Premium
Importance of Axial Length in the Detection of Carotid Artery Stiffness Induced by a High Fat Diet
Author(s) -
Abshire Caleb Michael,
ReverteRibo Virginia,
RosalesMartinez Carla,
Zimmerman Margaret A,
Miller Kristen S,
Prieto Minolfa,
Lindsey Sarah H
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1068.1
Subject(s) - electrical impedance myography , medicine , cardiology , common carotid artery , in vivo , arterial stiffness , carotid arteries , blood pressure , artery , anatomy , biology , vasodilation , microbiology and biotechnology
Cardiovascular disease (CVD) is the leading cause of death worldwide and in the United States. Arterial stiffness, characterized by reduced compliance in large conducting arteries, is a major risk factor for CVD. Individuals with cardiometabolic risk factors such as obesity and insulin resistance have stiffer arteries and an increased risk of developing CVD. Recent evidence suggests that ex vivo arterial stiffening can be more fully characterized by performing pressure myography at multiple fixed lengths. Therefore, the aims of this study were to characterize the effect of a high fat diet on murine carotid stiffness using biaxial mechanical phenotyping. At 4 weeks of age, some C57BL/6 male mice were placed the DIO Rodent Purified Diet with 45% Energy from fat (HFD, TestDiet 58V8) while control animals remained on a normal diet. At 39 weeks of age, common carotid arteries were harvested and cannulated for assessment of biaxial mechanical properties using pressure myography. After equilibration and pre‐conditioning, in vivo carotid artery length was estimated by finding the length at which the artery caused minimal change to longitudinal force when subjected to pressures ranging from 70–150 mmHg. Pressure‐diameter and force‐length curves were obtained at the estimated in vivo length as well as 5% above and below the estimated in vivo length. Statistical analysis was performed using 2‐way ANOVA with Graphpad Prism. Baseline diameter of carotid arteries pressurized at 10 mmHg tended to be larger in HFD (388 ± 7 μm, n=5) versus control arteries (360 ± 13 μm, n=4, P=0.08). Pressure‐diameter data obtained at the estimated in vivo length showed a significant interaction between diet and pressure (P<0.001) with the largest differences evident at pressures at and above 70 mmHg (P<0.05). HFD significantly decreased arterial compliance, a measure of the change in diameter at each 10 mmHg pressure step (P<0.05), especially at lower pressures. Finally, arterial distensibility was calculated as the percent change in outer diameter from the original diameter obtained at 10 mmHg. HFD significantly decreased distensibility (P<0.05), with the greatest differences found at pressures above 40 mmHg (P<0.05). Interestingly, the impact of diet on arterial compliance was significantly attenuated when experiments were performed at an axial stretch above or below the estimated in vivo length. These data show a significant impact of HFD on carotid stiffness in male C57BL/6 mice. Of note, this difference was only detected when experimental conditions closely approximated the in vivo state. Additional analysis of this data will determine the impact of HFD and axial length on the force‐length and stress‐strain relationships. In conclusion, our study shows the importance of axial length in the analysis of diet‐induced carotid artery stiffness.