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Research Papers

Alterations of Pulse Pressure Stimulate Arterial Wall Matrix Remodeling

[+] Author and Article Information
Qingping Yao1

Department of Mechanical Engineering, University of Texas at San Antonio, San Antonio, TX 78249

Danika M. Hayman

Department of Mechanical Engineering, University of Texas at San Antonio, San Antonio, TX 78249; Biomedical Engineering Program, UTSA-UTHSCSA, San Antonio, TX 78229

Qiuxia Dai

Department of Medicine/Cardiology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78249

Merry L. Lindsey

Department of Medicine/Cardiology, University of Texas Health Science Center at San Antonio; Biomedical Engineering Program, UTSA-UTHSCSA, San Antonio, TX 78229

Hai-Chao Han2

Department of Mechanical Engineering, University of Texas at San Antonio, San Antonio, TX 78249; Biomedical Engineering Program,  UTSA-UTHSCSA, San Antonio, TX 78229haichao.han@utsa.edu

1

Visiting scholar from the Institute of Mechanobiology & Medical Engineering, Shanghai Jiaotong University, China.

2

Corresponding author.

J Biomech Eng 131(10), 101011 (Sep 10, 2009) (6 pages) doi:10.1115/1.3202785 History: Received November 15, 2008; Revised July 13, 2009; Published September 10, 2009

The effect of pulse pressure on arterial wall remodeling has not been clearly defined. The objective of this study was to evaluate matrix remodeling in arteries under nonpulsatile and hyperpulsatile pressure as compared with arteries under normal pulsatile pressure. Porcine carotid arteries were cultured for 3 and 7 days under normal, nonpulsatile, and hyperpulsatile pressures with the same mean pressure and flow rate using an ex vivo organ culture model. Fenestrae in the internal elastic lamina, collagen, fibronectin, and gap junction protein connexin 43 were examined in these arteries using confocal microscopy, immunoblotting, and immunohistochemistry. Our results showed that after 7 days, the mean fenestrae size and the area fraction of fenestrae decreased significantly in nonpulsatile arteries (51% and 45%, respectively) and hyperpulsatile arteries (45% and 54%, respectively) when compared with normal pulsatile arteries. Fibronectin decreased (29.9%) in nonpulsatile arteries after 3 days but showed no change after 7 days, while collagen I levels increased significantly (106%) in hyperpulsatile arteries after 7 days. The expression of connexin 43 increased by 35.3% in hyperpulsatile arteries after 7 days but showed no difference in nonpulsatile arteries. In conclusion, our results demonstrated, for the first time, that an increase or a decrease in pulse pressure from its normal physiologic level stimulates structural changes in the arterial wall matrix. However, hyperpulsatile pressure has a more pronounced effect than the diminished pulse pressure. This effect helps to explain the correlation between increasing wall stiffness and increasing pulse pressure in vivo.

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Copyright © 2009 by American Society of Mechanical Engineers
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Figures

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Figure 1

Confocal microscope images of fenestrae (some are marked by arrows) in the IEL of porcine carotid arteries cultured under nonpulsatile pressure (non-p), normal pulsatile pressure (normal-p), and hyperpulsatile pressure (hyper-p) for 3 days and 7 days as compared with a fresh artery. The circumference of the artery aligns horizontally. These images are representative of n=3 arteries for each group.

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Figure 2

Comparisons of the average fenestrae size and the total fenestrae area ratio in arteries cultured under different pulse pressure. Data were plotted as mean±SD. Sample size is n=3 for each group. (*) p<0.05 versus 7 days normal pulsatile. (#) p<0.05 versus 3 days normal pulsatile.

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Figure 3

Western blot demonstrating the collagen I, collagen III, and FN in arteries cultured under different pulse pressure for 3 days. Bar graphs illustrate the relative intensities obtained from densitometric measurements [mean±SD, n=4 for each group, p<0.05 (#) versus normal pulsatile].

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Figure 4

Western blot demonstrating the collagen I, collagen III, and FN in arteries cultured under different pulse pressure for 7 days. Bar graphs illustrate the relative intensities obtained from densitometric measurements [mean±SD, n=4 for each group, p<0.05 (*) versus normal pulsatile].

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Figure 5

Distribution of connexin 43 in arteries cultured under nonpulsatile pressure (non-p), normal pulsatile pressure (normal-p), and hyperpulsatile pressure (hyper-p) conditions for 7 days. The connexin 43 was stained green, while the nuclei were stained red with propidium iodide. Bottom panels are the PI counterstaining only. These are representative images from n=3 arteries.

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Figure 6

Comparison of connexin 43 and β-actin expression in arteries cultured for 3 and 7 days under nonpulsatile, pulsatile, and hyperpulsatile pressure conditions and in fresh arteries. The top panels show typical blotting images, and the bottom panel compares the relative intensity (mean±SD, n=4 for each group) among different groups. (*) p<0.05 versus 7 days normal pulsatile; ($) p<0.05 between 3 and 7 days.

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