A Novel Murine Model of Arteriovenous Fistula Failure: The Surgical Procedure in Detail

Wong, Chi Fong; Vries, Margreet R. de; Wang, Yang; Vorst, Joost R. van der; Vahrmeijer, Alexander L.; Zonneveld, Anton Jan van; Hamming, Jaap F.; Roy‐Chaudhury, Prabir; Rabelink, Ton J.; Quax, Paul H.A.; Rotmans, Joris I.

doi:10.3791/53294

Cited by 21 publications

(20 citation statements)

References 16 publications

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“…Ten-week-old C57BL/6J mice (Jackson Laboratory, Bar Harbor, ME, USA) were anaesthetized, surgically prepped, and administered pre-emptive analgesics. As previously described in a joint paper by us and the Rotmans group, [7,8] AV fistulae were created with an end-to-side anastomosis between the jugular vein and carotid artery (Figure 5) [7,8]. Of note, there was no compression of the vein, and the very fine 11/0 sutures did not cause any luminal obstruction.…”

Section: Arteriovenous Fistula Model Developmentmentioning

confidence: 93%

“…This is likely due to insufficient knowledge about the interactions between haemodynamic injury and the vascular response to injury, especially oxidative stress (likely magnified by the presence of uraemia) [2,5]. We previously developed a mouse model characterized by significant stenosis at the AV anastomosis 14 d post-surgery to better understand the cellular and molecular mechanisms involved in early AVF failure [7,8]. We have also demonstrated rapid and early (2 d) macrophage infiltration in our pig model of AVF stenosis [9].…”

Section: Introductionmentioning

confidence: 99%

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Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention

Chan

Wang

Cornea

et al. 2021

IJMS

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Background: Arteriovenous fistula (AVF) stenosis remains an important cause of AVF maturation failure, for which there are currently no effective therapies. We examined the pattern and phenotype of cellular proliferation at different timepoints in a mouse model characterized by a peri-anastomotic AVF stenosis. Methods: Standard immunohistochemical analyses for cellular proliferation and macrophage infiltration were performed at 2, 7 and 14 d on our validated mouse model of AVF stenosis to study the temporal profile, geographical location and cellular phenotype of proliferating and infiltrating cells in this model. Results: Adventitial proliferation and macrophage infiltration (into the adventitia) began at 2 d, peaked at 7 d and then declined over time. Surprisingly, there was minimal macrophage infiltration or proliferation in the neointimal region at either 7 or 14 d, although endothelial cell proliferation increased rapidly between 2 d and 7 d, and peaked at 14 d. Conclusions: Early and rapid macrophage infiltration and cellular proliferation within the adventitia could play an important role in the downstream pathways of both neointimal hyperplasia and inward or outward remodelling.

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Section: Arteriovenous Fistula Model Developmentmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention

Chan

Wang

Cornea

et al. 2021

IJMS

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“…Adult male mice aged 10-13 wk were used for the experiments. AVFs were created in an end-to-side manner between the dorsomedial branch of the external jugular vein and the common carotid artery as previously described (5,34). Briefly, the animal was anesthetized using isoflurane before the skin of the ventral neck area was shaved and disinfected.…”

Section: Animalsmentioning

confidence: 99%

“…To study the effect of RXFP1 deficiency on AVF maturation, we created AVFs in WT and Rxfp1 2/2 mice in an endto-side fashion between the jugular vein and carotid artery as previously described (34). Given that most of the stenotic lesions in human AVFs occur in the venous outflow tract, we harvested the first 3 consecutive venous sections downstream of the anastomotic area for morphometric analysis.…”

Section: Effect Of Rxfp1 Deficiency On Avf Maturationmentioning

confidence: 99%

Relaxin receptor deficiency promotes vascular inflammation and impairs outward remodeling in arteriovenous fistulas

et al. 2018

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The pathophysiology of arteriovenous fistula (AVF) maturation failure is not completely understood but impaired outward remodeling (OR) and intimal hyperplasia are thought to be contributors. This adverse vascular response after AVF surgery results from interplay between vascular smooth muscle cells (VSMCs), the extracellular matrix (ECM), and inflammatory cells. Relaxin (RLN) is a hormone that acts on the vasculature via interaction with RLN/insulin-like peptide family receptor 1 (RXFP1), resulting in vasodilatation, ECM remodeling, and decreased inflammation. In the present study, we evaluated the consequences of RXFP1 knockout ( Rxfp1) on AVF maturation in a murine model of AVF failure. Rxfp1 mice showed a 22% decrease in vessel size at the venous outflow tract 14 d after AVF surgery. Furthermore, a 43% increase in elastin content was observed in the lesions of Rxfp1 mice and coincided with a 41% reduction in elastase activity. In addition, Rxfp1 mice displayed a 6-fold increase in CD45 leukocytes, along with a 2-fold increase in monocyte chemoattractant protein 1 (MCP1) levels, when compared with wild-type mice. In vitro, VSMCs from Rxfp1 mice exhibited a synthetic phenotype, as illustrated by augmentation of collagen, fibronectin, TGF-β, and platelet-derived growth factor mRNA. In addition, VSMCs derived from Rxfp1 mice showed a 5-fold increase in cell migration. Finally, RXFP1 and RLN expression levels were increased in human AVFs when compared with unoperated cephalic veins. In conclusion, RXFP1 deficiency hampers elastin degradation and results in induced vascular inflammation after AVF surgery. These processes impair OR in murine AVF, suggesting that the RLN axis could be a potential therapeutic target for promoting AVF maturation.-Bezhaeva, T., de Vries, M. R., Geelhoed, W. J., van der Veer, E. P., Versteeg, S., van Alem, C. M. A., Voorzaat, B. M., Eijkelkamp, N., van der Bogt, K. E., Agoulnik, A. I., van Zonneveld, A.-J., Quax, P. H. A., Rotmans, J. I. Relaxin receptor deficiency promotes vascular inflammation and impairs outward remodeling in arteriovenous fistulas.

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“…4 Although factors including handling of the tissues, suture technique, physiological changes related to increasing blood flow, shear stress, and (patient and surgeon) related variables have been implicated, the exact etiology of JAS still remains unclear. 5 So, it was hypothesized that technical modification to alter the outflow vein configuration using the modified technique would prevent JAS and improve AVF maturation. 6…”

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confidence: 99%

Modified technique of end to side distal radio-cephalic shunt to overcome juxta-anastomotic stenosis

et al. 2019

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Background: Juxta-anastomotic stenosis (JAS) is one of the predominant causes of arteriovenous fistula (AVF) failure, with the reported incidence of 65%, so that technical modification to alter the outflow vein configuration using the modified technique has been applied to prevent JAS and improve AVF maturation. The aim of the study to evaluate the modified technique of end-to-side distal radiocephalic A-V fistula regarding maturation, patency rate and the resultant juxta-anastomotic stenosis.Methods: This prospective study was carried out on 80 patients with end stage renal disease (ESRD) at vascular surgery unit in general surgery department, Menoufia university hospital that prepared for dialysis. 40 patients "intervention group" underwent the modified technique to establish a functioning radiocephalic fistula; the other group (40 patients, control group) had the conventional technique of end to side radiocephalic fistula. Follow up of patients was over 6 months regarding function, patency rate and development of juxta-anastomotic stenosis.Results: There was statistically significant difference between 2 groups regarding primary failure, patency and JAS. Primary failure was detected in 2 patients in group A and in 5 patients in group B (p-value is 0.04). Considering patency rate, after 3 months the ratio between group A and group B was 37:34 with significant P value of 0.02, and after 6 months the ratio was 35:33 with P value of 0.03. Regarding JAS, by the end of follow up period, 4 patients diagnosed with JAS in group A, while group B had 8 patients, with p value of 0.01.Conclusions: Modified technique of end to side anastomosis for primary radio-cephalic fistula creation has better patency rate and low incidence of JAS than conventional method.

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A Novel Murine Model of Arteriovenous Fistula Failure: The Surgical Procedure in Detail

Cited by 21 publications

References 16 publications

Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention

Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention

Relaxin receptor deficiency promotes vascular inflammation and impairs outward remodeling in arteriovenous fistulas

Modified technique of end to side distal radio-cephalic shunt to overcome juxta-anastomotic stenosis

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