Spinal cord protection: Development of a paraplegia-preventive solution

Ueno, Tetsuya; Furukawa, K; Katayama, Yukitoshi; Suda, Hisao; Itoh, Tsuyoshi

doi:10.1016/0003-4975(94)91083-9

Cited by 41 publications

(19 citation statements)

References 16 publications

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“…Particularly during early reperfusion, enormous amounts of superoxide radicals are produced; they disrupt cell membranes and promote an inflammatory state by activating monocytes and neutrophils via the production of inflammatory mediators. Eventually, the inflammatory response is perpetuated via the production of cytokines by microglia and activated neutrophils, thereby leading to further generation of these radicals [9,21] . Consequently, preventing lipid peroxidation appears to be important in the maintenance of cellular structural integrity and the prevention of neuronal injury associated with I/R [2][3][4] .…”

Section: Discussionmentioning

confidence: 99%

Methylene Blue Decreases Ischemia-Reperfusion (I/R)-Induced Spinal Cord Injury: An in vivo Study in an I/R Rabbit Model

Bardakçi¹,

Kaplan²,

Karadeniz³

et al. 2006

Eur Surg Res

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Objectives: To evaluate the effects of intravenous methylene blue (MB) administration on ischemia-reperfusion (I/R) injury of the spinal cord (SC). Methods: 16 rabbits were randomly assigned either to group M (n = 8; receiving MB, intervention group) or group C (n = 8; control group) and underwent a 30-min period of SC ischemia by clamping the abdominal aorta between the left renal artery and the aortic bifurcation. 15 min before clamping, rabbits received either intravenous MB (10 mg/kg; group M) or normal saline (group C). The two groups were compared 24 h postoperatively both histologically and for neurological function, using a Tarlov score. Measurements to determine levels of malondialdehyde (MDA) and glutathione (GSH) in the SC tissue were also performed. Results: Neurological impairment and spinal tissue MDA levels were significantly lower in animals treated with MB (p < 0.001). In contrast, spinal GSH levels were significantly higher in group M (p < 0.001). Histological examination revealed that the integrity of the SC was better preserved in the MB group, whereas cords from the control group exhibited evidence of acute neuronal injury. Conclusions: The prophylactic use of MB reduces neurological injury and improves clinical outcomes in the rabbit SC I/R model. These effects are probably mediated by the drug’s antioxidant properties.

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Section: Discussionmentioning

confidence: 99%

Methylene Blue Decreases Ischemia-Reperfusion (I/R)-Induced Spinal Cord Injury: An in vivo Study in an I/R Rabbit Model

Bardakçi¹,

Kaplan²,

Karadeniz³

et al. 2006

Eur Surg Res

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“…With each administration of 10 mg/kg dantrolene, mannitol was coadministered at 165 mg/kg; the total osmolarity of the injected solution was approximately 288 mosm, which is relatively isotonic. In studies showing reduced edema and neuroprotection by mannitol, dosages typically range between 1.0 -1.5 g/kg and produce a hypertonic bolus (e.g., Filbert et al, 1993;Ueno et al, 1994;Berger et al, 1994;Bareyre et al, 1997;Korenkov et al, 2000). However, mannitol has been reported to possess free radical scavenging properties (e.g., Willis et al, 1994;Jiang et al, 2001;Larsen et al, 2002) which may have provided an extra measure of neuroprotection.…”

Section: Discussionmentioning

confidence: 99%

A Viable Neuroprotection Strategy Following Soman-induced Status Epilepticus

Ballough¹,

Filbert²

2003

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information The present study examined the neuroprotective effectiveness of dantrolene in the prevention of soman-induced SRBD. (Dantrolene is FDA approved for the treatment of malignant hyperthermia.) The decision to consider this compound is based on its well-known mode of action in preventing the release of calcium from intracellular stores. In addition, we assessed possible synergistic overlap in the neuroprotective effectiveness of combined dantrolene and diazepam co-treatment. The combined neuroprotective effectiveness of diazepam+dantrolene is compared with that of diazepam+HU-2 I1 (dexanabinol). The present results provide strong evidence that, by blocking the release of calcium from intracellular stores, dantrolene synergistically augmented the neuroprotection produced by diazepam alone. ACKNOWLEDGMENTSThe authors wish to express their sincere gratitude to Joe Jaworski, Blair Hontz, Denise Fath, Mark Walters and Roy Railer for their expert technical assistance and efforts above and beyond the call of duty. In addition, the authors wish to extend special thanks to Dr. Harpal Mangat for greatly influencing the decision to administer dantrolene by i.v. injection. The authors are also grateful to MAJ Stephen Dalal for his expert instructions in rodent i.v. injection techniques. Considering that science does not progress in a vacuum, sincere appreciation is extended to Dr. Harpal Mangat and Dr. Robert Kan for stimulating and productive intellectual exchanges regarding various aspects of this study.111,o ABSTRACT It is well known that termination of seizures using anticonvulsant drug therapy is the most effective means of preventing soman-induced seizure-related brain damage (SRBD), i.e., neuronal necrosis resulting from glutamate-induced excitotoxicity. Somaninduced seizures, however, become refractive to anticonvulsant therapy within 40 minutes after onset and development of status epilepticus. Even in cases where seizure termination is successful, excitotoxicity that has already been initiated by seizures of sufficient duration (i.e., 15 minutes or longer) will continue to develop over the ensuing several hours in accordance with well-defined pathways leading to neuronal necrosis or apoptosis. Our laboratory has previously demonstrated proof of concept that a classical neuroprotective approach (i.e., the prevention of delayed calcium overload [Randall and Thayer, 1992]) can interrupt the excitotoxic sequence initiated by seizures and block the development of soman-induced SRBD; this has been accomplished...

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“…21) A number of pharmacological methods have been applied to treat traumatic spinal cord injury, reduce ischemic or reperfusion injury of the spinal cord, and prevent paraplegia. 20,22) The mechanism of I/R injury in peripheral nerves has been described in previous studies. 5,9,23,24) Ischemia, especially severe ischemia, results in the cessation of nerve blood flow, conduction block, and blood-nerve barrier disruption, with resulting endoneurial edema due to the generation of reactive oxygen species and subsequent IFD.…”

Section: Electrophysiological Assessmentsmentioning

confidence: 99%

Impact of Aortic Cross-Clamping Time on Peripheral Nerves: Experimental Model

Akdemır¹,

Akdemir

Çavuşoğlu

et al. 2015

ATCS

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Purpose: The present study investigated the correlation between extend aortic cross-clamping time and peripheral nerve injury on rats. Methods: 24 male, Sprague Dawley rats were divided into 3 groups; (a) control group: abdomen was directly closed after reached aorta, and followed by 72 hours, (b) shortterm ischaemia-reperfusion group: peripheral nerve ischemia was induced in rats by supraceliac aortic occlusion for 20 min followed by 72 h of reperfusion, (c) long-term ischaemia-reperfusion group: peripheral nerve ischemia was induced for 30 min followed by 72 h of reperfusion. Preoperative and postoperative, electromyography (EMG) recordings were done. End of 72 h, the sciatic nerves were harvested from each animal for histopathological and biochemical analysis. Results: The mean compound muscle action potential (CMAP) amplitude of long-term ischaemia-reperfusion group was statically significant reduced when compared to the control group (p <0.01). However, the mean distal latency value of long-term ischaemia-reperfusion group was statically significant increased (p <0.01). On the other hand, there were statically significant differences between the results of malondialdehyde, edema and ischemia fiber degeneration grades on control and long-term ischaemia-reperfusion group (p <0.001). Conclusion: This study demonstrated that the extending cross clamping time directly harms the peripheral nerve of rats.

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Spinal cord protection: Development of a paraplegia-preventive solution

Cited by 41 publications

References 16 publications

Methylene Blue Decreases Ischemia-Reperfusion (I/R)-Induced Spinal Cord Injury: An in vivo Study in an I/R Rabbit Model

Methylene Blue Decreases Ischemia-Reperfusion (I/R)-Induced Spinal Cord Injury: An in vivo Study in an I/R Rabbit Model

A Viable Neuroprotection Strategy Following Soman-induced Status Epilepticus

Impact of Aortic Cross-Clamping Time on Peripheral Nerves: Experimental Model

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