scholarly journals Vascular Injury After Stenting ― Insights of Systemic Mechanisms of Vascular Repair ―

2021 ◽  
Author(s):  
Pilar Jimenez-Quevedo ◽  
Esther Bernardo ◽  
Maria del Trigo ◽  
Shuji Otsuki ◽  
Luis Nombela-Franco ◽  
...  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Hang Wang ◽  
Yang-Guang Yin ◽  
Hao Huang ◽  
Xiao-Hui Zhao ◽  
Jie Yu ◽  
...  

2018 ◽  
Vol 08 (04) ◽  
pp. 258-262
Author(s):  
Ahsin Manzoor Bhatti ◽  
Junaid Mansoor ◽  
Haroon Sabir Khan

Objective: To analyze errors in primary treatment of vascular injuries and delayed presentations of missed vascular injuries as a surrogate indicator of need for improved vascular surgical training of upcoming general surgeons. Materials and methods: This retrospective observational study was carried out at vascular surgery department of two tertiary care hospitals of Armed Forces from Jan 2012 to June 2017. Hospital records of all patients with vascular trauma were analyzed for presence of pitfalls in primary treatment and delayed presentation of missed vascular injuries which resulted in redo surgeries or adverse outcomes. Results: Out of 256 patients with vascular injury sequel 41 had either a problem in primary treatment or presented with delayed complications of missed injuries. The omissions can be divided into: missed injuries (24/41), technical errors in initial repair (12/24), reperfusion of mangled Extremity (3/41) and non availability of a surgeon capable of undertaking vascular repair. The commonest operative fault was failure to debride the vessel adequately and vascular repair under tension. The commonest primary assessment problem was failure to timely appreciate hard signs of vascular injury. Conclusion: With better training and emphasizing the need of thorough clinical examination outcome of vascular trauma can be improved.


Author(s):  
Jing Yan ◽  
Wen-Bin Wang ◽  
Yang-Jing Fan ◽  
Han Bao ◽  
Na Li ◽  
...  

Endothelial progenitor cells (EPCs) play a vital role in endothelial repair following vascular injury by maintaining the integrity of endothelium. As EPCs home to endothelial injury sites, they may communicate with exposed vascular smooth muscle cells (VSMCs), which are subjected to cyclic stretch generated by blood flow. In this study, the synergistic effect of cyclic stretch and communication with neighboring VSMCs on EPC function during vascular repair was investigated. In vivo study revealed that EPCs adhered to the injury site and were contacted to VSMCs in the Sprague–Dawley (SD) rat carotid artery injury model. In vitro, EPCs were cocultured with VSMCs, which were exposed to cyclic stretch at a magnitude of 5% (which mimics physiological stretch) and a constant frequency of 1.25 Hz for 12 h. The results indicated that stretched VSMCs modulated EPC differentiation into mature endothelial cells (ECs) and promoted angiogenesis. Meanwhile, cyclic stretch upregulated the mRNA expression and secretion level of connective tissue growth factor (CTGF) in VSMCs. Recombinant CTGF (r-CTGF) treatment promoted endothelial differentiation of EPCs and angiogenesis, and increased their protein levels of FZD8 and β-catenin. CTGF knockdown in VSMCs inhibited cyclic stretch-induced EPC differentiation into ECs and attenuated EPC tube formation via modulation of the FZD8/β-catenin signaling pathway. FZD8 knockdown repressed endothelial differentiation of EPCs and their angiogenic activity. Wnt signaling inhibitor decreased the endothelial differentiation and angiogenetic ability of EPCs cocultured with stretched VSMCs. Consistently, an in vivo Matrigel plug assay demonstrated that r-CTGF-treated EPCs exhibited enhanced angiogenesis; similarly, stretched VSMCs also induced cocultured EPC differentiation toward ECs. In a rat vascular injury model, r-CTGF improved EPC reendothelialization capacity. The present results indicate that cyclic stretch induces VSMC-derived CTGF secretion, which, in turn, activates FZD8 and β-catenin to promote both differentiation of cocultured EPCs into the EC lineage and angiogenesis, suggesting that CTGF acts as a key intercellular mediator and a potential therapeutic target for vascular repair.


Vascular ◽  
2011 ◽  
Vol 21 (1) ◽  
pp. 27-30 ◽  
Author(s):  
Yunus Nazli ◽  
Necmettin Colak ◽  
Ismail Uras ◽  
Mahmut Komurcu ◽  
Omer Cakir

Although acute elbow dislocations are common orthopedic injuries, concomitant neurovascular injury is rare. Brachial artery transection can result from open elbow dislocation and responds well to vascular repair. Rapid evaluation and a high level of suspicion are essential to facilitate immediate treatment. Delay to identify vascular injury after elbow dislocation or reduction can potentially lead to limb ischemia, and potential loss of limb. We present a case of relatively rare transection of the brachial artery, with an accompanying traumatic open elbow dislocation in a 12-year-old boy.


2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Jiawen Lv ◽  
Junchao Zeng ◽  
Fukun Guo ◽  
Yiran Li ◽  
Mengying Xu ◽  
...  

2017 ◽  
Vol 3 (2g) ◽  
pp. 671-674
Author(s):  
Dr. Ramachandra N Badami ◽  
Dr. M Shantharam Shetty ◽  
Dr. M Ajith Kumar ◽  
Dr. Ashok Shetty ◽  
Dr. Lathika Shetty

2006 ◽  
Vol 203 (5) ◽  
pp. 1221-1233 ◽  
Author(s):  
Steffen Massberg ◽  
Ildiko Konrad ◽  
Katrin Schürzinger ◽  
Michael Lorenz ◽  
Simon Schneider ◽  
...  

The accumulation of smooth muscle and endothelial cells is essential for remodeling and repair of injured blood vessel walls. Bone marrow–derived progenitor cells have been implicated in vascular repair and remodeling; however, the mechanisms underlying their recruitment to the site of injury remain elusive. Here, using real-time in vivo fluorescence microscopy, we show that platelets provide the critical signal that recruits CD34+ bone marrow cells and c-Kit+ Sca-1+ Lin− bone marrow–derived progenitor cells to sites of vascular injury. Correspondingly, specific inhibition of platelet adhesion virtually abrogated the accumulation of both CD34+ and c-Kit+ Sca-1+ Lin− bone marrow–derived progenitor cells at sites of endothelial disruption. Binding of bone marrow cells to platelets involves both P-selectin and GPIIb integrin on platelets. Unexpectedly, we found that activated platelets secrete the chemokine SDF-1α, thereby supporting further primary adhesion and migration of progenitor cells. These findings establish the platelet as a major player in the initiation of vascular remodeling, a process of fundamental importance for vascular repair and pathological remodeling after vascular injury.


1996 ◽  
Vol 67 (2) ◽  
pp. 161-164 ◽  
Author(s):  
Martinus Bråten ◽  
Per Helland ◽  
Hans O Myhre ◽  
Anders Mølster ◽  
Terje Terjesen

Circulation ◽  
2016 ◽  
Vol 133 (11) ◽  
pp. 1093-1103 ◽  
Author(s):  
Xiaojia Huang ◽  
Zhiyu Dai ◽  
Lei Cai ◽  
Kai Sun ◽  
Jaehyung Cho ◽  
...  

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