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BACKGROUND: Spinal cord ischemia-reperfusion injury is commonly seen in surgical treatments during extracorporeal circulation. Once it occurs, the consequences are serious. Therefore, it is of great significance to avoid the occurrence of spinal cord ischemia-reperfusion injury. Tetrandrine seems to protect spinal cord ischemia-reperfusion injury through multiple approaches. OBJECTIVE: To study the protective effect and mechanism of tetrandrine preconditioning on spinal cord ischemia-reperfusion injury in rabbits. METHODS: Forty-eight New Zealand rabbits were randomly divided into three groups (n=16 per group). Rabbit spinal cord ischemia-reperfusion model was made by using abdominal aorta occlusion. The sham operation group only exposed the abdominal aorta, but did not clamp the abdominal aorta while the abdominal aorta was clamped in the ischemia-reperfusion group for 30 minutes. Tetrandrine (22.5 mg/kg) was injected through the ear vein of the rabbit at 1 hour before operation in the tetrandrine pretreatment group. The abdominal aorta was then clamped for 30 minutes after opening the abdominal cavity, and then the rabbits were perfused for 48 hours. The motor function of hind limbs was evaluated by Tarlov scores at 24 hours and 48 hours after spinal cord ischemia-reperfusion injury in rabbits. The rabbits in each group were sacrificed after deep anesthesia and the lumbar spinal cord was taken out. Hematoxylineosin staining was used to observe the necrosis of spinal nerve cells in rabbits. Evans blue was used to observe the permeability of blood-spinal barrier; enzyme linked immunosorbent assay (ELISA) was used to test the expression of tumor necrosis factor-α; and mitochondrial permeability transition pore kit was adopted to measure the changes in fluorescence intensity to reflect the open changes of mitochondrial permeability transition pore. RESULTS AND CONCLUSION: Motor function scores of hind limbs: Compared with the sham operation group, the Tarlov scores were significantly lower in the ischemia-reperfusion group and tetrandrine pretreatment group at 24 hours and 48 hours after operation (P < 0.05), and the Tarlov scores in the ischemiareperfusion group were lower than those in the tetrandrine pretreatment group at 24 hours and 48 hours after operation (P < 0.05). Hematoxylin-eosin staining indicated that: the cell morphology was normal in the sham operation group; the necrotic nerve cells were noted in the other two groups, but tetrandrine pretreatment group was superior to the ischemia-reperfusion group. The permeability of Evans blue decreased significantly in the sham operation group compared with the other two groups (P < 0.05). Moreover, the permeability of Evans blue in the ischemia-reperfusion group was significantly higher than that in the tetrandrine pretreatment group (P < 0.05). Tumor necrosis factor-α level in the spinal cord was extremely lower in the sham operation group than the other two groups (P < 0.05). Compared with the tetrandrine pretreatment group, the level of tumor necrosis factor-α in the spinal cord was significantly increased in the ischemia-reperfusion group (P < 0.05). The fluorescence intensity of mitochondrial permeability transition pore was stronger in the sham operation group than the other two groups (P < 0.05), and lower in the ischemia-reperfusion group than the tetrandrine pretreatment group (P < 0.05). To conclude, tetrandrine preconditioning has a protective effect on spinal cord ischemia-reperfusion injury in rabbits, and its mechanism may be associated with protecting blood-spinal cord barrier, inhibiting the expression of tumor necrosis factor-α and inhibiting the opening of mitochondrial permeability transition pore. [ABSTRACT FROM AUTHOR]

Purpose: Radical oxygen species produced after injury counteracts antioxidant activity and frequently causes severe oxidative stress for the tissues. Alpha-lipoic acid is a powerful metabolic antioxidant with immunomodulatory effects which provides neuroprotection. The aim of this study is to investigate the neuroprotective and anti-apoptotic effects of alpha-lipoic acid on spinal cord ischemia–reperfusion. Methods: Twenty-four adult, male, New Zealand rabbits were divided into sham ( n = 8), control ( n = 8), and treatment groups ( n = 8). The abdominal aorta was clamped for 30 min by an aneurysm clip, approximately 1 cm below the renal artery and 1 cm above the iliac bifurcation in control and treatment groups. Only laparotomy was performed in the sham group. Twenty-five cubic centimeters of saline in control group and 100 mg/kg lipoic acid were administered intraperitoneally in the treatment group after closure of the incision. The animals were killed 48 h later. Spinal cord segments between L2 and S1 were harvested for analysis. Levels of nitric oxide, glutathione, malondialdehyde, advanced oxidation protein products, and superoxide dismutase were analyzed as markers of oxidative stress and inflammation. Caspase-3 activity was analyzed to detect the effect of lipoic acid on apoptosis. Results: In all measured parameters of oxidative stress, administration of lipoic acid significantly demonstrated favorable effects. Both plasma and tissue levels of nitric oxide, glutathione, malondialdehyde, and advanced oxidation protein products significantly changed in favor of antioxidant activity. There was no significant difference between the plasma superoxide dismutase levels of the groups. Histopathological evaluation of the tissues also demonstrated significant decrease in cellular degeneration and infiltration parameters after lipoic acid administration. However, lipoic acid has no effect on caspase-3 activity. Conclusions: Although further studies considering different dose regimens and time intervals are required, the results of the present study prove that alpha-lipoic acid has favorable effects on experimental spinal cord ischemia–reperfusion injury. [ABSTRACT FROM AUTHOR]

Background: The purpose of the study was to investigate and compare iloprost and levosimendan on spinal cord ischemia in an experimental model. Materials and Methods: The study was done in two stages. For the 4-hour short survival study, 50 New Zealand white rabbits were randomly allocated into five groups. Spinal cord ischemia was induced by clamping the aorta just below the left renal artery and just proximal to the aortic bifurcation with bulldog artery clamps. The aortic clamps were removed after 40 min and restoration of blood flow was verified visually. The groups were analyzed at 1 and 4 h after reperfusion. For the 48-hour survival study, two different groups (iloprost plus levosimendan, n = 10; saline-treated controls, n = 10) were analyzed at 24 and 48 h after reperfusion. Results: The neurologic status of the animals in the treatment and sham groups was better than that in the control group both at 1 and 4 h after reperfusion. Viability index values in the levosimendan, iloprost and iloprost plus levosimendan groups were statistically higher than in the control group indicating less or no neuronal damage. Discussion: The results suggest that levosimendan, as well as iloprost, may reduce ischemic damage in transient spinal ischemia and provide better neurologic outcome. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Unlabelled: We aimed to investigate the protective effects of trapidil after the occlusion of abdominal aorta and the reperfusion injury in lung. Eighteen New Zealand albino rabbits were used in the study. In six animals [group 1, ischemia-reperfusion (IR) group], the abdominal aorta was exposed and a microvascular clamp was placed in the infrarenal abdominal aorta for 60 min. After the ischemic period, the microvascular clamp was removed and reperfusion was provided for 2 h. After the reperfusion period, the lungs were removed carefully and specimens were prepared for histopathological and biochemical studies in appropriate conditions. In group 2 (study group), trapidil (Rocarnal, Rentschler-UCB GmbH, Kerpen, Germany) was administered intraperitoneally as a single dose 1 h prior to trial, the IR procedure was performed and lung specimens were prepared similar to group 1. In group 3 (sham group), the infrarenal abdominal aorta was exposed and lung specimens were prepared for histopathological and biochemical studies at the end of the study. Histopathological changes, malondialdehyde (MDA), nitric oxide (NO) and total sulfhydryl group (T-SH) levels were evaluated. There was a statistical difference between the IR group and study group regarding NO and MDA levels (P < 0.05 and P < 0.01, respectively), but this was not detected between the IR group and the sham group (P > 0.05). There was no statistical difference among the three groups regarding T-SH levels (P > 0.05). While a statistical difference was found between the sham group and study group in the NO level (P < 0.05), no statistical difference was found in the MDA level (P > 0.05). There was a statistical difference in interstitial edema, PMN infiltration and hemorrhage scores among the groups (P < 0.05). There was a statistical difference between the IR group and study group in PMN infiltration (P < 0.05), but this was not detected between the groups in interstitial edema and hemorrhage scores (P > 0.05). There was a statistical difference between IR group and sham group in interstitial edema, PMN infiltration and hemorrhage scores (P < 0.05). Statistical difference was found between the sham group and study group in interstitial edema and hemorrhage scores (P < 0.05), but not in PMN infiltration (P > 0.05).Conclusions: Infrarenal abdominal aortic occlusion and reperfusion causes lung injury. We conclude that trapidil has preventive effects in the lung tissue after IR injury. [ABSTRACT FROM AUTHOR]

• Lidocaine regional perfusion through abdominal aorta attenuates spinal cord IRI. • Lidocaine treatment has a dose-dependent neuroprotective effect. • The inhibition of EAAs release may be one of the mechanisms involved. In our previous study, we found that lidocaine, infused through the abdominal aorta, could protect the spinal cord against the ischemia-reperfusion (I/R) injury caused by aortic occlusion. However, whether lidocaine protective effects have dose-dependent properties and its underlying mechanisms still remain unclear. This study was designed to investigate whether regionally infused lidocaine could dose-dependently protect spinal cord against I/R injury in rabbits and its underlying mechanism. 46 New Zealand white rabbits were randomized into six groups: Group NS (normal saline control); Group L10 (lidocaine 10 mg/kg); Group L20 (lidocaine 20 mg/kg); Group L40 (lidocaine 40 mg/kg); Group L80 (lidocaine 80 mg/kg) and Group Sham. In Group NS, Group L10, Group L20, Group L40 and Group L80, spinal cord ischemia was induced by infrarenal aortic occlusion for 30 min. The sham group did not receive spinal cord ischemia. During the occlusion, normal saline or lidocaine at different doses was infused continuously through a catheter into the clamped abdominal aorta respectively. Neurologic behavior functions were assessed according to the Tarlov scale system at the moments of 0, 6, 24 and 48 h after reperfusion. The neural injuries were evaluated by the histological examination and the count of normal α-motor neurons in the ventral horn. The levels of excitatory amino acids (EAAs) in the spinal cord, including glutamate (Glu) and aspartic acid (Asp), were analyzed by high performance liquid chromatography with fluorescence detection. The Tarlov scales in the Group L20 and the Group L40 were significantly higher than those in the Group NS at 24 and 48 h after reperfusion (P < 0.05). 12.5 % animals in Group L40 and 25 % animals in Group L20 were paraplegic versus 75 % animals in Group NS at 48 h after reperfusion (P < 0.05). The median of normal α-motor neurons in the L20, L40 and L80 groups was 7.5, 9 and 5 respectively which was significantly higher than in the NS group (count 0, P < 0.05). The levels of L-ASP and L-Glu remarkably decreased in the Group L10 and the Group L40 compared to Group NS (P < 0.05). These data revealed that regional administration of lidocaine through the abdominal aorta can provide dose-dependent protection on spinal cord I/R in rabbits. Inhibition of EAA release may be one of the underlying mechanisms. [ABSTRACT FROM AUTHOR]