spinal cord ischemia
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2022 ◽  
Vol 17 (3) ◽  
pp. 650-655
Author(s):  
Fjolla Hyseni ◽  
Diana Hla ◽  
Abu Bakar Siddik ◽  
Ilir Ahmetgjekaj ◽  
Valon Vokshi ◽  
...  

2021 ◽  
Author(s):  
Cheng Wu ◽  
Qinghua Zhu ◽  
Yi Yao ◽  
Zhaoyang Shi ◽  
Chaojie Jin ◽  
...  

Background: Spinal cord ischemia/reperfusion injury (SCIRI) is usually caused by spinal surgery or aortic aneurysm surgery and can eventually lead to paralysis or paraplegia and neurological dysfunction. Exosomes are considered as one of the most promising therapeutic strategies for SCIRI as they can pass the blood-spinal barrier. Previous studies have proved that exosomes secreted by osteocytes have a certain slowing effect on SCIRI. Aim: We aimed to explore the effect of osteoblast secreted exosomes on SCIRI. Methods: Firstly, neurons and osteoblasts were co-cultured under different conditions. GEO database was utilized to detect the expression of miR-23a-3p in osteoblast exosomes. SCIRI cells were treated with exosomes, and the detection was taken to prove whether miR-23a-3p could slow the progression of SCIRI. Downstream gene and the potential regulatory mechanism were explored through database and functional experiments. Results: MiR-23a-3p was highly expressed in exosomes and it slowed down the process of SCIRI. Downstream mRNA KLF3 could bind to miR-23a-3p and was highly expressed in IRI. Moreover, CCNL2 was regulated by KLF3 and was highly expressed in IRI. Rescue experiments verified that miR-23a-3p suppressed the transcription of CCNL2 by targeting KLF3. Conclusion: Exosome miR-23a-3p from osteoblast alleviates SCIRI by down-regulating KLF3-activated CCNL2 transcription.


2021 ◽  
pp. 152660282110594
Author(s):  
Christos Argyriou ◽  
Stavros Spiliopoulos ◽  
Konstantinos Katsanos ◽  
Nikolaos Papatheodorou ◽  
Miltos K. Lazarides ◽  
...  

Purpose: Thoracic endovascular aortic aneurysm repair (TEVAR) has emerged as an attractive alternative option in the treatment of thoracoabdominal aortic aneurysm (TAAA) diseases, reporting lower morbidity and mortality rates compared with open or hybrid repair. A challenging situation arises when the aneurysm involves the celiac artery (CA), precluding a safe distal landing zone. We investigated the safety and efficacy of CA coverage in the treatment of complex TAAA diseases during endovascular management. Materials and Methods: A review of the literature was conducted in accordance with the Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines. The electronic bibliographic sources searched were MEDLINE and SCOPUS databases. Primary outcomes of interest were perioperative and 30-day mortality. Any type of endoleak, mesenteric ischemia, perioperative spinal cord ischemia, and reintervention rates were secondary end points. A random-effects meta-analysis was performed. Summary statistics of event risks were expressed as proportions and 95% confidence interval (CI). Results: Ten observational cohort studies published between 2009 and 2020, reporting a total of 175 patients, were eligible for quantitative synthesis. Indications for TEVAR were primary TAAAs in 82% of patients, aortic dissection in 14% of patients, type Ib endoleak after previous endograft deployment in 3% of patients, and penetrating aortic ulcer in 1 patient. Reintervention rate was 9% (95% CI, 4%–20%) and spinal cord ischemia was 7% (95% CI, 4%–-12%). Type II endoleak was the predominant type of endoleak in 10% of patients (95% CI, 4%–22%), followed by type I endoleak in 5% of patients (95% CI, 2%–12%) and type III endoleak in 1% (95% CI, 0%–16%) of patients. Mesenteric ischemia occurred in 6% of patients (95% CI, 3%–10%). Thirty-day mortality was 5% (95% CI, 2%–13%) and the pooled estimate for overall mortality was 21% (95% CI, 14%–31%). Conclusions: Celiac artery coverage during TEVAR is a challenging but feasible option for the treatment of TAAA diseases, providing acceptable morbidity and mortality rates. Demonstration of adequate visceral collateral pathways before definitive CA coverage is the sine quo non for the success of the technique.


2021 ◽  
Vol 15 ◽  
Author(s):  
Zhengran Yu ◽  
Xing Cheng ◽  
Jiacheng Chen ◽  
Zhong Huang ◽  
Shaofu He ◽  
...  

Cervical spondylotic myelopathy (CSM) is a degenerative condition of the spine that caused by static and dynamic compression of the spinal cord. However, the mechanisms of motor and somatosensory conduction, as well as pathophysiological changes at dynamic neck positions remain unclear. This study aims to investigate the interplay between neurophysiological and hemodynamic responses at dynamic neck positions in the CSM condition, and the pathological basis behind. We first demonstrated that CSM patients had more severe dynamic motor evoked potentials (DMEPs) deteriorations upon neck flexion than upon extension, while their dynamic somatosensory evoked potentials (DSSEPs) deteriorated to a similar degree upon extension and flexion. We therefore generated a CSM rat model which developed similar neurophysiological characteristics within a 4-week compression period. At 4 weeks-post-injury, these rats presented decreased spinal cord blood flow (SCBF) and oxygen saturation (SO2) at the compression site, especially upon cervical flexion. The dynamic change of DMEPs was significantly correlated with the change in SCBF from neutral to flexion, suggesting they were more sensitive to ischemia compared to DSSEPs. We further demonstrated significant vascular redistribution in the spinal cord parenchyma, caused by angiogenesis mainly concentrated in the anterior part of the compressed site. In addition, the comparative ratio of vascular densities at the anterior and posterior parts of the cord was significantly correlated with the perfusion decrease at neck flexion. This exploratory study revealed that the motor and somatosensory conductive functions of the cervical cord changed differently at dynamic neck positions in CSM conditions. Compared with somatosensory conduction, the motor conductive function of the cervical cord suffered more severe deteriorations upon cervical flexion, which could partly be attributed to its higher susceptibility to spinal cord ischemia. The uneven angiogenesis and vascular distribution in the spinal cord parenchyma might underlie the transient ischemia of the cord at flexion.


2021 ◽  
Vol 29 (1) ◽  
Author(s):  
Kentaro Kiryu ◽  
Hiroshi Yamamoto ◽  
Takayuki Kadohama ◽  
Daichi Takagi ◽  
Yoshinori Itagaki ◽  
...  

Abstract Background Degenerative aortic arch aneurysms are known to develop through a pathological process of arterial atherosclerosis, which could be accompanied by peripheral artery diseases and resultant development of intrapelvic collateral arteries to the ischemic lower limbs. The aim of this study was to investigate the relationship between peripheral collateral circulation and postoperative paraplegia after total arch repair with a frozen elephant trunk in patients with degenerative aortic arch aneurysms and peripheral artery diseases. Methods Between October 2014 and March 2020, 27 patients (20 men; 69.8 ± 7.7 years old) underwent total arch repair with a frozen elephant trunk. Two of the 27 patients developed paraplegia postoperatively. The patients were divided into two groups, spinal cord ischemia (SCI) group (2 patients) and no-SCI group (25 patients). The aortic shagginess score, arterial calcification (subclavian artery; hypogastric artery) score, and the number of hypogastric artery branches, assessed using preoperative contrast-enhanced computed tomography images, were compared between the two groups. Results The ankle brachial artery pressure index (i.e., lower side value each patient) was lower in the SCI group than that in the no-SCI group (0.64, 0.71, and 1.09±0.07, respectively). There was no difference between the two groups in the arterial calcification scores or the aortic shagginess score. The number of hypogastric artery branches was greater in the SCI group than in the no-SCI group (66, 66, and 30.7±7.5, respectively). Conclusions Enhanced collateral circulation to the ischemic lower limbs in patients with combination of degenerative aortic arch aneurysms and peripheral artery diseases may be involved in paraplegia the upper thoracic spinal cord injury after total arch repair with a frozen elephant trunk.


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