scholarly journals Preventive Effect of Edaravone Injection before Aortic Clamping for Spinal Cord Ischemia in a Rabbit Model

2016 ◽  
Vol 56 (8) ◽  
pp. 109-115
Author(s):  
Masahiro Sagane ◽  
Kiyoshi Chiba ◽  
Satoshi Kinebuchi ◽  
Shota Kita ◽  
Daijun Ro ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Ischemia ◽  
Rabbit Model ◽  
Preventive Effect ◽  
Aortic Clamping

Thoracoabdominalis aortakirekesztés során fellépő elektrofiziológiai változások a gerincvelőben

2020 ◽  
Vol 73 (4) ◽  
pp. 160-166
Author(s):  
Csaba Dzsinich ◽  
Péter Gloviczki ◽  
Gabriella Nagy ◽  
Klaudia Vivien Nagy
Keyword(s):  
Spinal Cord ◽  
Motor Evoked Potentials ◽  
Spinal Cord Ischemia ◽  
Experimental Studies ◽  
Neuron Specific Enolase ◽  
Neurological Complications ◽  
Neurologic Outcome ◽  
Published Data ◽  
Aortic Clamping ◽  
Sensory Evoked

Összefoglaló. A thoracoabdominalis aortakirekesztés okozta gerincvelő ischemia súlyos neurológiai következményeit számos klinikai és kísérleti tanulmány bizonyítja. E nehezen kiszámítható, súlyos szövődmény megelőzésének érdekében régi törekvés megfelelő intra- és posztoperatív monitorizálás kifejlesztése, ami előre jelzi a gerincvelő-funkció romlását, illetve a kialakuló celluláris károsodást. A legelterjedtebb, a klinikai gyakorlatban széles körben alkalmazott megoldás a gerincvelői kiváltott motoros potenciál (MEP) folyamatos ellenőrzése. Ritkábban alkalmazott – bár ígéretes – eljárás a biokémiai változások nyomon követése, ami a sejtszintű károsodás markereit használja fel az ischemia okozta változások felismerésére. Korábbi dolgozatunkban kutyákon végzett kísérleteink azon eredményeit ismertettük, amelyekben a 60 perces thoracoabdominalis aortakirekesztés okozta neurológiai változások és a perfúzió adatainak összefüggéseit tárgyaltuk. Jelen tanulmányunkban a gerincvelői motoros (MEP) és szenzoros (SEP) kiváltott potenciálok változásait vizsgáljuk a neurológiai végállapot vonatkozásában. Megállapítottuk, hogy SEP változásai a neurológiai károsodás mértékével értékelhető összefüggést nem mutatnak. A MEP-amplitúdó és -latencia értékei biztonsággal jelzik a fenyegető gerincvelő ischemiát. A neurológiai deficit mélységét (Tarlov 2,1,0) a MEP-értékek változásai numerikusan nem értékelhetően követik. Summary. Severe neurological complications of the thoracoabdominal aortic clamping were published in numerous clinical and experimental studies. These hardly predictable, devastating consequences demanded to develop a monitoring system which might detect impending level of spinal cord ischemia in time – in order to introduce or enhance protective procedures and prevent permanent neurological deficit. The most widely used monitoring in clinical practice is the continuous surveillance of the motor evoked potentials (MEP) during and after thoracoabdominal aortic clamping. Much less used, but promising opportunity is to control the metabolic changes and cellular integrity utilizing specific markers like liquor lactate and neuron specific enolase (NSE) etc. In our earlier study we published data of our canine experiment related to coherencies between neurological outcome and specific perfusion of the spinal cord during and after one hour thoracoabdominal aortic clamping. In the present paper we investigate the behavior of motor evoked (MEP) and sensory evoked (SEP) potentials related to neurological changes. We conclude the behavior of SEP values hardly correlate with the neurologic outcome, meanwhile decrease of MEP amplitude provides reliable signal for developing spinal cord ischemia. We could not confirm a numeric correlation of these data and the level of the final neurologic outcome.

A new method of intrathecal PO2, PCO2, and pH measurements for continuous monitoring of spinal cord ischemia during thoracic aortic clamping in pigs

Surgery ◽  
2000 ◽  
Vol 127 (5) ◽  
pp. 571-576 ◽  
Author(s):  
Lennart Christiansson ◽  
Anders Hellberg ◽  
Itaru Koga ◽  
Stefan Thelin ◽  
David Bergqvist ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Continuous Monitoring ◽  
Spinal Cord Ischemia ◽  
New Method ◽  
Ph Measurements ◽  
Aortic Clamping

scholarly journals Blood flow and vascular permeability during motor dysfunction in a rabbit model of spinal cord ischemia.

Stroke ◽  
1992 ◽  
Vol 23 (3) ◽  
pp. 367-373 ◽  
Author(s):  
T P Jacobs ◽  
O Kempski ◽  
D McKinley ◽  
A J Dutka ◽  
J M Hallenbeck ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Vascular Permeability ◽  
Spinal Cord Ischemia ◽  
Rabbit Model ◽  
Motor Dysfunction

196. A Novel Peroxynitrite Decomposition Catalyst Prevents Paralysis in a Rabbit Model of Spinal Cord Ischemia in Thoracic Aortic Stenting

2008 ◽  
Vol 144 (2) ◽  
pp. 264
Author(s):  
Mark L. Manwaring ◽  
Dorian J. deFreitas ◽  
Ken Salleng ◽  
Jacqueline C. Gustafson ◽  
Michael C. Stoner
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Ischemia ◽  
Rabbit Model ◽  
Aortic Stenting

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 < 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.

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.

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