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Updated: Apr 21, 2026

Preclinical Model of Hind Limb Ischemia in Diabetic Rabbits
Published on: June 2, 2019
Hyperglycemia has no effect on development of restenosis after percutaneous transluminal angioplasty (PTA) in a
Xiaojun Zhou1, Jianjun Dong2, Li Zhang1
1Department of EndocrinologyShandong Provincial Qianfoshan Hospital, Shandong University, No. 16766, Jingshi Road, Lixia District, Jinan, Shandong Province, ChinaDepartment of EndocrinologyQilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of SonographyLaboratory of Microvascular MedicineMedical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong, ChinaDepartment of Hepatobiliary Surgerythe People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, China.
Abstract:
It is well known that hyperglycemia is a trigger of atherosclerosis in patients with diabetes mellitus. However, the role of hyperglycemia in restenosis remains unclear. In this study, we investigated the effects of hyperglycemia on restenosis. Stenosis was evaluated in two sets of diabetic rabbit models: i) diabetic restenosis versus nondiabetic restenosis and ii) diabetic atherosclerosis versus nondiabetic atherosclerosis. Our results indicated that there was no difference in rates of stenosis between the diabetic and the nondiabetic groups in restenosis rabbit models. However, the incidence of stenosis was significantly higher in the diabetic atherosclerosis group compared with the nondiabetic atherosclerosis group. Similarly, the intima-media thickness and cell proliferation rate were significantly increased in the diabetic atherosclerosis group compared with the nondiabetic atherosclerosis group, but there was no difference between the diabetic restenosis and the nondiabetic restenosis groups. Our results indicate that hyperglycemia is an independent risk factor for atherosclerosis, but it has no evident effect on restenosis. These findings indicate that the processes of atherosclerosis and restenosis may involve different pathological mechanisms.
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