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Updated: Jun 18, 2026

The Rabbit Model of Accelerated Atherosclerosis: A Methodological Perspective of the Iliac Artery Balloon Injury
Published on: October 3, 2017
The Effect of an Atherogenic Diet and Acute Hyperglycaemia on Endothelial Function in Rabbits Is Artery Specific
Alexander Tacey1,2, Tawar Qaradakhi1, Cassandra Smith1,2
1Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC 3011, Australia.
Insights
High glucose causes toxic effects on blood vessels, leading to endothelial dysfunction. This dysfunction is blood vessel-specific and worsened by an atherogenic diet, particularly in the aorta.
Area of Science:
- Cardiovascular Science
- Endocrinology
- Vascular Biology
Background:
- Hyperglycaemia (high blood glucose) is a known risk factor for coronary artery disease.
- The specific blood vessel types affected by hyperglycaemia-induced dysfunction and whether an atherogenic diet exacerbates this are not fully understood.
Purpose of the Study:
- To investigate if hyperglycaemia-induced endothelial dysfunction is blood vessel-specific.
- To determine if an atherogenic diet worsens hyperglycaemia-induced endothelial dysfunction.
Main Methods:
- Dissection of abdominal aorta, iliac, and mesenteric arteries from rabbits fed a normal or atherogenic diet.
- Ex vivo incubation of arteries in control or high glucose solutions (20 mM or 40 mM).
- Isometric tension myography to assess endothelial-dependent vasodilation.
Main Results:
- An atherogenic diet reduced vasodilation in the aorta, iliac, and mesenteric arteries.
- High glucose incubation impaired vasodilation in the aorta and iliac arteries of rabbits on an atherogenic diet.
- No hyperglycaemia-induced dysfunction was observed in the mesenteric arteries.
Conclusions:
- Hyperglycaemia-induced endothelial dysfunction is blood vessel-specific.
- The aorta appears to be the most suitable artery for studying therapeutic interventions for hyperglycaemia-induced endothelial dysfunction.
Abstract:
Hyperglycaemia has a toxic effect on blood vessels and promotes coronary artery disease. It is unclear whether the dysfunction caused by hyperglycaemia is blood vessel specific and whether the dysfunction is exacerbated following an atherogenic diet. Abdominal aorta, iliac, and mesenteric arteries were dissected from New Zealand White rabbits following either a 4-week normal or atherogenic diet (n = 6-12 per group). The arteries were incubated ex vivo in control or high glucose solution (20 mM or 40 mM) for 2 h. Isometric tension myography was used to determine endothelial-dependent vasodilation. The atherogenic diet reduced relaxation as measured by area under the curve (AUC) by 25% (p < 0.05), 17% (p = 0.06) and 40% (p = 0.07) in the aorta, iliac, and mesenteric arteries, respectively. In the aorta from the atherogenic diet fed rabbits, the 20 mM glucose altered EC50 (p < 0.05). Incubation of the iliac artery from atherogenic diet fed rabbits in 40 mM glucose altered EC50 (p < 0.05). No dysfunction occurred in the mesentery with high glucose incubation following either the normal or atherogenic diet. High glucose induced endothelial dysfunction appears to be blood vessel specific and the aorta may be the optimal artery to study potential therapeutic treatments of hyperglycaemia induced endothelial dysfunction.

