Background: The failure of autologous arteriovenous fistulas (AVFs) occurs primarily due to stenosis in the anastomotic site, which is mainly related to the development of neointimal hyperplasia (NIH). Therefore, we conducted a study to establish a novel approach to create aortocaval fistulas (ACFs) in adenine-induced (AD) chronic kidney disease (CKD) rats to study the NIH in the inferior vena cava.
Methods: Ten adult female rats received a 0.75% adenine-rich diet for 4 weeks to induce CKD and underwent ACF surgery. Ten healthy rats served as controls. A 5-10-mm segment of a vein immediately adjacent to that the portion of the vein used for creating the fistula was surgically removed at the time of creating the fistula, and reconstruction of the failed fistula from the same patient was used as controls. ACF was assessed using duplex scans and histopathological analyses.
Results: At the end of the experiment, AD rats showed higher serum creatinine and urea nitrogen than those of vehicle-treated rats. Remarkable histological changes in kidney tissues demonstrated successful CKD models. Sections of the ACF in AD rats and veins removed at the time of the reconstruction of the failed fistula of the patient demonstrated that the eccentric neointima formation is irregularly thickened, with several small vessels within a more cellular region of the neointima. Immunohistochemistry demonstrated the presence of myofibroblasts, contractile smooth muscle cells and macrophages within the neointima.
Conclusions: Our rat models with ACFs showed typical features of NIH in the formation of fistula stenosis, which can resemble clinical findings in uremic patients.
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http://dx.doi.org/10.1007/s10157-020-01927-3 | DOI Listing |
Eur Heart J
January 2025
State Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, Shanghai Heart Failure Research Center, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Background And Aims: Members of the CCN matricellular protein family are crucial in various biological processes. This study aimed to characterize vascular cell-specific effects of CCN5 on neointimal formation and its role in preventing in-stent restenosis (ISR) after percutaneous coronary intervention (PCI).
Methods: Stent-implanted porcine coronary artery RNA-seq and mouse injury-induced femoral artery neointima single-cell RNA sequencing were performed.
J Cardiothorac Surg
January 2025
The First Department of Cardiology, Beidahuang Industry Group General Hospital, Harbin, 150000, Heilongjiang Province, China.
Objective: it was to evaluate the efficacy and safety of rapamycin-eluting stents at different doses in the treatment of coronary artery narrowing in miniature pigs.
Methods: a total of 20 miniature pigs were randomly assigned into four groups: S1 group (low-dose rapamycin-coated stent, 55 µg/mm), S2 group (medium-dose rapamycin-coated stent, 120 µg/mm), S3 group (high-dose rapamycin-coated stent, 415 µg/mm), and D0 group (bare metal stent). The stent size was 3.
Acta Radiol
January 2025
Department of Radiology, Interventional Radiology, Sağlık Bilimleri Üniversitesi Ankara Dışkapı Yıldırım Beyazıt Eğitim ve Araştırma Hastanesi, Ankara, Türkiye.
Background: Carotid artery stenting (CAS) is an interventional management in preventing ischemic stroke caused by carotid artery stenosis. After the treatment with CAS, in-stent restenosis caused by neointimal hyperplasia may develop.
Purpose: This study aims to obtain a better determination of neointimal hyperplasia using superb microvascular imaging (SMI), which provides a high-quality visualization of the endoluminal lesions, and to compare these results with B-mode and Doppler ultrasound (US).
J Mater Sci Mater Med
January 2025
Department of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, PR China.
In-stent restenosis (ISR) following interventional therapy is a fatal clinical complication. Current evidence indicates that neointimal hyperplasia driven by uncontrolled proliferation of vascular smooth muscle cells (VSMC) is a major cause of restenosis. This implies that inhibiting VSMC proliferation may be an attractive approach for preventing in-stent restenosis.
View Article and Find Full Text PDFRegen Biomater
December 2024
Institute of Biomedical Engineering, College of Medicine, Southwest Jiaotong University, Chengdu, Sichuan 610031, China.
Modification of polylactic acid (PLA) is a promising strategy for the next generation of bioresorbable vascular stent biomaterials. With this focus, FeMOFs nanoparticles was incorporated in PLA, and then post loading of carbon monoxide (CO) was performed by pressurization. It showed FeMOFs incorporation increased hydrophilicity of the surface and CO loading, and CO release was sustained at least for 3 days.
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