Comparison of the protective effects of direct ischemic preconditioning and remote ischemic preconditioning in a rabbit model of transient spinal cord ischemia

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 < 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 < 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.

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

The Heart Surgery Forum ◽

10.1532/hsf.1969 ◽

2018 ◽

Vol 21 (3) ◽

pp. 209 ◽

Cited By ~ 3

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.

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Advance in spinal cord ischemia reperfusion injury: Blood–spinal cord barrier and remote ischemic preconditioning

Life Sciences ◽

10.1016/j.lfs.2016.03.046 ◽

2016 ◽

Vol 154 ◽

pp. 34-38 ◽

Cited By ~ 6

Author(s):

Qijing Yu ◽

Jinxiu Huang ◽

Ji Hu ◽

Hongfei Zhu

Keyword(s):

Spinal Cord ◽

Reperfusion Injury ◽

Ischemic Preconditioning ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Spinal Cord Ischemia ◽

Remote Ischemic Preconditioning ◽

Blood Spinal Cord Barrier

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

The Heart Surgery Forum ◽

10.1532/hsf98.20111039 ◽

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

Background: 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.Methods: 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.Results: 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) (P < .05).Conclusion: IPC is beneficial for protecting against neurologic damage after transient aortic occlusion in a rabbit model; however, the protective mechanisms are not clear.

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Limb Remote Ischemic Preconditioning Protects the Spinal Cord from Ischemia–Reperfusion Injury

Anesthesiology ◽

10.1097/aln.0b013e3181d0486d ◽

2010 ◽

Vol 112 (4) ◽

pp. 881-891 ◽

Cited By ~ 43

Author(s):

Hai-Long Dong ◽

Yi Zhang ◽

Bin-Xiao Su ◽

Zheng-Hua Zhu ◽

Qiu-Han Gu ◽

...

Keyword(s):

Spinal Cord ◽

Enzyme Activity ◽

Antioxidant Enzyme ◽

Ischemic Preconditioning ◽

Ischemia Reperfusion ◽

Spinal Cord Ischemia ◽

Antioxidant Enzyme Activity ◽

Remote Ischemic Preconditioning ◽

Radical Scavenger ◽

Neurologic Function

Background It remains to be established whether spinal cord ischemic tolerance can be induced by limb remote ischemic preconditioning (RIPC), and the mechanisms underlying the neuroprotective effects of RIPC on the spinal cord need to be clarified. Methods Spinal cord ischemia was studied in New Zealand White rabbits. In experiment 1, all rabbits were subjected to 20-min spinal cord ischemia by aortic occlusion. Thirty minutes before ischemia, rabbits were subjected to sham intervention or RIPC achieved by bilateral femoral artery occlusion (10 min ischemia/10 min reperfusion, two cycles). Dimethylthiourea (500 mg/kg, intravenously), a hydroxyl radical scavenger, or vehicle was given 1 h before RIPC. Antioxidant enzyme activity was measured along with spinal cord histology and neurologic function. In experiment 2, rabbits were subjected to spinal cord ischemia, with or without RIPC. In addition, rabbits were pretreated with various doses of hexamethonium. Results RIPC improved neurologic function and reduced histologic damage. This was associated with increased endogenous antioxidant activity. Dimethylthiourea inhibited the protective effects of RIPC. In contrast, there was no effect of hexamethonium on the protective effect of RIPC. Conclusions An initial oxidative stress acts as a trigger to upregulate antioxidant enzyme activity, rather than the neural pathway, and plays an important role in the formation of the tolerance against spinal cord ischemia by limb RIPC.

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