Rapid Ischemic Preconditioning with a Short Reperfusion Time Prevents Delayed Paraplegia in a Rabbit Model

2011 ◽  
Vol 14 (5) ◽  
pp. 317
Author(s):  
Mehmet Ozkokeli ◽  
Mehmet Ugur Es ◽  
Ugur Filizcan ◽  
Murat Ugurlucan ◽  
Ahmet Sasmazel ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ischemic Preconditioning ◽  
Spinal Cord Ischemia ◽  
Rabbit Model ◽  
Aortic Aneurysms ◽  
Aortic Occlusion ◽  
Control Group ◽  
Protective Mechanisms ◽  
Group 13 ◽  
Histologic Evaluation

<p><b>Background:</b> Surgery for thoracic and thoracoabdominal aortic aneurysms can be complicated by a significant incidence of neurogenic deficits due to spinal cord ischemia. In this study, we investigated whether ischemic preconditioning (IPC) improves neurologic outcome in a rabbit model.</p><p><b>Methods:</b> Forty rabbits underwent infrarenal aortic occlusion. The IPC group (n = 20) had 10 minutes of aortic occlusion to induce spinal cord ischemia, 40 minutes of reperfusion, and 30 minutes of ischemia, whereas the control group (n = 20) had only 30 minutes of ischemia. Tarlov scoring (0, paraplegia; 4, normal) was used to evaluate neurologic functions 7 days later, and spinal cord segments (L4-L6) were stained with hematoxylin and eosin for histologic evaluation.</p><p><b>Results:</b> Complete paraplegia (grade 0) occurred in 15 (75%) of the 20 control animals, whereas in the IPC group, 13 (65%) of 20 animals were completely normal (grade 4) (<i>P</i> < .05).</p><p><b>Conclusion:</b> IPC is beneficial for protecting against neurologic damage after transient aortic occlusion in a rabbit model; however, the protective mechanisms are not clear.</p>

Evaluation of Rapid Ischemic Preconditioning in a Rabbit Model of Spinal Cord Ischemia

2003 ◽  
Vol 99 (5) ◽  
pp. 1112-1117 ◽  
Author(s):  
Meiko Kakimoto ◽  
Masahiko Kawaguchi ◽  
Takanori Sakamoto ◽  
Satoki Inoue ◽  
Hitoshi Furuya ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ischemic Preconditioning ◽  
Sham Group ◽  
Neuronal Damage ◽  
Spinal Cord Ischemia ◽  
Rabbit Model ◽  
Infrarenal Aorta ◽  
New Zealand White Rabbits ◽  
Histopathologic Evaluation ◽  
Group 5

Background Rapid ischemic preconditioning (IPC) has been shown to reduce cellular injury after subsequent cardiac and cerebral ischemia. However, the data on rapid IPC of the spinal cord is limited. The authors investigated whether pretreatment with sublethal ischemia of spinal cord can attenuate neuronal injury after spinal cord ischemia in rabbits. Methods Forty-seven male New Zealand white rabbits were randomly assigned to one of three groups (n = 15 or 16 each). In the IPC(-) group, the infrarenal aorta was occluded for 17 min to produce spinal cord ischemia. In the IPC(+) group, 5 min of aortic occlusion was performed 30 min before 17 min of spinal cord ischemia. In the sham group, the aorta was not occluded. Hind limb motor function was assessed at 3 h, 24 h, 4 days, and 7 days after reperfusion using Tarlov scoring (0 = paraplegia; 4 = normal). Animals were killed for histopathologic evaluation at 24 h or 7 days after reperfusion. The number of normal neurons in the anterior spinal cord (L4-L6) was counted. Results Neurologic scores were significantly higher in the IPC(+) group than the IPC(-) group at 3 and 24 h after reperfusion (P &lt; 0.05). However, neurologic scores in the IPC(+) group gradually decreased and became similar to those in the IPC(-) group at 4 and 7 days after reperfusion. At 24 h after reperfusion, the numbers of normal neurons were significantly higher in the IPC (+) group than in the IPC(-) group (P &lt; 0.05) and were similar between the IPC(+) and sham groups. At 7 days after reperfusion, there was no difference in the number of normal neurons between the IPC(+) and IPC(-) groups. Conclusion The results indicate that rapid IPC protects the spinal cord against neuronal damage 24 h but not 7 days after reperfusion in a rabbit model of spinal cord ischemia, suggesting that the efficacy of rapid IPC may be transient.

scholarly journals Immunohistochemical Analysis of the Spinal Cord Ischemia– Effect of Remote Ischemic Preconditioning in a Porcine Model

2018 ◽  
Vol 21 (3) ◽  
pp. 209 ◽  
Author(s):  
Henri Johannes Haapanen ◽  
Johanna Herajärvi ◽  
Hannu-Pekka Honkanen ◽  
Caius Mustonen ◽  
Hannu Tuominen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ischemic Preconditioning ◽  
Neuroprotective Effect ◽  
Spinal Cord Ischemia ◽  
Immunohistochemical Analysis ◽  
Limb Ischemia ◽  
Remote Ischemic Preconditioning ◽  
Control Group ◽  
Segmental Artery

Background: In experimental settings, remote ischemic preconditioning (RIPC) has shown a positive effect regarding spinal cord protection after local ischemia. In this study, we conducted spinal cord immunohistochemistry to demonstrate the protective effect of RIPC after 24 hours of the regional ischemia. Methods: Twenty piglets were randomized into an RIPC group (n = 10) and a control group (n = 10). The RIPC group underwent transient left hind limb ischemia before systematic left subclavian artery and segmental artery occlusion at the level of the diaphragm. Twenty-four hours later, the thoracic and lumbar spinal cords were harvested, and the oxidative stress markers were immunohistochemically analysed. Results: A total of 18 animals survived the 4-hour follow up (10 in the RIPC group, 8 in the control group) and 14 animals survived the 24-hour follow up (7 in each group). In the single sections of the spinal cord, the antioxidant pathway activation was seen in the RIPC group, as OGG1 and DJ-1/PARK7 activation was higher (P = .038 and P = .047, respectively). Conclusions: The results indicate that the neuroprotective effect of RIPC on the spinal cord after local ischemic insult remains controversial.

Protection against spinal cord ischemia with insulin-induced hypoglycemia

1987 ◽  
Vol 67 (5) ◽  
pp. 739-744 ◽  
Author(s):  
Claudia S. Robertson ◽  
Robert G. Grossman
Keyword(s):  
Spinal Cord ◽  
Blood Glucose ◽  
Lactic Acid Production ◽  
Spinal Cord Ischemia ◽  
Lactate Concentration ◽  
Rabbit Model ◽  
Control Group ◽  
Early Reperfusion ◽  
Occlusion Time ◽  
Extracellular Lactate

✓ The effect of insulin-induced reduction in blood glucose to 65 ± 20 mg/dl (mean ± standard deviation) on recovery of electrophysiological function and extracellular lactate concentration was studied in a rabbit model of spinal cord ischemia. These results were compared to findings in animals with spinal cord ischemia that either were fasted overnight (fasted group: blood glucose 97 ± 26 mg/dl) or had no pretreatment (control group: blood glucose 172 ± 65 mg/dl). The aorta was occluded until the postsynaptic waves of the spinal somatosensory evoked potentials (SSEP's) had been absent for 20 minutes, a period of ischemia that produces paraplegia in 100% of untreated rabbits. The total aortic occlusion time was not significantly different in the three groups. Recovery of the SSEP's was significantly better in the insulin-treated animals than in the fasted or control animals. The N3 wave of the SSEP's, which has been found to correlate best with neurological recovery, returned to 65% ± 48% of the preischemia amplitude in the insulin-treated animals, compared to 40% ± 34% in the fasted group and 26% ± 24% in the control animals. Extracellular lactate concentration in the spinal cord increased immediately after occlusion of the aorta, reached a plateau as the postsynaptic waves disappeared from the SSEP's, and then increased a second time during the first 15 minutes of reperfusion. The peak lactate concentration during ischemia and during reperfusion correlated with the preischemia glucose concentration (r = 0.60336 and r = 0.76930, respectively). Lactate concentration in the spinal cord was higher during ischemia and throughout the first 2 hours of reperfusion in the control and fasted animals than in the insulin-treated animals. During the 2nd hour of reperfusion, lactate concentration was significantly higher in the control animals than in the fasted animals. Reduction in blood glucose with insulin improves recovery of electrophysiological function after spinal cord ischemia, probably because of reduced lactic acid production, especially during the early reperfusion period.

Effect of repetitive ischemic preconditioning on spinal cord ischemia in a rabbit model

Life Sciences ◽  
2006 ◽  
Vol 79 (15) ◽  
pp. 1479-1483 ◽  
Author(s):  
Qi Jing YU ◽  
Yan Ling Wang ◽  
Qing Shan Zhou ◽  
Hai Bo Huang ◽  
Shu Fang Tian ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ischemic Preconditioning ◽  
Spinal Cord Ischemia ◽  
Rabbit Model

Neuroprotective Effect of Epidural Electrical Stimulation against Ischemic Spinal Cord Injury in Rats

2005 ◽  
Vol 103 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Manabu Kakinohana ◽  
Hideki Harada ◽  
Yasunori Mishima ◽  
Tatsuhiko Kano ◽  
Kazuhiro Sugahara
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Electrical Stimulation ◽  
Neuroprotective Effect ◽  
Spinal Cord Ischemia ◽  
Aortic Occlusion ◽  
Cord Injury ◽  
Optimal Setting ◽  
Transient Aortic Occlusion ◽  
Ischemic Spinal Cord Injury

Background Electroconvulsion therapy is likely to serve as an effective preconditioning stimulus for inducing tolerance to ischemic brain injury. The current study examines whether electrical stimuli on the spinal cord is also capable of inducing tolerance to ischemic spinal cord injury by transient aortic occlusion. Methods Spinal cord ischemia was induced by occlusion of the descending thoracic aorta in combination with maintaining systemic hypotension (40 mmHg) during the procedure. Animals implanted with epidural electrodes were divided into four groups according to electrical stimulation and sham. Two groups consisted of rapid preconditioning (RE group, n = 8) and sham procedure (RC group, n = 8) 30 min before 9 min of spinal cord ischemia. In the two groups that underwent delayed preconditioning, rats were exposed to 9 min of aortic occlusion 24 h after either pretreatment with epidural electrical stimulation (DE group, n = 8) or sham (DC group, n = 8). In addition, rats were exposed to 6-11 min of spinal cord ischemia at 30 min or 24 h after epidural electrical stimulation or sham stimulation. The group P50 represents the duration of spinal cord ischemia associated with 50% probability of resultant paraplegia. Results Pretreatment with electrical stimulation in the DE group but not the RE group protected the spinal cord against ischemia, and this stimulation prolonged the P50 by approximately 15.0% in the DE group compared with the DC group. Conclusions Although the optimal setting for this electrical preconditioning should be determined in future studies, the results suggest that epidural electrical stimulation will be a useful approach to provide spinal protection against ischemia.

Percutaneous flexible bipolar epidural neuroelectrode for spinal cord stimulation

1984 ◽  
Vol 60 (6) ◽  
pp. 1317-1319 ◽  
Author(s):  
Alfred G. Kaschner ◽  
Wilhelm Sandmann ◽  
Heinz Larkamp
Keyword(s):  
Spinal Cord ◽  
Evoked Potentials ◽  
Epidural Space ◽  
Somatosensory Evoked Potentials ◽  
Spinal Cord Stimulation ◽  
Spinal Cord Ischemia ◽  
Aortic Occlusion ◽  
Content Type ◽  
Fine Print

✓ This article describes a new flexible bipolar neuroelectrode which is inserted percutaneously into the epidural space for segmental spinal cord stimulation. This electrode was used in experiments with dogs and monkeys for recording cortical somatosensory evoked potentials in order to identify intraoperative spinal cord ischemia during periods of aortic occlusion.

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