scholarly journals Inductions of 3-l-Nitrotyrosine in Motor Neurons after Transient Spinal Cord Ischemia in Rabbits

1998 ◽  
Vol 18 (11) ◽  
pp. 1233-1238 ◽  
Author(s):  
Masahiro Sakurai ◽  
Naoto Fukuyama ◽  
Shunya Takizawa ◽  
Koji Abe ◽  
Takeshi Hayashi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neurons ◽  
Cell Damage ◽  
Spinal Cord Ischemia ◽  
Control Group ◽  
Tyrosine Nitration ◽  
Transient Ischemia ◽  
Ischemic Group ◽  
Strong Immunoreactivity ◽  
Time Point

The induction and distribution of 3-l-nitrotyrosine (NO2-Tyr) were examined with HPLC and immunohistochemistry in rabbit spinal cords after 15 minutes of transient ischemia until 7 days of the reperfusion. After the 15-minute ischemia, there was a significant decrease of neurologic scores in the ischemic group compared with the sham-operated control group at 7 days of reperfusion ( P = 0.0017), and the majority of motor neurons was selectively lost at 7 days of reperfusion ( P = 0.0039). NO2-Tyr was transiently induced at 8 hours of reperfusion in the ventral part of the spinal cord (0.47% ± 0.86%, NO2-Tyr/total tyrosine; P = 0.0021), but was not induced at any time point of reperfusion in the dorsal part of the spinal cord. Strong immunoreactivity for NO2-Tyr was selectively induced in large pyramidal motor neurons at 8 hours of reperfusion and was still weakly present until 7 days of reperfusion. (There may be a difference in sensitivity between the two techniques.) These results suggested that protein tyrosine nitration by nitric oxide plays a role in the selective motor neuron cell damage after transient spinal cord ischemia.

scholarly journals Effect of coenzyme Q10 on spinal cord ischemia-reperfusion injury

2015 ◽  
Vol 22 (4) ◽  
pp. 432-438 ◽  
Author(s):  
Jin-Young Hwang ◽  
Seong-Won Min ◽  
Young-Tae Jeon ◽  
Jung-Won Hwang ◽  
Sang-Heon Park ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Reperfusion Injury ◽  
Motor Neurons ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coenzyme Q ◽  
Spinal Cord Ischemia ◽  
Neurological Function ◽  
Saline Control ◽  
Control Group

OBJECT Spinal cord ischemia remains a serious complication of thoracoabdominal aortic aneurysm surgery. Coenzyme Q10, a potent antioxidant, has been reported to exert a neuroprotective effect. In the present study, we evaluated the effect of coenzyme Q10 pretreatment on spinal cord ischemia-reperfusion injury. METHODS Male Sprague-Dawley rats were treated with either 300 mg/kg coenzyme Q10 (CoQ10 group, n = 12) or saline (control and sham groups, n = 12 for each group) for 5 days before ischemia. Spinal cord ischemia was induced in the control and CoQ10 groups. Neurological function was assessed using the Basso-Beattie-Bresnahan (BBB) motor rating scale until 7 days after reperfusion, and then the spinal cord was harvested for histopathological examinations and an evaluation of malondialdehyde level. RESULTS On post-reperfusion Day 1, the CoQ10 group showed higher BBB scores compared with those in the control group, although the difference was not significant. However, on Day 2, the CoQ10 group showed a significantly higher BBB score than the control group (14.0 [10.3–15.0] vs 8.0 [5.0–9.8], median [IQR], respectively; p = 0.021), and this trend was maintained until Day 7 (17.5 [16.0–18.0] vs 9.0 [6.5–12.8], respectively; p < 0.001). Compared with the control group, the CoQ10 group had more normal motor neurons (p = 0.003), fewer apoptotic changes (p = 0.003) and a lower level of tissue malondialdehyde (p = 0.024). CONCLUSIONS Pretreatment with 300 mg/kg coenzyme Q10 resulted in significantly improved neurological function and preservation of more normal motor neurons.

scholarly journals Profound Hypotension before Aortic Clamping Can Exacerbate Spinal Cord Ischemic Injury after Aortic Surgery in Rats

2020 ◽  
Vol 9 (11) ◽  
pp. 3395
Author(s):  
Chang-Hoon Koo ◽  
Jung-Hee Ryu ◽  
Jin-Young Hwang ◽  
Jin-Hee Kim ◽  
Hyun-Jung Shin ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neurons ◽  
Histopathological Examination ◽  
Aortic Surgery ◽  
Spinal Cord Ischemia ◽  
Motor Deficit ◽  
Control Group ◽  
Aortic Clamping ◽  
Cord Injury ◽  
Profound Hypotension

Spinal cord ischemia is one of the most serious complications of aortic repair in patients with acute aortic syndrome. However, the effect of hypotension before aortic clamping on spinal cord injury has not been documented. A total of 48 male Sprague-Dawley rats were randomly divided into four groups: the sham group; control group (mean arterial pressure (MAP) < 90% of baseline value before aortic clamping); mild hypotension group (MAP < 80%); and profound hypotension group (MAP < 60%). Spinal cord ischemia was induced using a balloon-tipped catheter placed in the descending thoracic aorta. Neurological function of the hind limbs was evaluated for seven days after reperfusion and recorded using a motor deficit index (MDI). The spinal cord was then harvested for histopathological examination and evaluation of oxidative stress and inflammation. The profound hypotension group demonstrated a significantly higher MDI 48 h post-reperfusion and lower number of normal motor neurons than the other groups (p < 0.001). The levels of tissue malondialdehyde and tumor necrosis factor-α (TNF-α) were also significantly increased in the profound hypotension group compared with other groups. Profound hypotension before aortic clamping can aggravate neurologic outcomes after aortic surgery by exacerbating neurologic injury and reducing the number of normal motor neurons.

Effects of HBO with reduction of iNOS and HIF -1α in motor neurons after transient spinal cord ischemia in rabbits

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S452-S452
Author(s):  
Noritaka Murakami ◽  
Masahiro Sakurai ◽  
Takashi Horinouchi ◽  
Jun Ito ◽  
Shin Kurosawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neurons ◽  
Spinal Cord Ischemia

scholarly journals Dexmedetomidine Attenuates Blood-Spinal Cord Barrier Disruption Induced by Spinal Cord Ischemia Reperfusion Injury in Rats

2015 ◽  
Vol 36 (1) ◽  
pp. 373-383 ◽  
Author(s):  
Bo Fang ◽  
Xiao-Qian Li ◽  
Bo Bi ◽  
Wen-Fei Tan ◽  
Gang Liu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neurons ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Beneficial Effects ◽  
Polymerase Chain ◽  
Underlying Mechanisms ◽  
Blood Spinal Cord Barrier ◽  
Metalloproteinase 9

Background/Aims: Dexmedetomidine has beneficial effects on ischemia reperfusion (I/R) injury to the spinal cord, but the underlying mechanisms are not fully understood. This study investigated the effects and possible mechanisms of dexmedetomidine on blood-spinal cord barrier (BSCB) disruption induced by spinal cord I/R injury. Methods: Rats were intrathecally pretreated with dexmedetomidine or PBS control 30 minutes before undergoing 14-minute occlusion of aortic arch. Hind-limb motor function was assessed using Tarlov criteria, and motor neurons in the ventral gray matter were counted by histological examination. The permeability of the BSCB was examined using Evans blue (EB) as a vascular tracer. The spinal cord edema was evaluated using the wet-dry method. The expression and localization of matrix metalloproteinase-9 (MMP-9), Angiopoietin-1 (Ang1) and Tie2 were assessed by western blot, real-time polymerase chain reaction, and immunofluorescence. Results: Intrathecal preconditioning with dexmedetomidine minimized the neuromotor dysfunction and histopathological deficits, and attenuated EB extravasation after spinal cord I/R injury. In addition, dexmedetomidine preconditioning suppressed I/R-induced increase in MMP-9. Finally, Dexmedetomidine preconditioning enhanced the Ang1-Tie2 system activity after spinal cord I/R injury. Conclusions: Dexmedetomidine preconditioning stabilized the BSCB integrity against spinal cord I/R injury by inhibition of MMP-9, and enhancing the Ang1-Tie2 system.

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.

scholarly journals The efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injury

2020 ◽  
pp. 254-260
Author(s):  
Yasar Karatas ◽  
Mehmet Fatih Erdi ◽  
Bulent Kaya ◽  
Fatih Keskin ◽  
İbrahim Kılınç ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Tnf Alpha ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Spinal Cord Tissue ◽  
Adalimumab Treatment

Objective: Paraplegia is a dangerous complication of thoracoabdominal aortic surgery. Various studies have been conducted on the prevention of this complication and some spinal cord protection methods have been proposed. However, there is not any modality that prevent the development of paraplegia certainly. In the I / R period, primary injury triggers secondary injury due to increased inflammation, apoptosis and free radical formation. In this study, we evaluated that the neuroprotective effect of adalimumab in spinal cord ischemia-reperfusion injury.  Materials and Methods: In total, 24 adult New Zealand rabbits were divided into three groups: Group 1, control; Group 2, ischemia-reperfusion by infrarenal aortic clamping; Group 3, adalimumab treated followed by ischemia. Tissue and plasma tumor necrosis factor alpha, interleukin 6, interleukin 10, thiobarbituric acid reactive substance, total oxidant status and total antioxidant status levels were analyzed as a marker of inflammation and oxidation. Histopathological evaluation of the tissues was performed, and apoptosis was evaluated by TUNNEL method. Results: I/R injury significantly increases plasma and spinal cord tissue at TNF alpha, TOS, TBARS, IL6 levels and reduces plasma and spinal cord tissue to TAS and IL10 levels. Adalimumab treatment significantly reduces plasma and spinal cord tissue to TNF alpha, TOS, TBARS, IL6 and increases plasma and tissue to TAS and IL10 levels. Conclusion: Adalimumab treatment significantly reduces the spinal cord neuronal damage score and the number of apoptotic cells. This paper aims to demonstrate the important neuroprotective effects of adalimumab on rabbit spinal cord I/R injury.

Neuroprotective Effects of Riluzole and Ketamine during Transient Spinal Cord Ischemia in the Rabbit

2000 ◽  
Vol 93 (5) ◽  
pp. 1303-1311 ◽  
Author(s):  
Jeroen Lips ◽  
Peter de Haan ◽  
Pieter Bodewits ◽  
Ivo Vanicky ◽  
Misa Dzoljic ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Ischemia ◽  
Initial Step ◽  
Balloon Occlusion ◽  
Saline Control ◽  
Control Group ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Lumbosacral Spinal Cord ◽  
Excitatory Neurotransmitters

Background Massive release of central excitatory neurotransmitters is an important initial step in ischemic neuronal injury, and modification of this process may provide neuroprotection. We studied the protective effects of the voltage-dependent sodium channel antagonist riluzole and the N-methyl-d-aspartate receptor antagonist ketamine on hind limb motor function and histopathologic outcome in an experimental model of spinal cord ischemia. Methods Temporary spinal cord ischemia was induced by 29 min of infrarenal balloon occlusion of the aorta in 60 anesthetized New Zealand white rabbits. Animals were randomly assigned to one of four treatment groups (n = 15 each): group C, saline (control); group R, riluzole, 8 mg/kg intravenously; group K, ketamine, 55 mg/kg intravenously; group RK, riluzole and ketamine. After reperfusion, riluzole treatment was continued with intraperitoneal infusions. Normothermia (38 degrees C) was maintained during ischemia, and rectal temperature was assessed before and after intraperitoneal infusions. Neurologic function, according to Tarlov's criteria, was evaluated every 24 h, and infarction volume and the number of eosinophilic neurons and viable motoneurons in the lumbosacral spinal cord was evaluated after 72 h. Results Neurologic outcome was better in groups R and RK than in groups C and K. All animals in group C (100%) and all animals but one in group K (93%) were paraplegic 72 h after the ischemic insult versus 53% in group R and 67% in group RK (P &lt; 0.01 each). More viable motoneurons were present in groups R and RK than in controls (P &lt; 0.05). Conclusions The data indicate that treatment with riluzole can increase the tolerance of spinal cord motoneurons to a period of normothermic ischemia. Intraischemic ketamine did not provide neuroprotection in this model.

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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