Thesis Type: Expertise In Medicine
Institution Of The Thesis: Gazi University, Tıp Fakültesi, Turkey
Approval Date: 2010
Thesis Language: Turkish
Student: Hakan ÖZGÜL
Supervisor: VOLKAN SİNCİ
Abstract:Introduction and Objective: The most important neurological complications experienced in TAA surgery are paraplegia and paraparesis which are the results of spinal cord ischemia. Despite of there are lots of preventive procedures developed to reduce these complications, unfortunately none of these methods is enough itself. To protect the ischemia-reperfusion injury of the spinal cord while cross clamping, increasing the ischemic tolerance of spinal cord by pharmacological agents is one of the methods that considered and tried. Considering lots of pharmaceutical substance have been tried in this aspect, none of these approved as a complete success by the authority. The aim of this study is to evaluate the usability of iloprost as an ischemiareperfusion injury protector and consider iloprost’s effectivity with the synergy of ascorbic acid. Material and Method: We used 28 New Zealand Rabbits weighted between 2300- 2700 grams in this study. Ischemia formed with buldog clamps applied on Aorta just above the Renal Arteries for 30 minutes. The test subjects divided four groups: Sham group (n:7), Control group (n:7), Đloprost group (n:7), Đloprost + ascorbic acid group. The blood specimens obtained before aortic oclusion, oclusion ending, 6.th and 24.th hours of reperfusion. Blood specimens studied for biochemical parameters of neuron specific enolase and S100 β. In 48.th hour, the subjects evaluated neurologically with tarlov scale. After neurologic evaluation, the subjects sacrified with high doses of ketamine+xylazine and their thoracolomber level spinal cords extracted to be examined histopathologically with electron microscope. This histopathological evaluation focused on neurodegenerational determinants espicially nucleus, organel level damage and edema, myelined neural fibers structural degeneration, axoneme structure and pericapillary edema. Findings: There is a statically meaningful difference between neurological evaluation of the groups (p<0.05) and histopathological evaluation (p<0.001). As a result of this research; iloprost and ascorbic acid found to reduce the ischemiareperfusion tissue edema and concluded that ascorbic acid is protective in capillary level and iloprost is protective in neuronal edema. Both of these agents are not protective in organel level. If biochemical parameters regarded; beside the sham group, the other groups S100ß results peaks at first 6.th hour, the change of the 24.th hour of iloprost and ascorbic acid groups is not meaningful and the control group shows minimal decrease. The iloprost group’s first 24.th hour S100β value decrease is meaningful and corralates with histopathologic and neurologic assesments. This finding supports the thesis of ilioprost’s spinal cord protectivity. NSE assesments of our work is not corralated with histopathologic and neurologic results. The cause of this is thought to be the result of iloprost’s and ascorbic acid’s lack of the organel level protectivity. Iloprost and ascorbic acid decrease the ischemia reperfusion injury just because they reduce pericapillary and perineural edema. In this case NSE values found to be high because of the organel level injury happened in the tissue. Result: This experimental work’s statistical analysis report shows that; iloprost and iloprost + ascorbic acid groups subjects benefited the treatments. This can be seen either in histopathological and neurological results or in statistical conclusions outcome. As a result; implementation of iloprost and ascorbic acid before the ischemia and at the beginning of reperfusion is valuable in spinal cord protection and combining this method with other protective techniques in TAA surgery will reduce neurologic complications in this patience group.