Background. Hypoperfusion of the central nervous system has been found to be an often diagnosis of patients with neurological deficits. This condition is usually seen as a consequence of an inadequate nervous tissue blood supply which may be caused by various extra- or intraarterial factors. Objective. NO (nitric oxide) – related structures were investigated in the area around the central canal. Possible changes of these structures following incomplete aortic ischemia were hypothesized to be a result of the pathophysiological contribution of NO. Materials and Methods. Twelve experimental animals – rabbits were used in this study. A new model of long-term 70% aortic stenosis was performed and lumbosacral part of the spinal cord was investigated. Immunohistochemical method for visualization of neuronal NO synthase and histochemical method for NADPH-diaphorase were used in order to characterize NO-related neural structures. Traditional hematoxylin-eosin (HE) staining was used as well. Results. Morphological shape of pericentral structures was investigated in transverse sections of the spinal cord by using light microscopy. There were three time periods in which experimental animals were evaluated: one week, one month and three months following surgery. No change was seen during all time periods on sections stained by hematoxylin-eosin comparing to control samples. Results obtained by histochemical and immunohistochemical methods were almost identical, the only difference was seen inNADPH-d staining of vessels,which appeared onemonth following surgery.Three months of aortic stenosis caused visible changes in the spinal cord. The influence of hypoxia was only slightly seen in the change of morphological shape of neuronal bodies themselves. On the other side, neuropil developed picture of huge amount of neural processes in the background and showed strong intensity of both NOS and NADPH-diaphorase of staining. Three months after surgery, there were well developed vessels, visible by using NADPH-diaphorase staining. Conclusion. These resuIts suggest that NO is involved in pathophysiological processes in the spinal cord during long-term hypoperfusion. Key words: long-term incomplete ischemia, nitric oxide, spinal cord

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