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Journal articles on the topic 'Intima Hyperplasia'
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1
Yan, Huifang, Xiwei Peng, Hao Xu, Jiahuan Zhu, and Changqing Deng. "Inhibition of Aortic Intimal Hyperplasia and Vascular Smooth Muscle Proliferation and Extracellular Matrix Protein Expressions by Astragalus–Angelica Combination." Evidence-Based Complementary and Alternative Medicine 2018 (August 13, 2018): 1–15. http://dx.doi.org/10.1155/2018/1508637.
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VSMC proliferation and ECM deposition always resulted in intimal hyperplasia. Astragalus–Angelica combination has a protective effect on the cardiovascular system. The inhibition effect of different Astragalus–Angelica combination on the hyperplastic intima after vascular balloon injury in rats was investigated in this study. Astragalus–Angelica combination can inhibit the intima hyperplasia after balloon injury, in which a 1:1 ratio shows excellent results. Astragalus–Angelica combination can enhance the expression of smooth muscleα-actin (SMа-actin) and inhibit the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin E, collagen I (Col-I), fibronectin (FN), and matrix metallopeptidase-9 (MMP-9) in hyperplastic intima, suggesting that Astragalus–Angelica combination can inhibit the intimal hyperplasia of blood vessels in rats. The mechanism is related to the inhibition of PI3K/Akt signaling pathway activation and thereby inhibits the phenotypic transformation and cell proliferation of VSMCs and thus inhibits the extracellular matrix (ECM) deposition of vascular wall during intimal hyperplasia.
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Mesfin, G. M., M. J. Higgins, W. P. Brown, and D. Rosnick. "Cardiovascular Complications of Chronic Catheterization of the Jugular Vein in the Dog." Veterinary Pathology 25, no. 6 (November 1988): 492–502. http://dx.doi.org/10.1177/030098588802500613.
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Cardiovascular changes associated with indwelling catheters were evaluated in 51 adult beagle dogs catheterized for 4 to 9 weeks. Pathologic changes consistent with traumatic injury were in the vena cava and endocardium of the right atrium of 88% of cannulated dogs. Lesions were characterized by surface denudation and diffuse intimal thickening due to myointimal hyperplasia and deposition of extracellular matrix. Affected intima was lined by hyperplastic, poorly differentiated endothelial cells and contained round to oval cells with characteristics of smooth muscle cells. After 9 weeks, thickened intima was vascularized and composed of spindle-shaped cells and fibrillar stroma. Intimal sclerosis and localized proliferative papillary projections in the vena cava cranial to areas of myointimal hyperplasia occurred infrequently. Traumatic lesions, regardless of location or severity, did not extend below the internal elastic membrane. Inflammatory cellular responses, when present, were minimal. The location, distribution, and morphogenesis of catheter-related cardiovascular lesions distinguishes them from those induced by chemical toxicity or pharmacotoxicity.
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Jalaeefar, Amirmohsen, Arash Mohammadi Tofigh, Atoosa Gharib, Mohsen Khandaghy, and Mohammad Reza Rahimi. "Effects of N-acetylcysteine on arterial neo-intimal hyperplasia in rat model of arteriovenous fistula." Journal of Vascular Access 20, no. 2 (August 24, 2018): 190–94. http://dx.doi.org/10.1177/1129729818793368.
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Introduction: Arteriovenous fistula is the best choice for vascular access in hemodialysis patients. However, arteriovenous fistula dysfunction is a major clinical issue. The most common cause of arteriovenous fistula failure is intimal hyperplasia. In this study, we have investigated the effect of N-acetylcysteine on neo-intimal hyperplasia after arteriovenous fistula creation in rats. Methods: This study was conducted in 24 rats which were randomly divided into two groups: control and N-acetylcysteine groups. An end-to-side anastomosis was made between the femoral artery and vein. The control group received distilled water intraperitoneally while the animals in N-acetylcysteine group received 300 mg/kg/day of N-acetylcysteine via the same route. After 28 days, the thickness of intima and media was measured using hematoxylin and eosin. Results: There was no significant difference between the two groups regarding age ( p = 0.6) and weight ( p = 0.1). The mean intima thickness in N-acetylcysteine group was significantly less than control group (17 ± 20 and 119 ± 46 µm, respectively; p < 0.001). The mean intima/media thickness in the N-acetylcysteine group was significantly less than control group (0.5 ± 0.63 vs 2.05 ± 1.17 µm; p < 0.001). Conclusion: N-acetylcysteine is effective in inhibiting neo-intimal hyperplasia in a rat model of arteriovenous fistula.
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Van Phung, Doan, Takeshi Kinoshita, Tohru Asai, and Tomoaki Suzuki. "Histological and Morphometric Properties of Skeletonized Gastroepiploic Artery and Risk Factors for Intimal Hyperplasia." Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery 7, no. 3 (May 2012): 191–94. http://dx.doi.org/10.1097/imi.0b013e318264f4cb.
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Objective The aim of the present study was to examine the histological and morphometric properties of skeletonized gastroepiploic artery (GEA) and the risk factors for intimal hyperplasia. Methods We obtained the redundant distal segments of skeletonized GEAs from 33 patients undergoing coronary bypass surgery and microscopically examined the transverse sections just distal to the most distal anastomoses. Intimal hyperplasia was evaluated on the basis of intima-to-media ratio and percentage of luminal narrowing. Risk factors were examined using multivariate linear regression analysis. Results The median (range) of lumen diameter at the most distal anastomosis was 3.8 (2.4–6.4) mm; width of intima, 82 (8–418) μm; width of media, 167 (88–351) μm; wall thickness, 250 (118–554) μm; intima-to-media ratio, 0.59 (0.04–3.88), and percentage of luminal narrowing, 12.3 (1.5–28.9). The number of elastic lamina in the media was 4.2 ± 1.8. Atherosclerosis was found in six patients, and medial calcification, in three patients. The median (range) of graft flow and pulsatile index measured by intraoperative transit-time flow meter was 65 (11–141) mL/min and 3.1 (1.4–5.9), respectively. All GEA grafts were patent at the coronary computed tomography angiography before discharge. Estimated glomerular filtration rate was independently associated with intima-to-media ratio (β coefficient = −0.016, P < 0.01) and percentage of luminal narrowing (β coefficient = −0.012, P < 0.01). Conclusions Skeletonized GEA had sufficient lumen diameter with excellent graft flow and early patency even when used as a sequential graft. Estimated glomerular filtration rate correlates significantly with intimal hyperplasia.
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Hirai, T., Y. Korogi, M. Harada, and M. Takahashi. "Prevention of Intimal Hyperplasia by Irradiation." Acta Radiologica 37, no. 1P1 (January 1996): 229–33. http://dx.doi.org/10.1177/02841851960371p147.
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Purpose: This experimental study was designed to investigate the effect of irradiation in prevention of intimal hyperplasia. Material and Methods: Twenty rabbits were divided into 4 groups, which were irradiated with 2, 5, 10, and 20 Gy, respectively. The intima of both femoral arteries was injured by air-drying, and irradiation was performed on the unilateral side. The contralateral femoral artery served as a control. Angiograms as well as histologic specimens were obtained 1 month later. Results: Marked intimal hyperplasia was observed in all control sites. There were no significant differences in thickness of intimal hyperplasia between irradiated and control sites in groups irradiated with 2 and 5 Gy. However, in the 10-Gy- and 20-Gy-irradiated groups, intimal hyperplasia of the irradiated site was significantly suppressed. Medial thinning and dilation of the lumen were observed in the 20-Gy-irradiated group. Conclusion: Radiation may prevent intimal hyperplasia. Further investigation of the optimal dose, timing of irradiation, and long-term patency of irradiated vessels may be needed.
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ARPA, Abdurrahman, and Pınar AYDIN OZTURK. "Histopathological effects of nimodipine and pentoxifylline on the vessel wall in end-to-end anastomoses in rat carotid arteries." Journal of Experimental and Clinical Medicine 39, no. 3 (August 30, 2022): 879–83. http://dx.doi.org/10.52142/omujecm.39.3.54.
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When reperfusion following ischemia occurs, oxygen returns to the ischemic tissue, increasing free oxygen radicals and inducing paradox secondary damage. Before infarction, revascularization may influence the morbidity rate. Successful revascularization is not always achieved due to stenosis incidence, proliferation of smooth muscle cells, and intimal hyperplasia. This study compares the effects of nimodipine that prevents vasospasm and pentoxifylline, which stimulates growth factors and reduces collagen synthesis on intimal hyperplasia. Eighteen randomly selected Sprague-Dawley rats were divided into three groups: Group 1, the control group; Group 2, intraperitoneally administered nimodipine; Group 3, orally administered pentoxifylline. Their right-sided carotid arteries were used for anastomosis and the left-sided ones for the control. After a 7-day treatment, both the right and left carotid arteries were removed. In the biopsy, the lumen’s area and diameter, thickness of tunica media thickness, thrombus, edema, intimal hyperplasia, vessel wall injury, and inflammation were analyzed. Pentoxifylline was effective in preventing intimal hyperplasia and tunica intima was similar to that in untreated carotid arteries. However, nimodipine inhibited intimal hyperplasia, but it was not as effective as pentoxifylline. The effects of pentoxifylline after anastomosis should be further assessed in vasoprotective treatment taking into account its efficacy against intimal hyperplasia.
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Qian, Kun, Li Feng, Yujie Sun, Bowen Xiong, Yi Ding, Panting Han, Hailun Chen, Xiao Chen, Ling Du, and Yuxue Wang. "Overexpression of Salusin-α Inhibits Vascular Intimal Hyperplasia in an Atherosclerotic Rabbit Model." BioMed Research International 2018 (July 12, 2018): 1–9. http://dx.doi.org/10.1155/2018/8973986.
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Inhibiting vascular endothelial foam is the focus of clinical attention. Using SonoVue (an ultrasound contrast agent), the salusin-α gene was transfected into the arterial intima of an atherosclerotic rabbit model induced by a high-fat diet in this study. Subsequently the model of blood lipid indexes, the pathological structure of the intima, and changes in molecules regulating atherosclerosis were investigated. The high-density lipoprotein C and apolipoprotein A values in the salusin-α gene overexpression (P) group were higher than those in the salusin-α gene interference (RP) group (P < 0.05), whereas the total cholesterol, low-density lipoprotein C, and apolipoprotein B values were reversed. Rabbits in the P group showed significantly thinner vascular intimal thickness than that of other experimental groups (P < 0.05). The expression of positive regulators of atherosclerosis (ABCA1, ABCG1) was higher in the P group than that in the RP group (P < 0.05), and the opposite effect was observed for negative regulators (ACAT1, CD36). Thus, our results showed that the overexpression of salusin-α gene inhibited the proliferation of the vascular intima, thereby throwing some light on understanding the mechanism how salusin-α gene expression interfered with the foaming of vascular intimal cells.
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Kachlik, David, Vaclav Baca, Petr Fara, Alois Lametschwandtner, Bernd Minnich, Vladimir Musil, Bohuslav Sosna, Josef Stingl, Zdenek Straka, and Marek Setina. "Blood vessels of the normal and pathologically changed wall of the human vena saphena magna." Open Medicine 3, no. 4 (December 1, 2008): 475–81. http://dx.doi.org/10.2478/s11536-008-0047-5.
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AbstractThe vascular supply of the wall of human vena saphena magna was qualitatively studied by the use of several morphological methods on both normal and pathologically changed veins. The material was obtained from patients undergoing aortocoronary bypass or surgery of the varices, and material from cadavers. Under physiological conditions, the wall of vena saphena magna is supplied by delicate system of vasa vasorum, organized in a form of feeding vessels branched into an irregular loose adventitial mesh and continuing further as a microcirculatory network supplying the two outer thirds of the media. Small local dilatations and tortuosities of adventitial veins were found on heavy varicose veins. Slight increase of vasa vasorum growing into the innermost layer of media was detected, but the hyperplastic intima remained avascular. In patients with recurrent varices or with vein thrombophlebitis intimal hyperplasia, degradation of media and thrombosis, were found. Apparent massive increase of vasa vasorum growing into the whole media, hyperplastic intima and into the organizing thrombi, were regularly observed. The increase of vasa vasorum is a part of the complex of pathophysiological reactions of the vein wall on the hypoxia developing during the most serious pathological changes, and not as the primary varicogenic factor. The vascular supply of the wall of the human vena saphena magna was qualitatively studied by the use of several morphological methods on both normal and pathologically changed veins. The material was obtained from patients undergoing aortocoronary bypass grafting or surgery of varices, as well as materials from cadavers. Under physiological conditions the wall of vena saphena magna is supplied by a delicate system of vasa vasorum. It is organized in a form of feeding vessels branched into an irregular loose adventitial mesh, which continues further as a microcirculatory network supplying the outer two thirds of the media. Small local dilatations and tortuosities of adventitial veins were found on severe varicose veins. A slight increase of the vasa vasorum growing into the innermost layer of media was detected, but the hyperplastic intima remained avascular. In patients with recurrent varices or vein thrombophlebitis, intimal hyperplasia, degradation of media and thrombosis, were found. It was regularly observed that there was an apparent, massive increase of the vasa vasorum growing into the entire media, hyperplastic intima, and into the organizing thrombi. The increase of the vasa vasorum is due to the pathophysiological reaction of the vein wall as a result of hypoxia, which develops during the most serious pathological changes. The increase is not the primary varicogenic factor.
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Vazquez-Padron, Roberto I., Juan C. Duque, Marwan Tabbara, Loay H. Salman, and Laisel Martinez. "Intimal Hyperplasia and Arteriovenous Fistula Failure: Looking Beyond Size Differences." Kidney360 2, no. 8 (June 3, 2021): 1360–72. http://dx.doi.org/10.34067/kid.0002022021.
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AbstractThe development of venous intimal hyperplasia (IH) has been historically associated with failure of arteriovenous fistulas (AVFs) used for hemodialysis. This long-standing assumption, made on the basis of histologic observations, has been recently challenged by clinical studies indicating that the size of the intima by itself is not enough to explain stenosis or AVF maturation failure. Irrespective of this lack of association, IH is present in most native veins and fistulas, is prominent in many patients, and suggests a role in the vein that may not be reflected by its dimensions. Therefore, the contribution of IH to AVF dysfunction remains controversial. Using only clinical data and avoiding extrapolations from animal models, we critically discuss the biologic significance of IH in vein remodeling, vascular access function, and the response of the venous wall to repeated trauma in patients receiving hemodialysis. We address questions and pose new ones such as the following: What are the factors that contribute to IH in preaccess veins and AVFs? Do cellular phenotypes and composition of the intima influence AVF function? Are there protective roles of the venous intima? This review explores these possibilities, with hopes of rekindling a critical discussion about venous IH that goes beyond thickness and AVF outcomes.
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Mitra, Amit K., Michael G. Del Core, and Devendra K. Agrawal. "Cells, cytokines and cellular immunity in the pathogenesis of fibroproliferative vasculopathies." Canadian Journal of Physiology and Pharmacology 83, no. 8-9 (August 1, 2005): 701–15. http://dx.doi.org/10.1139/y05-080.
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Atherosclerosis and restenosis are the result of vascular injury followed by an inflammatory and fibroproliferative response that involves a large number of growth factors, cytokines, and cellular elements. Platelet activation and leukocyte recruitment into the arterial intima play a crucial role, initiating a whole spectrum of reactions leading to vascular smooth muscle cell hyperplasia and intimal migration. The roles of macrophages and lymphocytes and mast cells as mediators of inflammation and immune response is discussed, as are the roles of growth factors and cytokines. New light on the 'old' problems will help us to devise newer and better therapeutic strategies to combat these clinical entities.Key words: atherosclerosis, cellular immunity, cytokines, growth factors, intimal hyperplasia, mast cells, restenosis, vasculopathies.
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Aydin, Unal, Murat Ugurlucan, Funda Gungor, Sedat Ziyade, Bekir Inan, Maciej Banach, Yusuf Kalko, and Tahsin Yasar. "Effects of Atorvastatin on Vascular Intimal Hyperplasia: An Experimental Rodent Model." Angiology 60, no. 3 (September 15, 2008): 370–77. http://dx.doi.org/10.1177/0003319708321102.
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Introduction Vascular intimal hyperplasia is associated with increased mortality and morbidity. The authors investigated the effects of atorvastatin on vascular intimal hyperplasia. Materials and methods Rats were divided into 4 groups. Groups 1, 2, and 3 had experimental aortic injury and received intraperitoneal injection of atorvastatin, solvent, or 0.9% NaCl, respectively. Group 4 was a nonintervention (laparotomy only) control group. Animals were sacrificed after 3 weeks. Blood samples and injured aortic segment were analyzed. Results Atorvastatin administration significantly lowered total and low-density lipoprotein cholesterol levels ( P = .012 and P = .001, respectively), intima—media ratio ( P = .002), and intimal smooth muscle cell accumulation ( P < .05) in group 1. Luminal narrowing in animals in group 1 was significantly lower than that in animals in groups 2 and 3, but was higher than in animals in group 4 ( P = .009). Conclusions Atorvastatin suppresses intimal hyerplasia and aids in intimal regeneration by lowering blood lipids and intimal smooth muscle cell accumulation.
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Galarza-Delgado, D. Á., J. R. Azpiri-López, I. J. Colunga-Pedraza, D. E. Flores Alvarado, O. Ilizaliturri Guerra, P. F. Frausto Lerma, A. Pérez Villar, M. A. Reyes Soto, I. C. Zárate Salinas, and A. C. Garza Acosta. "AB1212 PREVALENCE OF CAROTID SUBCLINICAL ATHEROSCLEROSIS IN PATIENTS WITH PSORIATIC ARTHRITIS VS RHEUMATOID ARTHRITIS: A CASE CONTROL STUDY." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1897. http://dx.doi.org/10.1136/annrheumdis-2020-eular.5197.
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Background:Rheumatic diseases such as Psoriatic Arthritis (PsA) and Rheumatoid Arthritis (RA) are associated with increased morbidity and mortality, mainly due to cardiovascular causes. Cardiovascular outcomes in patients with PsA and RA cannot be completely explained by traditional cardiovascular risk factors, suggesting that the systemic inflammation that characterizes these diseases may have an important role on accelerated atherosclerosis.1Objectives:To compare carotid intima-media thickness (cIMT) and asymptomatic carotid plaque (CP) prevalence, between patients with PsA, RA and controls.Methods:Cross-sectional observational study. Seventy patients, aged 35-75 years, with PsA and RA who fulfilled the CASPAR and ACR/EULAR 2010 classification criteria, respectively, who were active on a cardio-rheuma preventive clinic were recruited, matched with 70 healthy controls. All groups underwent a noninvasive examination using B-mode ultrasonography of the right and left common carotid artery. CP was defined as a focal narrowing ≥0.5 mm of the surrounding lumen or cIMT ≥1.2 mm; hyperplasia of the carotid intima was defined as cIMT ≥ 0.9 mm to 1.1 mm. Descriptive data were analyzed by continuous and categorical variables. Continuous variables with normal distribution are shown as mean ± standard deviation (SD), and non-normal distribution as median and quartiles (25q-75q). ANOVA, Kruskal Wallis,X2and Mann-Whitney U were used to compared data. Apvalue ≤0.05 was considered statistically significant. Statistical analysis was done using SPSS version 24 (IBM Corp., Armonk, NY, USA).Results:Clinical and demographic characteristics are shown in Table 1. The global prevalence of carotid atherosclerosis was 25.7% and 38.6% in RA and PsA respectively, and 27.1% in controls (p=0.170). Intimal hyperplasia was found in 20%, 12.9% and 0% in RA, PsA and controls (p=0.001), respectively (Table 2).Table 1.Clinical and demographic characteristicsRAn=70PsAn=70Controlsn=70PvalueGender Male9 (12.9%)31 (44.4%)11 (15.7%)<0.001 Female61 (87.1%)39 (55.7%)59 (84.3%)Age, years54.51±9.65753.1±10.8753.54±7.48NSBody Mass Index, BMI, kg/m228.99 (25.95-32.34)29.04 (26.23-31.92)27.44 (24.98-30.95)NSComorbidities Diabetes Mellitus11 (15.7%)14 (20%)8 (11.4%)NS Hypertension24 (34.3%)27 (38.6%)15 (21.4%)NS Dyslipidemia19 (27.1%)30 (42.9%)18 (25.7%)NS Active smoker7 (10%)16 (22.9%)15 (21.4%)NSDisease duration Duration, years8.45 (3.34-15.88)5 (2.75-8)-0.005Statins9 (12.9%)12 (17.1%)10 (14.3%)NSTable 2.Ultrasonographic characteristicsRAn=70PsAn=70Controlsn=70PvalueRight CIMT, mm0.8 (0.6-1.1)0.6 (0.5-0.9)0.6 (0.5-0.8)<0.001Left CIMT, mm0.8 (0.6-0.9)0.6 (0.5-0.7)0.6 (0.5-1.2)0.002Any Hyperplasia14 (20%)9 (12.9%)00.001Right intimal hyperplasia7 (10%)5 (7.1%)00.021Left intimal hyperplasia13 (18.6%)2 (2.9%)0<0.001Any plaque18 (25.7%)27 (38.6%)19 (27.1%)NSConclusion:This study shows the high prevalence of asymptomatic atherosclerosis in RA and PsA compared to general population. Even though it was shown a higher prevalence of CP in PsA, subclinical atherosclerosis in RA patients may have an increased clinical significance. The presence of carotid plaque between groups was not statistically significant. We observed increased prevalence of carotid intimal hyperplasia in RA and PsA compared with age-matched controls. We emphasize the value of ultrasonography in the detection of early atherosclerosis lesions.References:[1]Wah-Suarez, M. I., et.al. (2019). Carotid ultrasound findings in rheumatoid arthritis and control subjects: A case-control study.International Journal of Rheumatic Diseases,22(1), 25–31.Disclosure of Interests:None declared
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Sakarya, Ahmet, Hakan Uzun, Ayten Türkkanı, Ayşe Nur Çakar, Yun-Huan Hsieh, Galip Üstün, and Tunç Şafak. "Effects of Systemic and Local Caffeine on Vessel Diameter, Anastomosis Patency, and Intimal Hyperplasia in the Rat." Journal of Reconstructive Microsurgery 35, no. 04 (September 19, 2018): 244–53. http://dx.doi.org/10.1055/s-0038-1672130.
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Background The use of caffeine is not recommended prior to elective microsurgery due to its demonstrated negative effects on vessel anastomosis by the presumed sympathomimetic induction of vasoconstriction. In this study, we aimed to elucidate the systemic and local effects of caffeine on vessel diameter, anastomosis patency, and degree of intimal hyperplasia during the healing process. Methods Twenty-five rats were randomly assigned to five groups: (1) negative control, (2) preoperative systemic caffeine, (3) postoperative systemic caffeine, (4) perioperative systemic caffeine, and (5) a local caffeine group. Both the right and left femoral arteries were used. Ten anastomoses were performed per group. The arterial diameter was measured by micrometer, anastomosis patency was assessed surgically and histologically, and the histological examination was conducted 3 weeks postoperatively to determine intimal hyperplasia. Results The overall patency rate was 96%. Mild vasoconstriction was observed in the systemic caffeine groups (statistically insignificant); however, there were no negative effects on anastomosis patency. Local caffeine irrigation resulted in significant vasodilatation in the local caffeine group (p = 0.001); a similar effect was not observed in the other groups. There was a significant decrease in the intima/media ratio in the local caffeine group (p < 0.01), when compared with the control and systemic caffeine groups. No other intima/media ratio differences were observed among other comparison groups. Conclusion The systemic administration of caffeine, although statistically insignificant, has an observable effect on vasoconstriction. However, it does not appear to have negative effects on anastomosis patency regardless of its application period (pre-, post-, or perioperatively). The local application of caffeine resulted in considerable vasodilatation as opposed to the vasoconstriction effect in the systemic caffeine groups. Decreased intimal hyperplasia at the anastomosis edge, and antifibrotic properties in the surgical field were also observed in this group. Histologically, the local caffeine group demonstrated an additional beneficial effect on anastomosis remodeling.
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Kemahli, Mustafa Baris, Tugra Gencpinar, Huseyin Dursun, Cagatay Bilen, Pinar Akokay, Serdar Bayrak, and Abidin Cenk Erdal. "Effects Of Rivaroxaban And Apixaban On Intimal Hyperplasia In Rabbits." Turkish Journal of Vascular Surgery 31, no. 3 (November 15, 2022): 148–56. http://dx.doi.org/10.9739/tjvs.2022.09.03.
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Aim: Intimal hyperplasia causes vascular occlusion and its optimal treatment is unknown. In this study, we evaluated the effectiveness of Apixaban and Rivaroxaban treatment for preventing intimal hyperplasia in rabbits. Material and Methods: The rabbits (n = 15) were randomly divided into three groups. Reanastomoses are applied to the carotid artery. All groups received 100 U/kg heparin sodium during the operation period. Group A (n = 5) as a control group had no medication. Group B (n = 5) was given Rivaroxaban 3 mg/kg/day. In-group C (n = 5) Apixaban was administered per orally 10 mg/kg. At the end of the treatment on the 28th day, carotid artery specimens were excised and evaluated histologically. Results: Increased intima thickness was observed in the control group than the drug groups (P=0.019, P=0.007). It was found that there was no difference between groups in terms of lumen diameter, lumen area, tunica media area and tunica media thickness. There was difference between groups in terms of caspase 3 or TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) staining (p<0.05). Conclusion: Apixaban and Rivaroxaban may have protective efficacy against intimal hyperplasia after vascular surgical intervention.
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Asfar, Sami, Ali Shuaib, Fatemah Al-Otaibi, Sora S. Asfar, and Narayana Kilarkaje. "A New Technique to Induce Experimental Myointimal Hyperplasia." Medical Principles and Practice 27, no. 5 (2018): 415–19. http://dx.doi.org/10.1159/000492575.
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Background: Arterial myointimal hyperplasia (MIH) has a significant impact on the long-term outcomes of vascular procedures such as bypass surgery and angioplasty. In this study, we describe a new and innovative technique to induce MIH using a dental flossing cachet in Wistar rats. Methods: The intimal damage in the common carotid artery was induced by inserting the tip of the dental flossing cachet through the external carotid artery into the common carotid artery and turning it on for 3 rounds of 20 s each (n = 10). After 2 weeks, the rats were anesthetized and the common carotid arteries of the experimental side and the contralateral side (control) were harvested and preserved for histopathological studies. Results: The experimental carotid arteries showed significant intimal proliferation and thickening compared to the controls. The intima/media ratio of the experimental and normal (control) common carotid arteries were 1.274 ± 0.162 and 0.089 ± 0.023 (mean ± SEM), respectively (p < 0.001). Conclusion: This technique is simple, inexpensive, and highly reproducible and it induces sufficient MIH to study this phenomenon in animal models.
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Zhang, Dechuan, Tieying Yin, Feifei Du, Dingyuan Du, Lili Tan, Hans Gregersen, and Guixue Wang. "EVALUATION OF INTIMAL HYPERPLASIA AND THROMBOSIS AFTER IMPLANTATION OF PLATELET GLYCOPROTEIN IIIa MONOCLONAL ANTIBODY-ELUTING STENT IN NEW ZEALAND WHITE RABBIT AORTA OR ILIAC ARTERIES." Biomedical Engineering: Applications, Basis and Communications 27, no. 05 (October 2015): 1550046. http://dx.doi.org/10.4015/s1016237215500465.
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Since the percutaneous coronary intervention (PCI) was first introduced into China in 1984, this procedure has become widely accepted as an important step in coronary revascularization. This study aims to evaluate intimal hyperplasia and thrombosis after implantation of platelet glycoprotein IIIa monoclonal antibody (mAb)-eluting stent in the New Zealand white rabbit abdominal aorta or iliac artery by comparing CT angiography and pathological experiments. The antibody-eluting stents were prepared by the passive absorption method. Arterial intima in the stented segment and 0.5 cm adjacent to the stented site were observed and analyzed by scanning electron microscopy (SEM) and cross-sectional staining. Endothelialization and thrombosis on the stent surface were visualized by CT angiography and three-dimensional (3D) reconstruction technique in animals surviving from 1 to 12 weeks. Compared to stainless steel stents, the surface of antibody-eluting stents was covered with a complete endothelial layer after four weeks. Both CT angiography and pathological results showed intimal hyperplasia (p < 0.05) after 12 weeks. Therefore, pathological methods are the goldern standard for evaluation of intimal hyperplasia while CT angiography has a higher specificity in demonstrating the intimal changes after stent implantation for 12 weeks. The mAb-eluting stent has the potential to prevent thrombosis formation due to the interaction of stent with blood, and decreases the stenosis ratio by inhibiting neointima proliferation.
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Hariri, R. J., D. R. Alonso, D. P. Hajjar, D. Coletti, and M. E. Weksler. "Aging and arteriosclerosis. I. Development of myointimal hyperplasia after endothelial injury." Journal of Experimental Medicine 164, no. 4 (October 1, 1986): 1171–78. http://dx.doi.org/10.1084/jem.164.4.1171.
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Old Fischer 344 rats are more susceptible to vascular lesions after arterial endothelial injury than are young animals. Thus, 20-26-mo-old Fischer 344 rats developed greater and more persistent intimal proliferative lesions than did 2-5-mo-old rats after aortic endothelial denudation. 3 d after deendothelialization, intimal thickness was increased two-fold in both old and young animals. However, 14 d after endothelial injury, intimal thickness had increased nearly five times in old animals, but had regressed to normal in young animals. Intimal thickness of young aortic grafts transplanted into young recipients did not differ significantly from adjacent host aorta or autotransplanted aortic segments 6 wk after surgery. In contrast, intimal thickness of old grafts transplanted into young recipients was eight times greater than adjacent young host aorta 6 wk after surgery. The density of cell nuclei in the intima of old grafts was also much greater than that in young grafts. Thus, in two experimental models of vascular injury, old rats have consistently had greater myointimal hyperplasia than young rats. The increased proliferative response of aortic smooth muscle cells after vascular injury of old animals may contribute to the increased prevalence of vascular disease with age.
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Stolic, Radojica. "Dysfunction of the arteriovenous fistula for hemodialysis as a consequence of venous neointimal hyperplasia and treatment strategies." Srpski arhiv za celokupno lekarstvo 147, no. 9-10 (2019): 642–48. http://dx.doi.org/10.2298/sarh180413020s.
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One of the main problems related to inadequate planning of vascular access is dysfunction during maturation. Arteriovenous fistula dysfunction is most often a consequence of neointimal hyperplasia. Important causes for initial dysfunction of the fistula include narrow lumens of the arteries and veins used for anastomosis, damage to the vascular endothelium during fistula creation, previous venipuncture, postoperative development of venous collaterals, the impact force of friction on the arteriovenous anastomosis, a genetic predisposition for development of vascular stenosis, neointimal hyperplasia and previously persistent venous neointimal hyperplasia. Any damage to the endothelium is a stimulus for neointimal hyperplasia. During surgery for creating the fistula, endothelial cells separate on the intima, edema appears, fibrin is deposited, leukocytes and platelets infiltrate. Spotted edema and necrosis of smooth muscle cells appear in the media. In order to determine an adequate therapeutic strategy, the pathogenesis of intimal hyperplasia has been widely considered from different aspects. It is currently based on preoperative preservation of veins and careful selection of blood vessels, percutaneous transluminal angioplasty or surgical revision. Nevertheless, no current therapeutic strategies provide appropriate recommendations to improve maturation of the arteriovenous fistula. Notwithstanding considerable knowledge about the pathogenesis of venous neointimal hyperplasia, currently no prophylactic treatments would reduce its progression.
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Hollingsworth, S. J., C. B. Tang, and S. G. E. Barker. "The Effects of Heparin on Cultured Explants of Varicose Long Saphenous Vein." Phlebology: The Journal of Venous Disease 16, no. 2 (June 2001): 60–67. http://dx.doi.org/10.1177/026835550101600203.
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Objective: To examine the effects of heparin on smooth muscle cells (SMCs) in explants of varicose, long saphenous vein (LSV). Procedures: Explants of varicose LSV were cultured for 7 days either alone, or with heparin at 10, 100 or 1000 IU/ml (Monoparin). At 7 days, cultured explants were analysed for changes in intimal and medial thickness and by immuno-histochemistry. Comparisons were made with explants at initial isolation and with similar, cultured explants of normal LSV. Results: In normal LSV, by day 7, SMC-derived neo-intimal hyperplasia developed ( p<0.01) with an increase in intimal thickness ( p<0.02) and a decrease in medial thickness ( p<0.001). Heparin at 10 and 100 IU/ml further enhanced this neo-intima formation ( p<0.001). In contrast, at 1000 IU/ml, heparin inhibited neo-intima formation. In varicose explants, the pattern of intimal and medial changes was different. At isolation, varicose LSVs had substantially thicker intimal layers ( p<0.001). When cultured alone, a thicker media developed ( p<0.001) but there was little change in intimal thickness. Heparin at all concentrations had no effect on the thicker medial development seen in controls but did, however, reduce intimal thickness ( p<0.005). Conclusions: The response to heparin in explants of varicose LSV is different from that of normal LSV, which is biphasic and complex.
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Chang, Hong, Huan Lei, Yizhou Zhao, Ruixue Yang, Aiming Wu, Yingqiu Mao, Youliang Huang, et al. "Yiqihuoxuejiedu Formula Restrains Vascular Remodeling by Reducing the Inflammation Reaction and Cx43 Expression in the Adventitia after Balloon Injury." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/904273.
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Vascular remodeling is closely related to hypertension, atherosclerosis, and restenosis after PCI. Considerable evidence indicates that the activation and proliferation of adventitial fibroblasts play key roles in vessel injury. The inflammatory response and high expression of connexins contribute to adventitial remodeling. Therefore, reducing inflammation reaction and connexins expression in adventitia may become a new target to prevent vascular remodeling. Yiqihuoxuejiedu formula, composed of TCM therapeutic principle of supplementing qi, activating blood and detoxification, can inhibit restenosis after intimal injury. To further investigate the effect of Yiqihuoxuejiedu formula on inflammation and connexins, we established a carotid artery injury model. In model rats, hyperplasia in the intima was mild but obvious in the adventitia; CRP heightened; expressions of MCP-1, CD68, and Cx43 increased. Yiqihuoxuejiedu formula relieved intimal hyperplasia and adventitial area, obviously diminished the expressions of CD68 and Cx43 in the adventitia, and reduced CRP but did not lower MCP-1. These results indicated that Yiqihuoxuejiedu formula inhibited vascular remodeling especially adventitial hyperplasia by reducing the inflammation reaction including lowering macrophages infiltration and systemic nonspecific inflammatory response and also restraining gap junction connexins leading to less communication among cells. This study provides new ideas and methods for the prevention and treatment of vascular remodeling.
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Wang, Yung-Chun, Dunpeng Cai, Xiao-Bing Cui, Ya-Hui Chuang, William P. Fay, and Shi-You Chen. "Janus Kinase 3 Deficiency Promotes Vascular Reendothelialization—Brief Report." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 6 (June 2021): 2019–26. http://dx.doi.org/10.1161/atvbaha.121.316293.
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Objective: The objective of this study is to determine the role of JAK3 (Janus kinase 3) in reendothelialization after vascular injury. Methods and Results: By using mouse carotid artery wire injury and rat balloon injury model, we found that JAK3 regulates reendothelialization and endothelial cell proliferation after vascular injury. JAK3 and phospho-JAK3 levels were increased in neointimal smooth muscle cells in response to vascular injury in mice. JAK3 deficiency dramatically attenuated the injury-induced intimal hyperplasia in carotid arteries of both male and female mice. Importantly, JAK3 deficiency caused an increased rate of reendothelialization following mechanical injury. Likewise, knockdown of JAK3 in medial smooth muscle cells elicited an accelerated reendothelialization with reduced intimal hyperplasia following balloon injury in rat carotid arteries. Interestingly, knockdown of JAK3 restored the expression of smooth muscle cell contractile protein smooth muscle α-actin in injury-induced intimal smooth muscle cells while increased the proliferating endothelial cells in the intima area. Conclusions: Our results demonstrate a novel role of JAK3 in the regeneration of endothelium after vascular injury, which may provide a new strategy to enhance reendothelialization while suppressing neointimal formation for effective vascular repair from injury.
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Liu, Chengwei, Xuesong Zhang, Shi Wang, Mingxun Cheng, Chuanyu Liu, Shuqing Wang, Xinhua Hu, and Qiang Zhang. "Transfected Early Growth Response Gene-1 DNA Enzyme Prevents Stenosis and Occlusion of Autogenous Vein GraftIn Vivo." BioMed Research International 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/310406.
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The aim of this study was to detect the inhibitory action of the early growth response gene-1 DNA enzyme (EDRz) as a carrying agent by liposomes on vascular smooth muscle cell proliferation and intimal hyperplasia. An autogenous vein graft model was established. EDRz was transfected to the graft vein. The vein graft samples were obtained on each time point after surgery. The expression of the EDRz transfected in the vein graft was detected using a fluorescent microscope. Early growth response gene-1 (Egr-1) mRNA was measured using reverse transcription-PCR andin situhybridization. And the protein expression of Egr-1 was detected by using western blot and immunohistochemistry analyses. EDRz was located at the media of the vein graft from 2 to 24 h, 7 h after grafting. The Egr-1 protein was mainly located in the medial VSMCs, monocytes, and endothelium cells during the early phase of the vein graft. The degree of VSMC proliferation and thickness of intima were obviously relieved compared with the no-gene therapy group. EDRz can reduce Egr-1 expression in autogenous vein grafts, effectively restrain VSMC proliferation and intimal hyperplasia, and prevent vascular stenosis and occlusion after vein graft.
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Costa, Regina de Faria Bittencourt da, Djalma José Fagundes, Yara Juliano, Neil Ferreira Novo, and Wilma Therezinha Trench Vieira. "Effects of external gamma radiation on femoral artery reimplantation in rats: morphometrical analyzes." Acta Cirurgica Brasileira 18, no. 2 (March 2003): 86–96. http://dx.doi.org/10.1590/s0102-86502003000200004.
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PURPOSE: To investigate the effects of external gamma radiation on rat femoral artery reimplant. METHODS: Sixty-two male Wistar rats were distributed in two groups I (Control) and II (Irradiated), both formed by three observation subgroups: 2 (10 animals), 7 (11) and 21(10) postoperative days (PO). The right femoral artery of each animal was split up and reimplanted (end-to-end anastomosis), through microsurgery technique. In the first PO day group II animals were irradiated with a single dose of 15Gy, external source. The histological analysis, qualitative and descriptive analysis, was accomplished through hematoxylin and eosin (HE), Verhoeff and Masson trichromium methodology. Morphometric analysis was realized in the same slides used to histological analysis stained by HE. Computer software was used to quantify morphological alterations of the vascular wall, by processing captured images from a microscope. It was analyzed the intimal layer (intimal hyperplasia and endothelium cells formation) and the nuclei percentage of smooth muscular cell in the medium layer and in the intima hyperplasia. The data were treated applying the statistical tests: Fisher's exact, Chi-square, Mann-Whitney, Kruskal-Wallis and analysis of variance (p < .05). RESULTS: The patency graft was observed by microscope distal to the autograft in 93.5% (29/31). It was observed that the gamma-radiation reduced the degree of covering of the vascular wall for the neo-formed endothelium. The nuclei percentage of smooth muscular cells, in the media, was smaller compared to control animals, although it was no significant for the studied sample size. The irradiated group showed a significant lower luminal stenosis and the intimal hyperplasia occurrence. In this group the percentage of smooth muscular cells proliferation, in the media, were significantly lower for 7 and 21 days of observation. CONCLUSION: The external single dose of 15 Gy gamma-radiation delivered at first postoperative day may inhibit the endothelial cells regeneration and the percentage of lumen stenosis and prevents intimal hyperplasia, in the 2, 7 and 21 PO on femoral artery autograft in rats.
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Tatic, Vujadin, Vladimir Kanjuh, Sasa Rafajlovski, Dusan Suscevic, and Radoje Ilic. "Morphological changes in aorto-coronary vein graft: The analysis of autopsy and biopsy material." Vojnosanitetski pregled 61, no. 5 (2004): 499–506. http://dx.doi.org/10.2298/vsp0405499t.
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Background. Patients with implanted aortic coronary grafts have different survival time, which raises the question why the efficacy of graft implants is so poor. The aim of this study was to present the results of the analysis of morphological changes in the vein grafts taken after the death of patients who died after surgery in different time intervals, as well to present the analysis of the grafts obtained after surgical reintervention. Methods. The total number of 656 grafts of 308 dead patients was analyzed, as well as 76 grafts from 40 patients who underwent surgical reintervention. According to the duration of the graft since surgical intervention until death, all the analyzed changes were divided into two groups: a) early changes and complications, and b) late changes and complications in aorto-coronary vein grafts. Results. After the autopsy, 518 vein grafts from the first group were evaluated histopathologically. Changes were found in the form of small or large areas with peeled endothelium in 266 grafts, with the insudation of fibrin and thrombocytes in such places, subendothelial edema, and occlusive thrombosis of the graft lumen. Significant stenosis, which occurred distally from the anastomoses, was present in 118 grafts without changes in the walls of the graft, and there was significant narrowing of the graft lumen in 134 vein grafts due to intimal hyperplasia. In the second group, 138 grafts were histopathologically analyzed after autopsy. Significant hyperplasia was present in 117 grafts with the migration of smooth muscle cells from media into intima, and in 21 grafts there were atheromatous plaques. In 120 veins analyzed before the graft implantation, the lesion or the lack of endothelium was found, as well as the penetration of fibrin and blood elements and intimal hyperplasia. In 46 veins analyzed before the graft implantation, significant intimal hyperplasia with the elevated number of smooth muscle cells was found. Conclusion. The most frequent lesions in the grafts were the lesions of the endothelium, which caused thrombosis formation and lumen occlusion. Intimal hyperplasia in patients with longer survival time occurred due to the migration of smooth muscle cells from the media, or due to the formation of atherosclerotic plaques, which caused graft lumen stenosis or thrombosis.
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Kachlík, Stingl, Sosna, Straka, Lametschwandtner, Minnich, and Fára. "Morphological features of vasa vasorum in pathologically changed human great saphenous vein and its tributaries." Vasa 37, no. 2 (May 1, 2008): 127–36. http://dx.doi.org/10.1024/0301-1526.37.2.127.
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Background: The question whether the primary increase of vasa vasorum (VV) of venous wall (i) plays an initial role in varicogenesis or (ii) is an expression of impairment of the nutritional conditions in superficial veins of lower extremities is not unambiguously solved yet. The aim of the study was to describe the arrangement of the VV within the wall of the human great saphenous vein (GSV) qualitatively, and of its tributaries at different stages of varicosis and in other pathological states like thrombophlebitis or phlebosclerosis. Material and methods: 22 patients deserving an aorto-coronary bypass surgery or GSV surgery were subdivided into three groups according to the staging of their varices and other pathology. The harvested GSV were prepared for light and scanning electron microscopy. One cadaverous specimen of GSV was injected with India ink. Results: In specimens from reticular and primary large varices local intimal hyperplasia was regularly found, partially accompanied with a mild increase of VV. Tortuosities and irregular dilations of adventitial veins were also found. In patients with recurrent primary varices or thrombophlebitis severe intimal and medial hyperplasia, thrombosis and a striking increase of VV were found. The intima remained avascular in all cases. Conclusions: Remarkable increase of VV accompanies the most severe forms of varices as well as all cases of the extreme grades of phlebosclerosis, medial hyperplasia and thrombosis. We hypothesize that this increase in VV is rather a secondary vascular reaction to the impaired metabolic conditions within the venous wall than a primary varicogenic factor.
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Gregory, Elaine K., Antonio R. Webb, Janet M. Vercammen, Megan E. Flynn, Guillermo A. Ameer, and Melina R. Kibbe. "Periadventitial atRA citrate-based polyester membranes reduce neointimal hyperplasia and restenosis after carotid injury in rats." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 10 (November 15, 2014): H1419—H1429. http://dx.doi.org/10.1152/ajpheart.00914.2013.
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Oral all-trans retinoic acid (atRA) has been shown to reduce the formation of neointimal hyperplasia; however, the dose required was 30 times the chemotherapeutic dose, which already has reported side effects. As neointimal formation is a localized process, new approaches to localized delivery are required. This study assessed whether atRA within a citrate-based polyester, poly(1,8 octanediolcitrate) (POC), perivascular membrane would prevent neointimal hyperplasia following arterial injury. atRA-POC membranes were prepared and characterized for atRA release via high-performance liquid chromatography with mass spectrometry detection. Rat adventitial fibroblasts (AF) and vascular smooth muscle cells (VSMC) were exposed to various concentrations of atRA; proliferation, apoptosis, and necrosis were assessed in vitro. The rat carotid artery balloon injury model was used to evaluate the impact of the atRA-POC membranes on neointimal formation, cell proliferation, apoptosis, macrophage infiltration, and vascular cell adhesion molecule 1 (VCAM-1) expression in vivo. atRA-POC membranes released 12 μg of atRA over 2 wk, with 92% of the release occurring in the first week. At 24 h, atRA (200 μmol/l) inhibited [3H]-thymidine incorporation into AF and VSMC by 78% and 72%, respectively (* P = 0.001), with negligible apoptosis or necrosis. Histomorphometry analysis showed that atRA-POC membranes inhibited neointimal formation after balloon injury, with a 56%, 57%, and 50% decrease in the intimal area, intima-to-media area ratio, and percent stenosis, respectively ( P = 0.001). atRA-POC membranes had no appreciable effect on apoptosis or proliferation at 2 wk. Regarding biocompatibility, we found a 76% decrease in macrophage infiltration in the intima layer ( P < 0.003) in animals treated with atRA-POC membranes, with a coinciding 53% reduction in VCAM-1 staining ( P < 0.001). In conclusion, perivascular delivery of atRA inhibited neointimal formation and restenosis. These data suggest that atRA-POC membranes may be suitable as localized therapy to inhibit neointimal hyperplasia following open cardiovascular procedures.
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Pei, Fang, Hua Pei, Chunhua Su, Lin Du, Jifen Wang, Fusheng Xie, Qi Yin, and Zhao Gao. "Fisetin Alleviates Neointimal Hyperplasia via PPARγ/PON2 Antioxidative Pathway in SHR Rat Artery Injury Model." Oxidative Medicine and Cellular Longevity 2021 (April 21, 2021): 1–15. http://dx.doi.org/10.1155/2021/6625517.
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The phenotypic transformation of proliferation and migration in vascular smooth muscle cells (VSMCs) from media to intima is the basic pathology of neointimal hyperplasia after angioplasty in hypertensive patients. Angiotensin II (AngII) stimulates oxidative stress in VSMC, inducing VSMC proliferation and migration, which is a critical factor in both developments of hypertension and angioplasty-induced arterial restenosis. Fisetin, a plant flavonoid polyphenol, has been reported to be antioxidative and potent senolytic. It is unknown whether fisetin would inhibit neointimal hyperplasia. Therefore, we investigated the role of fisetin in neointimal formation in vitro and in vivo. The rat thoracic aortic smooth muscle cells (A10 cells) stimulated by AngII were used as the in vitro neointimal hyperplasia model, where AngII significantly induced the proliferation and migration in A10 cells. We found that fisetin could dose-dependently inhibit the effect of AngII via inducing the expression of an antioxidant, paraoxonase-2 (PON2), whose overexpression could inhibit the proliferation and migration of A10 cells and downexpression by siRNA had the opposite effect. Furthermore, we found the mechanism of fisetin’s inducing PON2 expression involved PPARγ. Rosiglitazone, a PPARγ agonist, could increase PON2 expression in A10 cells, while the PPARγ inhibitor prevented the effect of fisetin on PON2. The in vivo neointimal hyperplasia model was established 2 weeks after the carotid artery balloon injury in SHR rats. Administration of fisetin (ip 3 mg/kg daily for 2 weeks) right after the injury significantly increased PON2 expression in the artery, inhibiting ROS production, and efficiently reduced carotid neointimal hyperplasia. These results indicate that fisetin increases the expression of antioxidant PON2 via activation of PPARγ, reducing oxidative stress, inhibiting VSMC proliferation and migration, and alleviates neointimal hyperplasia after intimal injury. PON2 may be a potential therapeutic target to reduce arterial remodeling after angioplasty in hypertensive patients.
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Jahan, Reza, Timothy D. Solberg, Daniel Lee, Paul Medin, Satoshi Tateshima, James Sayre, Antonio De Salles, Harry V. Vinters, and Fernando Vinuela. "Stereotactic Radiosurgery of the Rete Mirabile in Swine: A Longitudinal Study of Histopathological Changes." Neurosurgery 58, no. 3 (March 1, 2006): 551–58. http://dx.doi.org/10.1227/01.neu.0000197335.93538.bd.
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Abstract OBJECTIVE: Stereotactic radiosurgery is an established, effective treatment for brain arteriovenous malformations. The mechanisms of vessel occlusion in arteriovenous malformations has not been extensively evaluated. To better understand these mechanisms, we report histopathological changes in the swine rete mirabile after stereotactic radiosurgery. METHODS: Thirty-five swine were used, 15 as nonradiated controls and 20 as radiated. Two in the control group and five in the radiated group were sacrificed before the study endpoint. Tissue was obtained from 13 nonradiated (4 at 3 mo, 5 at 6 mo, 4 at 9 mo) and 15 radiated swine (2 at 3 mo, 3 at 6 mo, 10 at 9 mo) for histological, immunohistochemical, and morphometric analysis. RESULTS: Radiated vessels showed increasing intimal hyperplasia over the follow-up period. Histometrical analysis confirmed this with evidence of progressive luminal narrowing over the follow-up period. Immunohistochemical analysis showed intimal cells to be proliferating smooth muscle cells with surrounding extracellular collagen Type IV. Adventitial fibrosis composed of collagen Type IV was also seen with smooth muscle cells interspersed within the collagen matrix. The nonradiated animals showed no intimal hyperplasia or change in the appearance or size of the vessels over the same follow-up period. Adventitial fibrosis was minimal in the nonradiated animals. CONCLUSION: The vessels show an intimal response to radiation with progressive occlusion caused by migrating, proliferating smooth muscle cells, a likely source of the extracellular collagen in the intima. Cytokine mediated pathways likely produce these morphological changes. Future studies will be directed toward elucidating these underlying molecular mechanisms.
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Chen, Yuh-Fung, Kuo-Jen Wu, Lian-Ru Siao, and Huei-Yann Tsai. "Trilinolein, a Natural Triacylglycerol, Protects Cerebral Ischemia through Inhibition of Neuronal Apoptosis and Ameliorates Intimal Hyperplasia via Attenuation of Migration and Modulation of Matrix Metalloproteinase-2 and RAS/MEK/ERK Signaling Pathway in VSMCs." International Journal of Molecular Sciences 23, no. 21 (October 24, 2022): 12820. http://dx.doi.org/10.3390/ijms232112820.
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Cerebrovascular disease is one of the leading causes of disability and death worldwide, and seeking a potential treatment is essential. Trilinolein (TriL) is a natural triacylglycerol presented in several plants. The effects of TriL on cerebrovascular diseases such as cerebral ischemia and carotid stenosis have never been studied. Accordingly, we investigated the protection of TriL on cerebral ischemia/reperfusion (I/R) and vascular smooth muscle cell (VSMC) migration in vivo and in vitro. The cerebral infarction area, the intima to media area (I/M ratio), and proliferating cell nuclear antigen (PCNA)-staining of the carotid artery were measured. Platelet-derived growth factor (PDGF)-BB-stimulated A7r5 cell migration and potential mechanisms of TriL were investigated by wound healing, transwell, and Western blotting. TriL (50, 100, and 200 mg/kg, p.o.) reduced: the cerebral infarction area; neurological deficit; TUNEL-positive apoptosis; intimal hyperplasia; and PCNA-positive cells in rodents. TriL (5, 10, and 20 µM) significantly inhibited PDGF-BB-stimulated A7r5 cell migration and reduced matrix metalloproteinase-2 (MMP-2), Ras, MEK, and p-ERK protein levels in PDGF-BB-stimulated A7r5 cells. TriL is protective in models of I/R-induced brain injury, carotid artery ligation-induced intimal hyperplasia, and VSMC migration both in vivo and in vitro. TriL could be potentially efficacious in preventing cerebral ischemia and cerebrovascular diseases.
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Grudzinska, Monika K., Krzysztof Bojakowski, Joanna Soin, Frank Stassen, Cecilia Söderberg-Nauclér, and Piotr Religa. "RCMV increases intimal hyperplasia by inducing inflammation, MCP-1 expression and recruitment of adventitial cells to intima." Herpesviridae 1, no. 1 (2010): 7. http://dx.doi.org/10.1186/2042-4280-1-7.
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Szabo, Balazs, Balazs Gasz, Laszlo Adam Fazekas, Adam Varga, Levente Kiss-Papai, Orsolya Matolay, Zsofia Rezsabek, Mohammad W. Al-Smadi, and Norbert Nemeth. "Heterogeneous Maturation of Arterio-Venous Fistulas and Loop-Shaped Venous Interposition Grafts: A Histological and 3D Flow Simulation Comparison." Biomedicines 10, no. 7 (June 25, 2022): 1508. http://dx.doi.org/10.3390/biomedicines10071508.
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Vascular graft maturation is associated with blood flow characteristics, such as velocity, pressure, vorticity, and wall shear stress (WSS). Many studies examined these factors separately. We aimed to examine the remodeling of arterio-venous fistulas (AVFs) and loop-shaped venous interposition grafts, together with 3D flow simulation. Thirty male Wistar rats were randomly and equally divided into sham-operated, AVF, and loop-shaped venous graft (Loop) groups, using the femoral and superficial inferior epigastric vessels for anastomoses. Five weeks after surgery, the vessels were removed for histological evaluation, or plastic castings were made and scanned for 3D flow simulation. Remodeling of AVF and looped grafts was complete in 5 weeks. Histology showed heterogeneous morphology depending on the distribution of intraluminal pressure and WSS. In the Loop group, an asymmetrical WSS distribution coincided with the intima hyperplasia spots. The tunica media was enlarged only when both pressure and WSS were high. The 3D flow simulation correlated with the histological findings, identifying “hotspots” for intimal hyperplasia formation, suggesting a predictive value. These observations can be useful for microvascular research and for quality control in microsurgical training.
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Toshmatova, Mahfuza, Sentaro Nakanishi, Yukiharu Sugimura, Vera Schmidt, Artur Lichtenberg, Alexander Assmann, and Payam Akhyari. "Influence of Laminin Coating on the Autologous In Vivo Recellularization of Decellularized Vascular Protheses." Materials 12, no. 20 (October 15, 2019): 3351. http://dx.doi.org/10.3390/ma12203351.
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Decellularization of non-autologous biological implants reduces the immune response against foreign tissue. Striving for in vivo repopulation of aortic prostheses with autologous cells, thereby improving the graft biocompatibility, we examined surface coating with laminin in a standardized rat implantation model. Detergent-decellularized aortic grafts from donor rats (n = 37) were coated with laminin and systemically implanted into Wistar rats. Uncoated implants served as controls. Implant re-colonization and remodeling were examined by scanning electron microscopy (n = 10), histology and immunohistology (n = 18). Laminin coating persisted over eight weeks. Two weeks after implantation, no relevant neoendothelium formation was observed, whereas it was covering the whole grafts after eight weeks, with a significant acceleration in the laminin group (p = 0.0048). Remarkably, the intima-to-media ratio, indicating adverse hyperplasia, was significantly diminished in the laminin group (p = 0.0149). No intergroup difference was detected in terms of medial recellularization (p = 0.2577). Alpha-smooth muscle actin-positive cells originating from the adventitial surface invaded the media in both groups to a similar extent. The amount of calcifying hydroxyapatite deposition in the intima and the media did not differ between the groups. Inflammatory cell markers (CD3 and CD68) proved negative in coated as well as uncoated decellularized implants. The coating of decellularized aortic implants with bioactive laminin caused an acceleration of the autologous recellularization and a reduction of the intima hyperplasia. Thereby, laminin coating seems to be a promising strategy to enhance the biocompatibility of tissue-engineered vascular implants.
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Bodnar, P. Ya. "Structural features of the lower limb deep vein remodeling as a morphologic component in the pathogenesis of pulmonary thromboembolism in cancer patients." Reports of Morphology 25, no. 4 (December 19, 2019): 11–16. http://dx.doi.org/10.31393/morphology-journal-2019-25(4)-02.
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Oncological patients are at high risk of developing thromboembolic complications, which is a manifestation of a complex set of symptoms – cancer. At the same time, the analysis of the literature shows that the question of the involvement of structural changes of the vascular wall in the pathogenesis of possible primary thrombus formation in cancer patients remains open. The aim of the study – to study the structural features of remodeling of the deep vein of the lower extremity as a morphological link of pathogenesis of pulmonary embolism in cancer patients. Retrospective analysis of 54 protocols of autopsy of deaths from cardiopulmonary shock caused by pulmonary embolism in 2014-2018 was performed. In parallel, all patients were determined the number of free-circulating endothelial cells in the citrate blood by Hladovez J. method, in modification of Sivak V.V. and co-authors (2007). Statistical processing of digital data was performed using the software “Excel” and “STATISTICA” 6.0. In retrospective analysis of autopsy protocols, the highest proportion of pulmonary embolism was report in patients with cancer of the uterus and colon. Morphological changes of the deep vein of the lower extremities in cancer patients were manifested by endothelium desquamation and circular and focal muscular-fibrous hyperplasia of the intima, which caused disturbances of laminar flow of blood; muscular-fibrous atrophy with neovascularization of the middle membrane and sclerosis of vasa vasorum vessels of adventitia. The process of remodeling was also manifest by the inflammatory transformation of the vascular wall, the formation of obstructing and floating blood clots with their subsequent organization, vascularization and recanalization. The cause of intimal thickening, atrophy, and sclerosis with midbrain neovascularization is most likely a hypoxic mechanism of activation of transforming connective tissue growth factors that stimulate collagenogenesis and neoangiogenesis. Desquamation of endothelial cells can also be considered as a significant contributor to thrombus formation. Endothelial cells have a protective function aimed at eliminating damage to the vascular wall by thrombus formation and the development of fibrous intima hyperplasia. In addition, tumor cells are themselves capable of producing excess platelet growth factor, which causes intima proliferation. So, a component of pathomorphogenesis of pulmonary artery thromboembolism in cancer patients is a complex structural reconstruction of the wall of the deep vein of the lower extremity, which causes the development of its thrombosis. Deep vein remodeling in cancer patients is characterized by endothelial cell desquamation, intima and middle-membrane thickening and sclerosis in combination with vasa vasorum fibrous degeneration and perforant vein thrombosis. In response to hemodynamic disorders, compensatory remodeling develops: the combination of leiomyocyte atrophy with their hypertrophy and neovascularization of the middle membrane.
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Kim, Jung-Hwan, Eui Hwa Jang, Ji-Yeon Ryu, Jiyong Lee, Jae Ho Kim, Wonhyoung Ryu, and Young-Nam Youn. "Sirolimus-Embedded Silk Microneedle Wrap to Prevent Neointimal Hyperplasia in Vein Graft Model." International Journal of Molecular Sciences 24, no. 4 (February 7, 2023): 3306. http://dx.doi.org/10.3390/ijms24043306.
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We investigated the role of a sirolimus-embedded silk microneedle (MN) wrap as an external vascular device for drug delivery efficacy, inhibition of neointimal hyperplasia, and vascular remodeling. Using dogs, a vein graft model was developed to interpose the carotid or femoral artery with the jugular or femoral vein. The control group contained four dogs with only interposed grafts; the intervention group contained four dogs with vein grafts in which sirolimus-embedded silk-MN wraps were applied. After 12-weeks post-implantation, 15 vein grafts in each group were explanted and analyzed. Vein grafts applied with the rhodamine B–embedded silk-MN wrap showed far higher fluorescent signals than those without the wrap. The diameter of vein grafts in the intervention group decreased or remained stable without dilatation; however, it increased in the control group. The intervention group had femoral vein grafts with a significantly lower mean neointima-to-media ratio, and had vein grafts with an intima layer showing a significantly lower collagen density ratio than the control group. In conclusion, sirolimus-embedded silk-MN wrap in a vein graft model successfully delivered the drug to the intimal layer of the vein grafts. It prevented vein graft dilatation, avoiding shear stress and decreasing wall tension, and it inhibited neointimal hyperplasia.
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Planas-Rigol, Ester, Nekane Terrades-Garcia, Marc Corbera-Bellalta, Ester Lozano, Marco A. Alba, Marta Segarra, Georgina Espígol-Frigolé, et al. "Endothelin-1 promotes vascular smooth muscle cell migration across the artery wall: a mechanism contributing to vascular remodelling and intimal hyperplasia in giant-cell arteritis." Annals of the Rheumatic Diseases 76, no. 9 (June 12, 2017): 1624–34. http://dx.doi.org/10.1136/annrheumdis-2016-210792.
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BackgroundGiant-cell arteritis (GCA) is an inflammatory disease of large/medium-sized arteries, frequently involving the temporal arteries (TA). Inflammation-induced vascular remodelling leads to vaso-occlusive events. Circulating endothelin-1 (ET-1) is increased in patients with GCA with ischaemic complications suggesting a role for ET-1 in vascular occlusion beyond its vasoactive function.ObjectiveTo investigate whether ET-1 induces a migratory myofibroblastic phenotype in human TA-derived vascular smooth muscle cells (VSMC) leading to intimal hyperplasia and vascular occlusion in GCA.Methods and resultsImmunofluorescence/confocal microscopy showed increased ET-1 expression in GCA lesions compared with control arteries. In inflamed arteries, ET-1 was predominantly expressed by infiltrating mononuclear cells whereas ET receptors, particularly ET-1 receptor B (ETBR), were expressed by both mononuclear cells and VSMC. ET-1 increased TA-derived VSMC migration in vitro and α-smooth muscle actin (αSMA) expression and migration from the media to the intima in cultured TA explants. ET-1 promoted VSMC motility by increasing activation of focal adhesion kinase (FAK), a crucial molecule in the turnover of focal adhesions during cell migration. FAK activation resulted in Y397 autophosphorylation creating binding sites for Src kinases and the p85 subunit of PI3kinases which, upon ET-1 exposure, colocalised with FAK at the focal adhesions of migrating VSMC. Accordingly, FAK or PI3K inhibition abrogated ET-1-induced migration in vitro. Consistently, ET-1 receptor A and ETBR antagonists reduced αSMA expression and delayed VSMC outgrowth from cultured GCA-involved artery explants.ConclusionsET-1 is upregulated in GCA lesions and, by promoting VSMC migration towards the intimal layer, may contribute to intimal hyperplasia and vascular occlusion in GCA.
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Mejia-Vilet, J. M., Y. J. López-Hernández, J. I. Santander-Vélez, M. Trujeque-Matos, C. Cruz, C. A. Carranza de la Torre, V. Espinosa-Cruz, R. Espinosa-González, N. O. Uribe-Uribe, and L. E. Morales-Buenrostro. "Angiotensin II receptor agonist antibodies are associated with microvascular damage in lupus nephritis." Lupus 29, no. 4 (February 10, 2020): 371–78. http://dx.doi.org/10.1177/0961203320904787.
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Angiotensin II type 1 receptor agonist antibodies (AT1R-AAs) have been associated with hypertension, atherosclerosis and vascular inflammation in human diseases. The aim of the study was to evaluate the prevalence of AT1R-AAs in active lupus nephritis (LN) patients and their association with vascular damage. One hundred and seven active LN patients underwent a complete clinical examination, measurement of AT1R-AAs, ambulatory blood pressure monitoring, carotid intima-media thickness measurement and morphometric analysis of subintimal fibrosis and medial hyperplasia of the vessels in the kidney tissue. Plasma AT1R-AAs were positive in 58 (54.2%) patients. The Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) score, complement C3 and C4 levels and titers of anti-dsDNA antibodies were higher in the group with positive AT1R-AAs compared with those with negative AT1R-AAs. The AT1R-AA titers correlated with anti-dsDNA antibody titers and with complement C3 and C4 serum levels. In the kidney biopsy, the percentage of subintimal fibrosis and the area of medial hyperplasia were greater in the AT1R-AA-positive patients. No differences in arterial pressure, carotid intima-media thickness and response to therapy were detected. In conclusion, AT1R-AAs are prevalent in active LN patients and are associated with histologic features of microvascular damage.
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Albayrak, Gokhan, Erdem Silistreli, Bekir Ergur, Sule Kalkan, Ozalp Karabay, A. Cenk Erdal, and Unal Acikel. "Inhibitory effect of adenosine on intimal hyperplasia and proliferation of smooth muscle cells in a carotid arterial anastomosis animal model." Vascular 23, no. 2 (May 6, 2014): 124–31. http://dx.doi.org/10.1177/1708538114533962.
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Purpose The effect of adenosine (9-β-0-ribifuranosyladenine) on the endothelial cell proliferation and neointimal hyperplasia is investigated in the rabbit carotid artery anastomosis model. Methods Twenty-eight New Zealand white rabbits were arranged in four groups of seven animals each. The right carotid arteries of each animal were transsected and re-anastomosed. The left sides remained as control. In Group A, no medication was used. In Group B, subcutaneous Adenosine was applied for 3 days. In Group C, the same dose was applied for 7 days, and in Group D for 21 days. After 28 days, the luminal diameters, luminal areas, intima/media ratios were all measured by using histopathological evaluation. Findings The mean luminal diameters and areas of the four groups were smaller than the control ones. Massive thickening of smooth muscle cell proliferation and dense intensifying in the connecting tissues were observed most prominently in Group A, in decreasing degrees within other groups. Intima/media ratio was highest in Group A. Scoring the quantity of e-NOS positive staining also revealed a significant difference between the experimental groups and their control associates. Conclusion The process of endothelial cell proliferation and neointimal hyperplasia can be significantly reduced by the use of adenosine.
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Kural, Mehmet H., Guohao Dai, Laura E. Niklason, and Liqiong Gui. "An Ex Vivo Vessel Injury Model to Study Remodeling." Cell Transplantation 27, no. 9 (August 10, 2018): 1375–89. http://dx.doi.org/10.1177/0963689718792201.
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Objective: Invasive coronary interventions can fail due to intimal hyperplasia and restenosis. Endothelial cell (EC) seeding to the vessel lumen, accelerating re-endothelialization, or local release of mTOR pathway inhibitors have helped reduce intimal hyperplasia after vessel injury. While animal models are powerful tools, they are complex and expensive, and not always reflective of human physiology. Therefore, we developed an in vitro 3D vascular model validating previous in vivo animal models and utilizing isolated human arteries to study vascular remodeling after injury. Approach: We utilized a bioreactor that enables the control of intramural pressure and shear stress in vessel conduits to investigate the vascular response in both rat and human arteries to intraluminal injury. Results: Culturing rat aorta segments in vitro, we show that vigorous removal of luminal ECs results in vessel injury, causing medial proliferation by Day-4 and neointima formation, with the observation of SCA1+ cells (stem cell antigen-1) in the intima by Day-7, in the absence of flow. Conversely, when endothelial-denuded rat aortae and human umbilical arteries were subjected to arterial shear stress, pre-seeding with human umbilical ECs decreased the number and proliferation of smooth muscle cell (SMC) significantly in the media of both rat and human vessels. Conclusion: Our bioreactor system provides a novel platform for correlating ex vivo findings with vascular outcomes in vivo. The present in vitro human arterial injury model can be helpful in the study of EC-SMC interactions and vascular remodeling, by allowing for the separation of mechanical, cellular, and soluble factors.
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Jahan, Reza, Timothy D. Solberg, Daniel Lee, Paul Medin, Satoshi Tateshima, Antonio De Salles, James Sayre, Harry V. Vinters, and Fernando Viñuela. "An Arteriovenous Malformation Model for Stereotactic Radiosurgery Research." Neurosurgery 61, no. 1 (July 1, 2007): 152–59. http://dx.doi.org/10.1227/01.neu.0000279736.07683.1e.
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Abstract OBJECTIVE To introduce the utilization of a swine arteriovenous malformation (AVM) model for stereotactic radiosurgery research and to describe the morphological changes in the vessels after radiation. METHODS The model was created in six animals by creation of a right-sided carotid-jugular fistula. Pre- and postsurgical hemodynamic evaluation was performed. The left rete was radiated in four animals; two animals were not radiated. All animals were sacrificed 4 months after surgery, and the bilateral retia were obtained at autopsy. RESULTS There were no procedure-related complications. A pressure gradient of 20 mmHg across the nidus was obtained after surgery. The peak velocity in the arterial feeder increased from 18.5 to 83 cm/s. Microscopic examination of the control animals showed intimal hyperplasia and disrupted internal elastic lamina, similar to human AVMs. The radiated retia showed more prominent intimal hyperplasia. This was confirmed by histometric studies showing greater luminal occlusion in radiated specimens. Adventitial fibrosis was prominent in the radiated retia and was absent in the control animals. Immunohistochemical studies showed proliferating smooth muscle cells in the intima. The adventitial fibrosis consisted of smooth muscle cells surrounded by collagen Type IV extracellular matrix. CONCLUSION The nidus component and high-flow vasculopathy make this an attractive model for stereotactic radiosurgery research. Histology of the radiated models is similar to those described in radiated human AVMs. Further studies of the model are warranted to gain a better understanding of the cellular and molecular events in AVM vessels after stereotactic radiosurgery.
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Yang, Genhuan, Rong Zeng, Xitao Song, Changwei Liu, and Leng Ni. "Sophocarpine Alleviates Injury-Induced Intima Hyperplasia of Carotid Arteries by Suppressing Inflammation in a Rat Model." Journal of Clinical Medicine 10, no. 22 (November 22, 2021): 5449. http://dx.doi.org/10.3390/jcm10225449.
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Introduction: Balloon angioplasty is a commonly applied procedure for treating atherosclerotic vascular diseases. However, the maintenance of long-term lumen patency is relatively difficult due to the occurrence of restenosis. Previous research has shown that the occurrence of vascular wall inflammation is associated with higher rates of restenosis. Sophocarpine (SPC) can exert various therapeutic effects such as anti-oxidation, anti-inflammation, anti-tumor, antivirus and immune regulation. This study aimed to investigate whether SPC can alleviate intimal hyperplasia following balloon injury in a rat carotid artery model. Methods: Twenty Sprague–Dawley rats were randomly assigned to four groups: (i) control, (ii) balloon injury, (iii) balloon injury followed by saline injection, and (iv) balloon injury followed by SPC administration. Each group contained five rats. A high-pressure balloon of 3 mm × 20 mm was placed in the carotid artery. The balloon was inflated to a pressure of 8 atmospheres to carry out rat carotid artery balloon injury model. The areas of neointimal and media were determined by Verhoeff_Van Gieson staining, and the intima-to-media (I:M) ratios were subsequently evaluated. After that, the protein levels of IL-6, IL-1β, MCP-1, NF-κB, TNF-α, VCAM-1, ICAM-1 and eNOS were measured. Results: The ratio of I:M was remarkably higher in the balloon injury group than in the control group (p < 0.01). SPC could significantly decrease the ratio of I:M compared with the balloon injury group (p < 0.01). Besides, the protein levels of IL-6, IL-1β, MCP-1, NF-κB, TNF-α, ICAM-1 and VCAM-1 were increased in rat carotid arteries exposed to balloon injury (p < 0.01), and treatment with SPC could attenuate these effects (p < 0.05). Furthermore, balloon injury inhibited the protein expression of eNOS (p < 0.01), and SPC could elevate its level (p < 0.05). Conclusions: SPC could alleviate an intimal hyperplasia in balloon-injured carotid artery, and the mechanisms underlying this protective effect might be due to its inhibitory potency against inflammation signals. Our study also implies the potential applicability of SPC in treating restenosis after balloon angioplasty.
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Roy, Joy, Phan Kiet Tran, Karin Lundmark, Adnan Rahman, and Ulf Hedin. "Control of Smooth Muscle Cell Proliferation – The Role of the Basement Membrane." Thrombosis and Haemostasis 82, S 01 (1999): 23–26. http://dx.doi.org/10.1055/s-0037-1615548.
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SummaryIn atherogenesis and in response to vessel injury, arterial smooth muscle cells (SMCs) are activated from a quiescent, differentiated state into an actively proliferating and synthetic phenotype which migrate into the intima where the cells participate in the formation of a fibrous plaque or intimal hyperplasia. The mechanisms involved in the control of SMC function are not clear and no preventive therapy against SMC activation is available. Interactions between SMCs and the extracellular matrix have been shown to influence SMC structure and function through integrin-mediated signaling processes. The SMC basement membrane is a specific form of extracellular matrix which seems to be crucial for the maintenance of SMC quiesence and the disruption of these interactions is part of cellular activation after atherogenic or traumatic stimuli. This concept of “negative growth control” may constitute a future target for the development of new strategies in the prevention of SMC activation in atherogenesis and restenosis formation.
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Basi, David L., Neeta Adhikari, Ami Mariash, Qinglu Li, Esther Kao, Sureni V. Mullegama, and Jennifer L. Hall. "Femoral artery neointimal hyperplasia is reduced after wire injury in Ref-1+/− mice." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (January 2007): H516—H521. http://dx.doi.org/10.1152/ajpheart.00246.2006.
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Redox factor-1 (Ref-1) is a multifunctional protein that regulates redox, DNA repair, and the response to cell stress. We previously demonstrated that Ref-1+/− mice exhibit a significantly reduced Ref-1 mRNA and protein levels within the vasculature, which are associated with increased oxidative stress. The goal of this study was to test the hypothesis that partial loss of Ref-1 altered the cellular response to vascular injury. Fourteen days after femoral artery wire injury, we found that vessel intima-to-media ratio was significantly reduced in Ref-1+/− mice compared with that in wild-type mice ( P < 0.01). Bromodeoxyuridine labeling and transferase-mediated dUTP nick-end labeling staining at 14 days did not differ in the Ref-1+/− mice. In vitro studies found no significant changes in either serum-induced proliferation or baseline apoptosis in Ref-1+/− vascular smooth muscle cells. Exposure to Fas ligand; however, did result in increased susceptibility of Ref-1+/− vascular smooth muscle cells to apoptosis ( P < 0.001). Ref-1+/− mice exhibited an increase in circulating baseline levels of IL-10, IL-1α, and VEGF compared with those in wild-type mice but a marked impairment in these pathways in response to injury. In sum, loss of a single allele of Ref-1 is sufficient to reduce intimal lesion formation and to alter circulating cytokine and growth factor expression.
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Koniari, Ioanna, Dimosthenis Mavrilas, Efstratios Apostolakis, Evangelia Papadimitriou, Helen Papadaki, Apostolos Papalois, Evangelia Poimenidi, Ioanna Xanthopoulou, George Hahalis, and Dimitrios Alexopoulos. "Inhibition of Atherosclerosis Progression, Intimal Hyperplasia, and Oxidative Stress by Simvastatin and Ivabradine May Reduce Thoracic Aorta’s Stiffness in Hypercholesterolemic Rabbits." Journal of Cardiovascular Pharmacology and Therapeutics 21, no. 4 (November 25, 2015): 412–22. http://dx.doi.org/10.1177/1074248415617289.
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Aims: This study aims to evaluate atherosclerosis, oxidative stress, and arterial stiffness attenuation by simvastatin and ivabradine in hyperlipidemic rabbits. Methods and Results: Forty rabbits were randomly divided into 4 groups: atherogenic diet (group C), atherogenic diet plus simvastatin (group S), atherogenic diet plus ivabradine (group I), and atherogenic diet plus simvastatin and ivabradine (group S + I). After 9 weeks, rabbits were euthanized and descending aortas excised for mechanical testing. Atherogenic diet induced the development of significant atherosclerotic lesions in group C animals but in none of groups S, I, and S + I. RAM-11 and HHF-35–positive cells were significantly reduced in groups S, I, and S + I compared with group C ( P < .001). A significant neointimal hyperplasia and intima–media ratio reduction was demonstrated in groups S ( P = .015 and P < .001), I ( P = .021 and P < .001), and S + I ( P = .019 and P < .001) compared with group C. Protein nitrotyrosine levels were significantly decreased in group S compared with group C ( P = .009), and reactive oxygen species levels were decreased in group I compared with group C ( P = .011). Aortic stiffness was significantly reduced in groups S, I, and S + I compared with group C ( P = .003, P = .011, and P = .029). Conclusion: Simvastatin and ivabradine significantly inhibited intimal hyperplasia and oxidative stress contributing to aortic stiffness reduction in hyperlipidemic rabbits.
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Sundt, Thoralf M., and Thoralf M. Sundt. "Principles of preparation of vein bypass grafts to maximize patency." Journal of Neurosurgery 66, no. 2 (February 1987): 172–80. http://dx.doi.org/10.3171/jns.1987.66.2.0172.
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✓ Experience in cardiovascular and peripheral vascular surgery with saphenous vein bypass conduits is reviewed. It is clear that meticulous technique and graft preparation are crucial to short-term and long-term patency. The risk of early thrombosis is related to damage to the graft 's native intima, graft flow, and coagulability of the patient 's blood. Attention to atraumatic harvesting techniques and perfection of anastomoses are crucial to minimizing intimal damage. Graft inflow and outflow are fundamental principles. The use of vitamin K antagonists and platelet inhibitors may improve graft survival. Subacute occlusion is related to structural alterations in the grafts themselves. These include intimal hyperplasia and medial fibrosis as the grafts become “arterialized,” valve fibrosis, aneurysmal dilatation, clamp stenosis, and suture stenosis. Long-term patency is threatened primarily by atherosclerosis in the graft itself. There is some evidence that care in vein harvesting and implantation as well as the use of anticoagulant agents affect the development of this complication. A technique for graft preparation is presented that is based on the experience of the authors in harvesting grafts for both cerebral and coronary bypass conduits.
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MAGUIRE, Janet J., Julie C. M. YU, and Anthony P. DAVENPORT. "ETA receptor antagonists inhibit intimal smooth muscle cell proliferation in human vessels." Clinical Science 103, s2002 (September 1, 2002): 184S—188S. http://dx.doi.org/10.1042/cs103s184s.
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We have determined the ability of the endothelin (ET)A receptor antagonist, PD156707 (CI 1020), to inhibit intimal proliferation in human saphenous veins maintained in organ culture. After 28 days in culture, veins exposed to 1µM PD156707 exhibited a significant reduction in intima to intima-plus-media ratio (I:I+M ratio) (0.14±0.02, n = 15) and an increase in lumen area (3.1±0.8mm2) compared with veins cultured without the antagonist (I:I+M, 0.29±0.02; lumen area, 2.5±0.7mm2; n = 23) but were not significantly different from pre-cultured controls (I:I+M, 0.15±0.02; lumen area, 4.4±1.2mm2; n = 17) (Dunn's test for non-parametric multiple comparisons: α<0.05). In organ bath experiments, ET-1 and 5-hydroxytryptamine constricted pre-cultured control vessels with pD2 values (where pD2 is defined as the negative logarithm of the molar EC50 value of an agonist) of 8.9±0.4 and 7.0±0.4 (n = 3) and Emax (efficacy) values of 86±3% and 71±13% (compared with constriction induced by KCl) respectively. There was no difference in the responsiveness of veins cultured for 14 days to either agonist, indicating that the vessels maintained in organ culture remain viable. Crucially, vein segments cultured with 1µM PD156707 (a concentration that antagonized ET-1 responses in pre-cultured control vessels) contracted to ET-1 with a potency comparable to that obtained in vessels cultured in the absence of the antagonist (pD2 = 8.9±0.4 and 8.0±0.6 respectively, n = 3) confirming that PD156707 was not toxic to the tissue at the concentration used. In conclusion we have shown that the ETA-selective antagonist, PD156707, completely blocked intimal hyperplasia in human saphenous veins in organ culture, suggesting that ETA antagonists may be beneficial in preventing or delaying saphenous vein graft disease in patients receiving bypass grafts for coronary artery disease.
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Xie, Tingfei, Yunpeng Xu, Lecai Ji, Xiaolu Sui, Aisha Zhang, Yanzi Zhang, and Jihong Chen. "Heme Oxygenase 1/Peroxisome Proliferator-Activated Receptor Gamma Pathway Protects Intimal Hyperplasia and Mitigates Arteriovenous Fistula Dysfunction by Regulating Oxidative Stress and Inflammatory Response." Cardiovascular Therapeutics 2022 (June 12, 2022): 1–13. http://dx.doi.org/10.1155/2022/7576388.
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Purpose. An arteriovenous fistula (AVF) is the preferred vascular access mode for maintenance hemodialysis, and access stenosis and thrombosis are the primary causes of AVF dysfunction. This study is aimed at exploring the molecular mechanisms underlying AVF development and the roles of the heme oxygenase 1/peroxisome proliferator-activated receptor gamma (HO-1/PPAR-γ) pathway in AVF. Method. AVF model mice were established, and the vascular tissues from the arteriovenous anastomosis site were sent for mRNA sequencing. Differentially expressed mRNAs (DEmRNAs) were screened and subjected to functional analysis. Thereafter, the mice with HO-1 knockdown and coprotoporphyrin IX chloride (COPP) pretreatment were used to investigate the roles of the HO-1/PPAR-γ pathway in AVF. Results. By sequencing, 2514 DEmRNAs, including 1323 upregulated and 1191 downregulated genes, were identified. These DEmRNAs were significantly enriched in the PPAR signaling pathway, AMPK signaling pathway, glucagon signaling pathway, IL-17 signaling pathway, and Toll-like receptor signaling pathway. High expression of HO-1 and PPAR-γ reduced endothelial damage and intimal hyperplasia during AVF maturation. After AVF was established, the levels of transforming growth factor-β (TGF-β), interleukin-1β (IL-1β), interleukin-18 (IL-18), and reactive oxygen species (ROS) were significantly increased ( P < 0.05 ), and HO-1 normal expression and COPP pretreatment evidently decreased their levels in AVF ( P < 0.05 ). Additionally, AVF significantly upregulated HO-1 and PPAR-γ and downregulated MMP9, and COPP pretreatment and HO-1 normal expression further upregulated and downregulated their expression. Conclusion. The HO-1/PPAR-γ pathway may suppress intimal hyperplasia induced by AVF and protect the intima of blood vessels by regulating MMP9 and ROS, thus mitigating AVF dysfunction.
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Tarbell, John, Marwa Mahmoud, Andrea Corti, Luis Cardoso, and Colin Caro. "The role of oxygen transport in atherosclerosis and vascular disease." Journal of The Royal Society Interface 17, no. 165 (April 2020): 20190732. http://dx.doi.org/10.1098/rsif.2019.0732.
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Atherosclerosis and vascular disease of larger arteries are often associated with hypoxia within the layers of the vascular wall. In this review, we begin with a brief overview of the molecular changes in vascular cells associated with hypoxia and then emphasize the transport mechanisms that bring oxygen to cells within the vascular wall. We focus on fluid mechanical factors that control oxygen transport from lumenal blood flow to the intima and inner media layers of the artery, and solid mechanical factors that influence oxygen transport to the adventitia and outer media via the wall's microvascular system—the vasa vasorum (VV). Many cardiovascular risk factors are associated with VV compression that reduces VV perfusion and oxygenation. Dysfunctional VV neovascularization in response to hypoxia contributes to plaque inflammation and growth. Disturbed blood flow in vascular bifurcations and curvatures leads to reduced oxygen transport from blood to the inner layers of the wall and contributes to the development of atherosclerotic plaques in these regions. Recent studies have shown that hypoxia-inducible factor-1α (HIF-1α), a critical transcription factor associated with hypoxia, is also activated in disturbed flow by a mechanism that is independent of hypoxia. A final section of the review emphasizes hypoxia in vascular stenting that is used to enlarge vessels occluded by plaques. Stenting can compress the VV leading to hypoxia and associated intimal hyperplasia. To enhance oxygen transport during stenting, new stent designs with helical centrelines have been developed to increase blood phase oxygen transport rates and reduce intimal hyperplasia. Further study of the mechanisms controlling hypoxia in the artery wall may contribute to the development of therapeutic strategies for vascular diseases.
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Duque, Juan C., Laisel Martinez, Marwan Tabbara, Punam Parikh, Angela Paez, Guillermo Selman, Loay H. Salman, Omaida C. Velazquez, and Roberto I. Vazquez-Padron. "Vascularization of the arteriovenous fistula wall and association with maturation outcomes." Journal of Vascular Access 21, no. 2 (October 14, 2019): 161–68. http://dx.doi.org/10.1177/1129729819863584.
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Background and objectives: The venous vasa vasorum is the mesh of microvessels that provide oxygen and nutrients to the walls of large veins. Whether changes to the vasa vasorum have any effects on human arteriovenous fistula outcomes remains undetermined. In this study, we challenged the hypothesis that inadequate vascularization of the arteriovenous fistula wall is associated with maturation failure. Design, setting, participants, and measurements: This case–control pilot study includes pre-access veins and arteriovenous fistula venous samples (i.e. tissue pairs) from 30 patients undergoing two-stage arteriovenous fistula creation (15 matured and 15 failed to mature). Using anti-CD31 immunohistochemistry, we quantified vasa vasorum density and luminal area (vasa vasorum area) in the intima, media, and adventitia of pre-access veins and fistulas. We evaluated the association of pre-existing and postoperative arteriovenous fistula vascularization with maturation failure and with postoperative morphometry. Results: Vascularization of veins and arteriovenous fistulas was predominantly observed in the outer media and adventitia. Only the size of the microvasculature (vasa vasorum area), but not the number of vessels (vasa vasorum density), increased after arteriovenous fistula creation in the adventitia (median vasa vasorum area 1366 µm2/mm2 (interquartile range 495–2582) in veins versus 3077 µm2/mm2 (1812–5323) in arteriovenous fistulas, p < 0.001), while no changes were observed in the intima and media. Postoperative intimal thickness correlated with lower vascularization of the media ( r 0.53, p = 0.003 for vasa vasorum density and r 0.37, p = 0.045 for vasa vasorum area). However, there were no significant differences in pre-existing, postoperative, or longitudinal change in vascularization between arteriovenous fistulas with distinct maturation outcomes. Conclusion: The lack of change in intimal and medial vascularization after arteriovenous fistula creation argues against higher oxygen demand in the inner walls of the fistula during the vein to arteriovenous fistula transformation. Postoperative intimal hyperplasia in the arteriovenous fistula wall appears to thrive under hypoxic conditions. Vasa vasorum density and area by themselves are not predictive of maturation outcomes.
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Yu, Wen Yan, and Jian Guo Wang. "Finite Element Model and Fluid-Structure Interaction Analysis of the Intravascular Stent." Advanced Materials Research 712-715 (June 2013): 1167–70. http://dx.doi.org/10.4028/www.scientific.net/amr.712-715.1167.
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The 316L stainless steel stent was analyzed about the effect on interaction with plaque and vessels and blood flow during and after implantation using finite element method (FEM) and computational fluid dynamics (CFD). The results showed that tilted ends are likely to damage the intima which may stimulate thrombus formation and neointimal hyperplasia and will cause the restenosis. Stagnant zones formed by the stent may cause the backflow phenomenon, which also contribute to the important elements of in-stent restenosis (ISR).
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Piollet, Marie, Adrian Sturza, Stéphanie Chadet, Claudie Gabillard-Lefort, Lauriane Benoist, Danina-Mirela Muntean, Oana-Maria Aburel, Denis Angoulvant, and Fabrice Ivanes. "P2Y11 Agonism Prevents Hypoxia/Reoxygenation- and Angiotensin II-Induced Vascular Dysfunction and Intimal Hyperplasia Development." International Journal of Molecular Sciences 22, no. 2 (January 16, 2021): 855. http://dx.doi.org/10.3390/ijms22020855.
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Vascular dysfunction in cardiovascular diseases includes vasomotor response impairments, endothelial cells (ECs) activation, and smooth muscle cells (SMCs) proliferation and migration to the intima. This results in intimal hyperplasia and vessel failure. We previously reported that activation of the P2Y11 receptor (P2Y11R) in human dendritic cells, cardiofibroblasts and cardiomyocytes was protective against hypoxia/reoxygenation (HR) lesions. In this study, we investigated the role of P2Y11R signaling in vascular dysfunction. P2Y11R activity was modulated using its pharmacological agonist NF546 and antagonist NF340. Rat aortic rings were exposed to angiotensin II (AngII) and evaluated for their vasomotor response. The P2Y11R agonist NF546 reduced AngII-induced vascular dysfunction by promoting EC-dependent vasorelaxation, through an increased nitric oxide (NO) bioavailability and reduced AngII-induced H2O2 release; these effects were prevented by the use of the P2Y11R antagonist NF340. Human vascular SMCs and ECs were subjected to AngII or H/R simulation in vitro. P2Y11R agonist modulated vasoactive factors in human ECs, that is, endothelial nitric oxide synthase (eNOS) and endothelin-1, reduced SMC proliferation and prevented the switch towards a synthetic phenotype. H/R and AngII increased ECs secretome-induced SMC proliferation, an effect prevented by P2Y11R activation. Thus, our data suggest that P2Y11R activation may protect blood vessels from HR-/AngII-induced injury and reduce vascular dysfunctions. These results open the way for new vasculoprotective interventions.