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Long-Term Type 1 Diabetes Enhances In-Stent Restenosis after Aortic Stenting in Diabetes-Prone BB Rats

机译:长期型1型糖尿病可增强糖尿病人BB大鼠主动脉支架置入后的支架内再狭窄

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摘要

Type 1 diabetic patients have increased risk of developing in-stent restenosis following endovascular stenting. Underlying pathogenetic mechanisms are not fully understood partly due to the lack of a relevant animal model to study the effect(s) of long-term autoimmune diabetes on development of in-stent restenosis. We here describe the development of in-stent restenosis in long-term (~7 months) spontaneously diabetic and age-matched, thymectomized, nondiabetic Diabetes Prone BioBreeding (BBDP) rats (n = 6-7 in each group). Diabetes was suboptimally treated with insulin and was characterized by significant hyperglycaemia, polyuria, proteinuria, and increased HbA1c levels. Stented abdominal aortas were harvested 28 days after stenting. Computerized morphometric analysis revealed significantly increased neointima formation in long-term diabetic rats compared with nondiabetic controls. In conclusion, long-term autoimmune diabetes in BBDP rats enhances in-stent restenosis. This model can be used to study the underlying pathogenetic mechanisms of diabetes-enhanced in-stent restenosis as well as to test new therapeutic modalities.
机译:1型糖尿病患者血管内支架置入术后发生支架内再狭窄的风险增加。根本的致病机制尚未完全被理解,部分原因是缺乏相关的动物模型来研究长期自身免疫性糖尿病对支架内再狭窄发展的影响。我们在这里描述了长期(〜7个月)自发性糖尿病和年龄匹配,经胸腺切除术的非糖尿病性糖尿病生物繁殖(BBDP)大鼠(每组6-7个)的支架内再狭窄的发展。糖尿病患者用胰岛素治疗效果欠佳,其特征是血糖明显升高,多尿,蛋白尿和HbA1c水平升高。支架置入术后28天,收集腹主动脉支架。计算机形态计量学分析显示,与非糖尿病对照组相比,长期糖尿病大鼠的新内膜形成明显增加。总之,BBDP大鼠的长期自身免疫性糖尿病会加剧支架内再狭窄。该模型可用于研究糖尿病增强型支架内再狭窄的潜在致病机制,并测试新的治疗方式。

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