Abstract:Abdominal aortic aneurysm is a common arterial dilatation disease, with insidious onset and complicated pathogenesis. Due to the lack of early diagnosis and effective intervention measures, the mortality rate of aneurysm is high once ruptured. Therefore, it is urgent to further explore its pathogenesis and find effective treatment measures. Due to many limitations in human trials, it is necessary to replicate animal models for the study of abdominal aortic aneurysms. This article will classify and introduce some classic and innovative animal models according to different research purposes, as well as their respective characteristics and application values, and provide help for researchers to choose appropriate animal model.

Abstract:Aortic aneurysm (AA) is a pathological dilatation disease of the aorta that is affected by multiple factors and has a potential risk of rupture. AA can be divided into thoracic aortic aneurysm (TAA) and abdominal aortic aneurysm (AAA) based on the location of aneurysm. The occurrence of TAA is highly relevant to genetic factors, and shows no age and gender differences. In contrast, the occurrence of AAA is related to age, gender, and atherosclerosis, but is not related with genetic factors. Most AA patients are asymptomatic, and generally have the characteristics of insidious onset and rupture to death. Therefore, AA is a serious life-threatening chronic disease, but its pathogenesis is not fully understood. The animal model of AA is of great significance to investigate the underlying pathophysiological mechanism, to develop and evaluate therapeutic drugs. Currently, there are many well-established animal models of AAA, but less of TAA. In fact, many established methods to induce AAA can also induce TAA. This review describes the AA animal models classified into non-dissected AA animal model and dissected AA animal model, and discusses the development methods and phenotypes of them, which may help us to find more efficient and reliable solutions against human aortic aneurysm.

Abstract:Aim To investigate the modeling methods and application of atherosclerotic vulnerable plaque (VP) animal model. Methods The related literature about VP animal modeling published in CNKI, Pubmed and Wanfang databases from October 2016 to October 2021 were retrieved. The modeling animals, modeling methods, modeling cycles, model evaluation methods and corresponding detection indexes in the literatures were statistically analyzed. Results The most commonly used experimental animals were mice with apolipoprotein E gene deficient at 6～12 weeks, New Zealand white rabbits at 12～16 weeks, and familial hypercholesterolemia pigs at 34 weeks. Modeling methods were followed by high-fat and high-cholesterol diet induction, arterial ligation, or combined with aortic endothelial balloon strain, chemical triggering, immune induction, etc. The modeling cycle ranged from 8 weeks to 1 year, with 12 to 18 weeks being the most. The evaluation methods were mostly pathological staining, combined with enzyme-linked immunosorbent assay, Western blot, real-time fluorescence quantitative PCR, flow cytometry and other methods; color Doppler ultrasound, cardiac perfusion imaging and in vivo live cell tracking technology were used for VP live detection. Conclusion High-fat and high-cholesterol diet feeding, or combined with surgical injury to establish VP model has good reproducibility. If a cost-effective in vivo detection method can be developed, the research efficiency of atherosclerotic diseases will be greatly improved.

Abstract:Cardiovascular diseases are the leading cause of human death. Among them, vascular stenosis diseases account for a high proportion of cardiovascular diseases, which seriously endanger peoples physical and mental health. Stent intervention is currently the most commonly used method for the treatment of vascular stenosis, but the proportion of restenosis after percutaneous intervention of coronary, carotid and peripheral arteries is very high, which seriously affects the prognosis of interventional patients. Therefore, a stable animal model can provide a tool for research and resolution of restenosis after percutaneous intervention. This article summarizes the method of creating ballon injury animal model and its application, in order to provide basis for the prevention and treatment of cardiovascular diseases.

Abstract:Aim Atherosclerosis is a chronic inflammatory disease, but the regression of plaques suggests the possibility of reversal of atherosclerotic disease. Thus, the establishment of a model of atherosclerosis regression in mice is of great significance for elucidating the mechanism of plaque regression. Methods In ApoE－/－ mice, three types of carotid ligation were performed to induce different types of blood flow. To establish the regression model, partial carotid ligation with a slipknot was firstly used to induce disturbed flow. After feeding on a high-fat diet for 2 weeks, the slipknot was removed, and followed by a chow diet for two weeks. The ultrasonic testing was performed to monitor the blood flow in real time caused afterligation or plaque formation; Sudan Ⅳ staining was used to assess atherosclerotic lesions; immunofluorescence staining with anti MOMA2 was applied to examine monocyte-macrophage infiltration. Results Three types of ligation induced different types of blood flow. The disturbed flow induced the largest atherosclerotic plaque area in ApoE－/－ mice. After restore of blood flow combined with chow diet, atherosclerotic plaques can be significantly reduced and reversed, and the macrophage infiltration also significantly decreased. Conclusion A novel atherosclerosis regression model in mice based on carotid ligation surgery was successfully constructed, which will help to understand the underlying mechanism of atherosclerosis regression.

Abstract:Arteriosclerosis obliterans (ASO) has become a serious threat to peoples physical and mental health of primary peripheral vascular disease, and early diagnosis and treatment is urgent and necessary. In recent years, as the research on the non-protein mechanism of post-transcriptional mechanism become clear, part of the research focused on exploring the relationship between microRNA and ASO. Therefore, this paper based on the regulation of microRNA in atherosclerosis model, animal model and patients with vascular smooth muscle cells proliferation, migration, differentiation, phenotypic transformation, apoptosis, senescence, inflammation and oxidative stress related to learning and research. From the aspects of gene regulation, microRNA research could better explain the occurrence and development of hardening of the ASO, but because of the many factors, such as complicated regulatory mechanism and the lack of the pharmacokinetics and pharmacodynamics research data, many target genes and so on, its clinical application is still restricted. In the future, the microRNA healing potion applied to the treatment of vascular diseases, especially in lower limb arteriosclerosis occlusion disorder will reduce the damage effectively.

Abstract:Aim To prepare the no-reflow model after myocardial ischemia-reperfusion injury in rats and to explore the key points in the establishment of the model, so as to provide reference for the successful replication of the disease model. Methods Twenty SD rats were randomly divided into no-reflow group (n＝15) and sham group (n＝5). In the no-reflow group, the left anterior descending artery (LAD) was ligated 45 min and then perfused 120 min. The sham group rats underwent the same surgical procedures except that LAD was not ligated. At the end of reperfusion, thioflavin S staining was performed to determine the area of no-reflow (ANR), while monitoring the changes of respiration and electrocardiogram (ECG) in rats. Results Twenty rats were all survived, at the selected condition of ischemia and reperfusion time, all the rats in the no-reflow group showed obviously myocardial no-reflow phenomenon. After no-reflow model was established, the heart rate accelerated and ST segment elevation increased in the ischemic stage. Along with a progress of reperfusion, the heart rate and amplitude increased first and then decreased, while the increase values of ST segment drop less than 30%. Conclusion The method can successfully replicate the animal model of no-reflow and the method has high success rate and high animal survival rate.

Abstract:Aortic dissection (AD) is a high-risk vascular disease, and more and more scholars pay attention to the research of its pathogenesis, prevention and treatment. At present, the animal models of AD can be divided into in vivo models and in vitro models. In vivo models include mechanical modeling, chemical induced modeling and genetic engineering modeling. In vitro model is to simulate the formation of AD in vitro. In this paper, the research progress of AD model is reviewed.

Abstract:Aim To establish the animal model of vein graft restenosis after coronary artery bypass grafting in patients with coronary artery disease. Methods 26 New Zealand rabbits were randomly divided into three groups:(1)high fat graft group(n＝10):rabbits treated by autologous external jugular vein grafting to common carotid artery and fed by high fat diet;(2)pure graft group(n＝10):rabbits treated by autologous external jugular vein grafting to common carotid artery and fed by normal diet;(3)normal control group(n＝6):rabbits fed by normal diet. The graft groups were performed by the external jugular vein anastomosis to the carotid artery bypass surgery. Blood flow was detected by color Doppler ultrasound, and the patency of vein graft was proved. Two months later, Doppler was used to detect the blood flow and intima thickness of vein graft, and the tissue specimens were taken for pathological examination, in order to understand whether there is thrombus in vein graft, proliferation and transfer of endothelial cell and smooth muscle cell, and proliferation of vascular matrix, etc. Results (1)All vein grafts were unobstructed after operation.(2)Two months after operation, color Doppler ultrasound examination showed that there were plaque formation, obvious stenosis and intima thickening of the vein grafts in high fat graft group, compared with the pure graft group and the normal control group.(3)The pathological examination showed that there were typical atherosclerotic changes such as shedding of the endothelial cells, intimal hyperplasia, smooth muscle cell migration, proliferation and lipid deposition on vein grafts in high fat graft group, while the changes in pure graft group and normal control group were not obvious. Conclusions The animal model of rabbit external jugular vein anastomosis to the carotid artery is reliable. It provides a simple and ideal model for the study of restenosis after vein grafts.

Abstract:Vulnerable atherosclerotic plaque rupture leading to thrombosis is the major cause of acute coronary syndromes. While early detection or prevention the vulnerable plaque would be the only way to reduce the risk of this catastrophic life-threatening event, there is frustratingly little progress in either. Lack of suitable animal models has considerably hampered the research progress in understanding the mechanisms occurring in the development of plaque rupture. This review summarizes the currently available vulnerable plaque animal models and invasive and noninvasive imaging modalities used to detect vulnerable plaques, including high frequency duplex ultrasound, coronary tomographic angiography (CTA), magnetic resonance imaging (MRI), intravascular ultrasound (IVUS), optical coherence tomography (OCT), intravascular ultrasound elastography, and inflammatory markers.