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.

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 Development and Treatments of Inflammatory Cells and Cytokines in Spinal Cord Ischemia-Reperfusion Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Ping Zhu ◽  
Jia-xin Li ◽  
Masayuki Fujino ◽  
Jian Zhuang ◽  
Xiao-Kang Li
Keyword(s):  
Spinal Cord ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Aortic Surgery ◽  
Spinal Cord Ischemia ◽  
Inflammatory Cells ◽  
Cord Injury ◽  
Cytokine Antagonist ◽  
Anti Inflammatory Cytokine

During aortic surgery, interruption of spinal cord blood flow might cause spinal cord ischemia-reperfusion injury (IRI). The incidence of spinal cord IRI after aortic surgery is up to 28%, and patients with spinal cord IRI might suffer from postoperative paraplegia or paraparesis. Spinal cord IRI includes two phases. The immediate spinal cord injury is related to acute ischemia. And the delayed spinal cord injury involves both ischemic cellular death and reperfusion injury. Inflammation is a subsequent event of spinal cord ischemia and possibly a major contributor to spinal cord IRI. However, the development of inflammatory mediators is incompletely demonstrated. And treatments available for inflammation in spinal cord IRI are insufficient. Improved understanding about spinal cord IRI and the development of inflammatory cells and cytokines in this process will provide novel therapeutic strategies for spinal cord IRI. Inflammatory cytokines (e.g., TNF-αand IL-1) may play an important role in spinal cord IRI. For treatment of several intractable autoimmune diseases (e.g., rheumatoid arthritis), where inflammatory cytokines are involved in disease progression, anti-inflammatory cytokine antagonist is now available. Hence, there is great potential of anti-inflammatory cytokine antagonist for therapeutic use of spinal cord IRI. We here review the mediators and several possibilities of treatment in spinal cord IRI.

scholarly journals mRNA and miRNA expression profile reveals the role of miR-31 overexpression in neural stem cell

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Pengfei Li ◽  
Yuantao Gao ◽  
Xiao Li ◽  
Feng Tian ◽  
Fei Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neurons ◽  
Early Stage ◽  
Expression Profiles ◽  
Mirna Expression Profile ◽  
Control Group ◽  
Cord Injury ◽  
Candidate Target ◽  
Mirnas Expression

Abstract A detailed understanding of the character and differentiation mechanism of neural stem cells (NSCs) will help us to effectively utilize their transplantation to treat spinal cord injury. In previous studies, we found that compared with motor neurons (MNs), miR-31 was significantly high-expressed in NSCs and might play an important role in the proliferation of NSCs and the differentiation into MNs. To better understand the role of miR-31, we characterized the mRNA and miRNAs expression profiles in the early stage of spinal cord-derived NSCs after miR-31 overexpression. There were 35 mRNAs and 190 miRNAs differentially expressed between the miR-31 overexpression group and the control group. Compared with the control group, both the up-regulated mRNAs and miRNAs were associated with the stemness maintenance of NSCs and inhibited their differentiation, especially to MNs, whereas the down-regulated had the opposite effect. Further analysis of the inhibition of miR-31 in NSCs showed that interfering with miR-31 could increase the expression of MNs-related genes and produce MNs-like cells. All these indicated that miR-31 is a stemness maintenance gene of NSCs and has a negative regulatory role in the differentiation of NSCs into MNs. This study deepens our understanding of the role of miR-31 in NSCs, provides an effective candidate target for effectively inducing the differentiation of NSCs into MNs, and lays a foundation for the effective application of NSCs in clinic.

scholarly journals IKVAV-Containing Cell Membrane Penetrating Peptide Treatment Induces Changes in Cellular Morphology after Spinal Cord Injury

2016 ◽  
Vol 10 (11) ◽  
pp. 149 ◽  
Author(s):  
Soheila Kazemi ◽  
Wendy Baltzer ◽  
Hadi Mansouri ◽  
Karl Schilke ◽  
John Mata
Keyword(s):  
Spinal Cord ◽  
Cell Membrane ◽  
Motor Neurons ◽  
Light And Electron Microscopy ◽  
Cellular Morphology ◽  
Control Group ◽  
Spinal Cord Tissue ◽  
Compression Injury ◽  
Cord Injury ◽  
Membrane Spanning

A cell membrane spanning peptide was used to increase the concentration of the IKVAV motif within damaged mouse spinal cord tissue. This peptide was injected directly to the lesion 24 hours after spinal cord compression injury. Because the membrane-spanning portion of the peptide adheres to tissue upon injection with a long half-life we hypothesized that the bioactive IKVAV sequence will provide a sustained regenerative signal at the sight of injury. Five different groups of mice were used and cellular morphology observations were undertaken using light and electron microscopy. Three surgical control groups: IKVAV, peptide and mannitol; one surgical treatment group: IKVAV-peptide; and one non-surgical control group: normal, were used in this experiment. In this study, treatment with IKVAV-peptide after SCI resulted in an increased number of protoplasmic astrocytes, large active motor neurons, and regeneration of muscle bundles followed by behavioral improvement. In this paper, we describe the cellular differences between all groups.

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 Induction of Parkinson Disease-Related Proteins in Motor Neurons after Transient Spinal Cord Ischemia in Rabbits

2009 ◽  
Vol 29 (4) ◽  
pp. 752-758 ◽  
Author(s):  
Masahiro Sakurai ◽  
Takae Kawamura ◽  
Hidekazu Nishimura ◽  
Hiroyoshi Suzuki ◽  
Fumiaki Tezuka ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Western Blot ◽  
Motor Neurons ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Early Stage ◽  
Spinal Cord Ischemia ◽  
Balloon Catheter ◽  
Cord Injury ◽  
Double Label

The mechanism of spinal cord injury has been thought to be related to the vulnerability of spinal motor neuron cells against ischemia. However, the mechanisms of such vulnerability are not fully understood. We investigated a possible mechanism of neuronal death by immunohistochemical analysis for DJ-1, PINK1, and α-Synuclein. We used a 15-min rabbit spinal cord ischemia model, with use of a balloon catheter. Western blot analysis for DJ-1, PINK1, and α-Synuclein; temporal profiles of DJ-1, PINK1, and α-Synuclein immunoreactivity; and double-label fluorescence immunocytochemical studies were performed. Western blot analysis revealed scarce immunoreactivity for DJ-1, PINK1, and α-Synuclein in the sham-operated spinal cords. However, they became apparent at 8 h after transient ischemia, which returned to the baseline level at 1 day. Double-label fluorescence immunocytochemical study revealed that both DJ-1 and PINK1, and DJ-1 and α-Synuclein were positive at 8 h of reperfusion in the same motor neurons, which eventually die. The induction of DJ-1 and PINK1 proteins in the motor neurons at the early stage of reperfusion may indicate oxidative stress, and the induction of α-Synuclein may be implicated in the programmed cell death change after transient spinal cord ischemia.

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

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.

PROTECTIVE EFFECT OF SOME SALTS 2-AMINOETHANESULFONIC ACID IN AN EXPERIMENTAL MODEL OF DEGENERATIVE SPINAL CORD INJURY

2020 ◽  
pp. 41-47
Author(s):  
Semeleva E.V. ◽  
Blinova E.V. ◽  
Zaborovsky A.V. ◽  
Vasilkina O.V. ◽  
Shukurov A.S.
Keyword(s):  
Spinal Cord ◽  
Morphological Changes ◽  
Male Rats ◽  
Zinc Salt ◽  
Control Group ◽  
Morphological Studies ◽  
Cord Injury ◽  
The Central Nervous System ◽  
Acid Compound ◽  
Lateral Sclerosis

In this work, we studied the pharmacological activity of zinc and magnesium salts of 2-aminoethanesulfonic acid in white non-linear male rats with amyotrophic lateral sclerosis, which was modeled by neurotoxicantsimplication into the pelvic part of spinal cord. After the reproduction of the pathology in animals, the indices of motor activity were recorded in the Rotarod test, and morphological studies of spinal cord sections stained according to Nisl in the Belshovsky modification were carried out. It was shown that the magnesium salt of 2-aminoethanesulfonic acid (compound LHT-317) to a greater extent reduces the development of motor disorders in experimental animals compared with the control group on the 4th day of observation. The course of intravenous administration of the studied compounds of 2-aminoethanesulfonic acid did not inhibit morphological changes in the spinal cord that develop in degenerative-dystrophic pathology of the central nervous system: connections. Moreover, if, against the background of treatment with zinc salt, the total area of motor zones in animals of the experimental group exceeded that of control rats, then the number of motoneurons did not differ from the control.

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