[Show abstract][Hide abstract] ABSTRACT: Despite recent advances in surgical techniques and perioperative management, the mortality rate in patients with type-A aortic dissection remains high. The establishment of an animal model that exhibits the clinical features of acute aortic dissection would facilitate investigations of the pathogenesis of aortic dissection and the development of appropriate treatments.
Twelve beagle dogs were divided into two groups: (1) an experimental group treated with the modified surgical procedure to generate an ascending aortic dissection (n = 6); and (2) a control group treated with a median sternotomy but without aortic dissection. All animals received continuous intravenous infusion of adrenaline to achieve controlled hypertension. The tearing length of the aortic intima, the pathological changes, the plasma levels of inflammatory mediators, and the organ functions were dynamically examined and compared.
The modified surgical procedure plus controlled hypertension successfully established a novel canine model of acute type-A aortic dissection. In the experimental group, the tearing length of the aortic intima reached the abdominal aorta (average 17 cm), and a false lumen was formed in the aortic media. The lung and intestinal tract had obvious structural injuries. The plasma levels of all inflammatory mediators tested, including tumor necrosis factor-α, interleukin-6, interleukin-10, and endotoxin, were significantly higher in the experimental animals than in the control group. The functional examination of the liver and kidneys revealed substantial disturbances, as reflected by the elevated plasma levels of alanine aminotransferase, aspartate aminotransferase, creatinine, and blood urea nitrogen in the experimental group.
A novel canine model of acute Stanford type-A aortic dissection has been developed, which showed multiple organ dysfunction that mimicked the clinically relevant features observed in man. This aortic dissection model is unique, and may further improve our understanding of the underlying pathogenesis of aortic dissections.