Objective To investigate the relationship between graded spinal cord ischemia/reperfusion injury and somatosensory evoked potentials(SEP),neurologic function score（NFS）and the histopathological changes of spinal cord. Methods Forty rabbits were randomized and equally divided into 4 groups: shamoperation group, ischemia for 30min, 45min and 60min groups. The spinal cord ischemiareperfusion injury model was created by occlusion of the abdominal aorta in rabbits. SEP was monitored before ischemia,5,10minutes after ischemia, 15, 30 minutes, 1,2, 24 and 48 hours after reperfusion. NFS was evaluated at 6,12,24 and 48 hours after reperfusion.The pathological changes of spinal cord were observed after reperfusion 48 hours. Results The pathological characters with mild,moderate and severe spinal cord ischemia/reperfusion injury could be simulated by declamping after 30， 45 and 60 minutes infrarenal aorta crossclamping. SEP amplitude returned to normal after reperfusion 15 minutes（Pgt;0.05）and SEP latency returned to normal after reperfusion 30 minutes（Pgt;0.05）during mild spinal cord ischemia/reperfusion injury.SEP amplitude returned to normal after reperfusion 30 minutes（Pgt;0.05）and SEP latency returned to normal after reperfusion 60 minutes（Pgt;0.05）during moderate spinal cord ischemia/reperfusion injury. SEP latency increased and SEP amplitude decreased during severe spinal cord ischemia/reperfusion injury,compared with other groups, there were significant differences in SEP latency and SEP amplitude by clamping the infrarenal aorta for 60min（Plt;0.01）. With graded spinal cord ischemia/reperfusion injury, compared with shamoperation group, spinal cord ischemiareperfusion groups had significant differences in NFS（Plt;0.01）. Conclusion SEP is much quicker in the recovery of amplitude than latency during spinal cord ischemia/reperfusion. SEP is a sensitive and accurate index for spinal cord function during ischemia/reperfusion injury. SEP monitoring spinal cord ischemia/reperfusion injury during operation provides experimental basis for clinical application.
Objective To investigate the targeted combination and anti-inflammatory effects of anti-intercellular adhesion molecule 1 (ICAM-1) targeted perfluorooctylbromide (PFOB) particles on myocardial ischemia-reperfusion injury in rat model. Methods Seventy-six adult Sprague Dawley rats (male or female, weighing 250-300 g) were selected for experiment. The models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery for 30 minutes in 30 rats. The expression of ICAM-1 protein was detected by immunohistochemistry staining at 6 hours after reperfusion, and the normal myocardium of 10 rats were harvested as control; then the content of interleukin 8 (IL-8) in serum was tested every 6 hours from 6 hours to 48 hours after reperfusion. The other 36 rats were randomly divided into 6 groups (n=6): ischemia-reperfusion injury model/targeted PFOB particles group (group A), ischemia-reperfusion injury model/untargeted PFOB group (group B), normal control/targeted PFOB particles group (group C), normal control/untargeted PFOB particles group (group D), ischemia-reperfusion injury model/normal saline group (group E), and sham operation group (group F). The ischemia-reperfusion injury models were established in groups A, B, and E; while a thread crossed under the coronary artery, which was not ligated after open-chest in group F. After 6 hours of reperfusion, 1 mL of corresponding PFOB particles was injected through juglar vein in groups A, B, C, and D, while 1 mL of nomal saline was injected in group E. Ultrasonography was performed in groups A, B, C, and D before and after injection. The targeted combination was tested by fluorescence microscope. The content of IL-8 was tested after 6 and 24 hours of reperfusion by liquid chip technology in groups A, B, E, and F. Results After 6 hours of reperfusion, the expression of ICAM-1 protein significantly increased in the anterior septum and left ventricular anterior wall of the rat model. The content of IL-8 rised markedly from 6 hours after reperfusion, and reached the peak at 24 hours. Ultrasonography observation showed no specific acoustic enhancement after injection of PFOB particles in groups A, B, C, and D. Targeted combination was observed in the anterior septum and left ventricular anterior wall in group A, but no targeted combination in groups B, C, and D. There was no significant difference in the content of IL-8 among groups A, B, and E after 6 hours of reperfusion (P gt; 0.05), but the content in groups A, B, and E was significantly higher than that in group F (P lt; 0.05). After 24 hours of reperfusion, no sigificant difference was found in the content of IL-8 between groups A and B (P gt; 0.05), but the content of IL-8 in groups A and B were significantly lower than that in group E (P lt; 0.05). Conclusion Anti-ICAM-1 targeted PFOB particles can target to bind and pretect injured myocardium of rat by its anti-inflammation effects.