Study of the Biomechanical and Histological Properties of the Abdominal Aorta of Diabetic Rats Exposed to Cigarette Smoke

Abstract

<b><i>Introduction:</i></b> In spite of the great relevance of abdominal aortic aneurysm, its etiopathogenesis is not fully understood. The biomechanical and histological study of the aortic wall may contribute to this elucidation. <b><i>Methods:</i></b> Seventy-five male Wistar rats were divided into 4 groups: control (CG), smoker (SG), diabetic (DG), and diabetic + smoker (DSG). The SG and DSG rats were exposed to cigarette smoke for 30 min/day, 5 days a week. Diabetes was induced by the intravenous injection of streptozotocin. After 16 weeks, the abdominal aorta was collected for biomechanical, histological, and matrix metalloproteinase 2 (MMP-2) activity analyses. <b><i>Results:</i></b> The valid biomechanical tests of 52 specimens were analyzed: 11 in the CG, 10 in the DG, 16 in the SG, and 15 in the DSG. The biomechanical analysis of the fragments showed no differences between the control, DG, SG, and DSG. Collagen deposition also did not present a significant difference between the studied groups. The total count of elastic fibers was higher in diabetic rats (DG and DSG) than in the SG. The inflammatory response observed in all experimental groups was significantly more intense than in the CG. Compared to the DSG, MMP-2 activity showed a significant decrease in the DG. <b><i>Conclusions:</i></b> Resistance and elasticity did not present a difference between the CG and the DG, SG, and DSG. Compared to the CG, the total count of elastic fibers, fragmentation of the elastic lamina, pericellular matrix deposition, and cell loss/substitution in the tunica media showed significant alterations in the aortic walls of the DG, SG, and DSG. MMP-2 activity was lower in the DG aorta than in the DSG aorta.

Potential influencing factors of aortic diameter at specific segments in population with cardiovascular risk

“…One epidemiological study indicates that smoking history is the strongest factor associated with AAA progression [ 23 ]. Mechanistic research report that smoking promotes the degradation of collagen and elastin and consequent weakening of the arterial wall by highly expressed matrix metalloproteinase in aortic wall, finally leading to aortic aneurysm formation [ 24 ]. Although we observed that smoking had a robust association with the diameter of almost all segments apart from ascending aorta in the unadjusted model, the strength of this association could not be further demonstrated by fully adjusted analysis.…”

“…In contrast, diabetes mellitus plays a protective role in dilated aortic diseases [ 8 , 27 ], characterized by the accumulation of collagen in the aortic wall and subsequent increases in matrix volume [ 28 ]. Interestingly, a rat study found that the total count of elastic fibers, fragmentation of the elastic lamina, pericellular matrix deposition, and cell loss/substitution in the tunica media were higher in the diabetic + smoker group (DSG) aorta than those in the smoker group (SG) aorta [ 24 ].The negative relationship between the presence of DM and aortic diameter was supported by a few other reports [ 8 , 15 ]. However, we found only that DM was inversely related with the diameters of annulus, mid and distal arch in univariate analysis.…”

Aerobic Exercise versus Electronic Cigarette in Vascular Aging Process: First Histological Insight

“…Previous study demonstrated that exposure to e-cigarette is composed of 18 mg/ml of nicotine, 70% of propylene glycol, and 30% of vegetable glycerine for 1 h/day, 6 days a week for 4 weeks, resulting in cardiac fibrosis. Exposure to cigarette smoke for 30 minutes a day, 5 days/week for 16 weeks, causes changes in the aortic wall, such as the elastic fiber count, elastic lamina fragmentation, deposition of pericellular matrix, and cell substitution and loss in the tunica media significantly [14][15][16].…”

The effect of smoking on quantification of aortic stiffness by ultrasound time-harmonic elastography

“…The fact that one reader was not blinded to smoking status may have introduced a possible bias, but it was shown that excellent inter-rater agreement was achieved with the blinded reader. Second, THE estimates effective aortic stiffness only, which reflects elastic properties of the vessel wall and surrounding tissue and in part the prevailing arterial blood pressure at the time of measurement 29 – 31 . Additionally, with current technology THE does not allow determination of SWS throughout the cardiac cycle because the traveling pulse wave causes deflection of the aortic wall during systole precluding determination of systolic SWS within the vessel wall.…”