Abstract
Abdominal aortic aneurysm (AAA) is a vascular disease involving the gradual dilation of the abdominal aorta. It has been reported that development of AAA is associated with inflammation of the vascular wall; however, the mechanism of AAA rupture is not fully understood. In this study, we investigated the mechanism underlying AAA rupture using a hypoperfusion-induced animal model. We found that the administration of triolein increased the AAA rupture rate in the animal model and that the number of adipocytes was increased in ruptured vascular walls compared to non-ruptured walls. In the ruptured group, macrophage infiltration and the protein levels of matrix metalloproteinases 2 and 9 were increased in the areas around adipocytes, while collagen-positive areas were decreased in the areas with adipocytes compared to those without adipocytes. The administration of fish oil, which suppresses adipocyte hypertrophy, decreased the number and size of adipocytes, as well as decreased the risk of AAA rupture ratio by 0.23 compared to the triolein administered group. In human AAA samples, the amount of triglyceride in the adventitia was correlated with the diameter of the AAA. These results suggest that AAA rupture is related to the abnormal appearance of adipocytes in the vascular wall.
Highlights
Outpatient clinic until the size reaches 55 mm, at which point surgeons recommend that the patient undergo surgery[8]
We found that the administration of triolein, a triglyceride (TG) species, increased the Abdominal aortic aneurysm (AAA) rupture rate in the animal model
We found that the administration of triolein, a kind of TG, increased rupture rates in the experimental model, which enabled us to assess the difference between ruptured and non-ruptured AAA (Fig. 1)
Summary
Outpatient clinic until the size reaches 55 mm, at which point surgeons recommend that the patient undergo surgery[8]. The decision to perform AAA surgery is derived from the balance between the patient’s operative risk and the risk of aneurysm rupture. There is no effective medicine available for inhibiting aneurysm growth or for preventing aneurysm rupture; this can be attributed to the undefined mechanisms of AAA development. Using a hypoperfusion-induced animal model, we demonstrated that hypoperfusion of the vascular wall caused AAA development[10]. The rate of AAA rupture was too low (around 15%) to obtain enough samples for pathological analysis of the ruptured vascular wall. We found that the administration of triolein, a triglyceride (TG) species, increased the AAA rupture rate in the animal model. We performed pathological analysis of the ruptured vascular walls to clarify the mechanism of AAA rupture
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