scholarly journals Mechanism of Vascular Injury and Repair ― Importance of Lesion Morphology ―

2022 ◽  
Author(s):  
Setsu Nishino ◽  
Masashi Sakuma ◽  
Shichiro Abe ◽  
Shigeru Toyoda ◽  
Teruo Inoue
Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Alfonso Eirin ◽  
Sandra M Herrmann ◽  
Monika L Gloviczki ◽  
Xiangyang Zhu ◽  
Hui Tang ◽  
...  

Introduction: Morbidity and mortality attributable to hypertension are higher in African American (AAEH) compared to Caucasian essential hypertensive (EH) patients, possibly related to a differential effect on vascular injury and repair. While circulating endothelial progenitor cells (EPC) preserve endothelial integrity IEC detach from sites of injury and represent markers of vascular damage. We hypothesized that plasma levels of IEC and inflammatory markers would be higher in AAEH compared to EH patients. METHODS: Inferior vena cava levels of CD34+/KDR+ (EPC) and VAP-1+ (IEC) cells were measured by FACS in EH and AAEH under fixed sodium intake (150 mEq/d) and blockade of the renin-angiotensin-system, and compared to systemic levels in normotensive control subjects (n=19 each). Systemic levels of inflammatory cytokines and EPC homing factors were measured by Luminex. Results: Blood pressure, serum creatinine, lipids, antihypertensive medications, and EPC levels did not differ between EH and AAEH patients. Circulating IEC were higher in AAEH, and inversely correlated with EPC levels (Figure). Systemic levels of inflammatory cytokines and EPC homing factors were higher in AAEH compared to EH patients (Table), and correlated directly with IEC. Conclusion: Despite preserved kidney function and controlled BP, circulating inflammatory markers were elevated in AAEH and correlated with increased IEC and decreased EPC levels. Increased release of cytokines and IEC in AAEH may impair EPC reparative capacity and predispose to hypertensive vascular injury. This process may aggravate vascular damage and accelerate hypertension-related morbidity/mortality rates in AAEH.


2019 ◽  
Vol 9 (1) ◽  
pp. 204589401982694 ◽  
Author(s):  
Ashley S. Lindsey ◽  
Lydia M. Sullivan ◽  
Nicole A. Housley ◽  
Anna Koloteva ◽  
Judy A. King ◽  
...  

Herein we describe lung vascular injury and repair using a rodent model of Pseudomonas aeruginosa pneumonia-induced acute respiratory distress syndrome (ARDS) during: 1) the exudative phase (48-hour survivors) and 2) the reparative/fibro-proliferative phase (1-week survivors). Pneumonia was induced by intratracheal instillation of P. aeruginosa strain PA103, and lung morphology and pulmonary vascular function were determined subsequently. Pulmonary vascular function was assessed in mechanically ventilated animals in vivo (air dead space, PaO2, and lung mechanics) and lung permeability was determined in isolated perfused lungs ex vivo (vascular filtration coefficient and extravascular lung water). At 48 hours post infection, histological analyses demonstrated capillary endothelial disruption, diffuse alveolar damage, perivascular cuffs, and neutrophil influx into lung parenchyma. Infected animals displayed clinical hallmarks of ARDS, including increased vascular permeability, increased dead space, impaired gas exchange, and decreased lung compliance. Overall, the animal infection model recapitulated the morphological and functional changes typically observed in lungs from patients during the exudative phase of ARDS. At 1 week post infection, there was lung histological and pulmonary vascular functional evidence of repair when compared with 48 hours post infection; however, some parameters were still impaired when compared with uninfected controls. Importantly, lungs displayed increased fibrosis and cellular hyperplasia reminiscent of lungs from patients during the fibro-proliferative phase of ARDS. Control, sham inoculated animals showed normal lung histology and function. These data represent the first comprehensive assessment of lung pathophysiology during the exudative and reparative/fibro-proliferative phases of P. aeruginosa pneumonia-induced ARDS, and position this pre-clinical model for use in interventional studies aimed at advancing clinical care.


2003 ◽  
Vol 1 (8) ◽  
pp. 1699-1709 ◽  
Author(s):  
C. Davis ◽  
J. Fischer ◽  
K. Ley ◽  
I. J. Sarembock

2015 ◽  
Vol 11 (1) ◽  
pp. 45-60 ◽  
Author(s):  
Andrew Mitchell ◽  
Takeshi Fujisawa ◽  
David Newby ◽  
Nicholas Mills ◽  
Nicholas L Cruden

2020 ◽  
Vol 127 (12) ◽  
pp. 1488-1490
Author(s):  
Daniel Pérez-Cremades ◽  
Henry S. Cheng ◽  
Mark W. Feinberg

2015 ◽  
Vol 135 (1) ◽  
pp. 301-308 ◽  
Author(s):  
Kevin Casey ◽  
Jennifer Sabino ◽  
Elliot Jessie ◽  
Barry D. Martin ◽  
Ian Valerio

2009 ◽  
Vol 69 (Suppl 1) ◽  
pp. i57-i60 ◽  
Author(s):  
A J van Zonneveld ◽  
H C de Boer ◽  
E P van der Veer ◽  
T J Rabelink

VASA ◽  
2019 ◽  
Vol 48 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Cheong J. Lee ◽  
Rory Loo ◽  
Max V. Wohlauer ◽  
Parag J. Patel

Abstract. Although management paradigms for certain arterial trauma, such as aortic injuries, have moved towards an endovascular approach, the application of endovascular techniques for the treatment of peripheral arterial injuries continues to be debated. In the realm of peripheral vascular trauma, popliteal arterial injuries remain a devastating condition with significant rates of limb loss. Expedient management is essential and surgical revascularization has been the gold standard. Initial clinical assessment of vascular injury is aided by readily available imaging techniques such as duplex ultrasonography and high resolution computed tomographic angiography. Conventional catheter based angiography, however, remain the gold standard in the determination of vascular injury. There are limited data examining the outcomes of endovascular techniques to address popliteal arterial injuries. In this review, we examine the imaging modalities and current approaches and data regarding endovascular techniques for the management popliteal arterial trauma.


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