images in both groups were characterised by argyrophilia and the swelling of grey matter neurons. However, in the dogs with traumatic SCIs, the changes only reached about 750 μm cranially and caudally from the necrotic epicentre. These findings indicated that the events taking part in secondary spinal cord injury mechanisms are similar in both, ischemic as well as in traumatic SCI.
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