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Aortic and Arterial Mechanics
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
The heart acts as a pulsatile pump that propels blood into the vascular system during its contraction (systole). Part of the blood ejected during systole is stored during distension of the aorta and the proximal arteries. The function of the large elastic arteries is to relay the contraction of the heart when it enters its relaxation phase (diastole), thanks to their compliance. After closing the aortic valve, the aorta and the proximal arteries retract elastically and restore the volume of blood stored. This is the Windkessel effect, by which blood pressure is maintained and blood flow is increased in diastole, which ensure a continuous and nonpulsatile flow in the peripheral arteries and the capillaries. This function of diastolic relay of the cardiac contraction is directly related to the elastic properties of the large arteries, which are conferred on them by the large quantity of elastic fibers and type III collagen in the media [1,2].
General Introductory Topics
Published in Vadim Backman, Adam Wax, Hao F. Zhang, A Laboratory Manual in Biophotonics, 2018
Vadim Backman, Adam Wax, Hao F. Zhang
Other luminal organs have a similar organization. For example, blood vessels have a thin layer of simple squamous cells (endothelium) lining their inner surfaces. The combination of the endothelium and the underlying elastic lamina forms what is called the intima. In healthy blood vessels (in reality this only exists in children), the endothelium of large blood vessels is only one cell thick. Beneath it, there is a smooth muscle layer, the media. Depending on the size of the blood vessel, the media may be mostly muscular (in muscular arteries) or have a significant component of elastin fibers intermixed with smooth muscle cells. The latter is characteristic of elastic arteries. Elastic and muscular arteries serve different roles in our circulatory system. Elastic arteries are the largest arteries in our body, such as the aorta, carotid arteries, etc. Their job is to serve as pressure reservoirs during the heart relaxation phase (diastole) and to expand easily during heart contraction (systole). Accordingly, their walls are very elastic in order to be able to expand and generate elastic recoil. Muscular arteries, on the other hand, are charged with pressure regulation, and they contract and relax to rectify the blood pressure and flow to the end organs, thus their thick muscular walls. Below the media is located the layer of adventitia, which is a mixture of different types of connective tissue: loose connective tissue and some inclusion of the adipose tissue.
Pulmonary Vascular Mechanobiology
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Diana M. Tabima Martinez, Naomi C. Chesler
While mean pressures are lower in the pulmonary circulation, pulsatility is inherently greater compared to the systemic circulation. The ratio of pulse pressure to mean pressure in the pulmonary artery is about one, whereas in the aorta, pulse pressure is about 40% of mean pressure.110 It is not surprising, therefore, that the compliance of large pulmonary arteries—or their percent deformation for a given change in pressure—is much greater than the compliance of large systemic arteries. When the elastic arteries become stiffened, as occurs with aging or hypertension, this cushioning effect is impaired and highly pulsatile pressures in the microcirculation likely result.
Adverse cardiovascular effects of exposure to cadmium and mercury alone and in combination on the cardiac tissue and aorta of Sprague–Dawley rats
Published in Journal of Environmental Science and Health, Part A, 2021
Sandra Arbi, Megan Jean Bester, Liselle Pretorius, Hester Magdalena Oberholzer
Alternating bands of collagen and elastin as typically found in the connective tissue of elastic arteries was observed in the control group (Figure 7a). Cadmium exposure caused the disruption of the elastic fibers by collagen (Figure 7b, label C), while an area of new collagen deposition and elastin destruction was observed adjacent to the elastin band (Figure 7b, arrow). In the Hg exposed group, interruptions in the horizontal elastic bands were observed. In the areas where elastin was lost, collagen was present (Figure 7c). In the co-exposure group, electron dense elastin strands are present and with areas of lighter density along the main elastin fiber which appears to be newly deposited elastin and similarly arranged elastin is located individually among the collagen bundles (Figure 7d, thick arrow, label E).
Characterization of a heparinized decellularized scaffold and its effects on mechanical and structural properties
Published in Journal of Biomaterials Science, Polymer Edition, 2020
Ji Li, Zhiwen Cai, Jin Cheng, Cong Wang, Zhiping Fang, Yonghao Xiao, Zeng-Guo Feng, Yongquan Gu
Mechanical strength is one of the key parameters that determine the suitability of a vessel graft for clinical implantation [84]. Therefore, mechanical testing was carried out to determine the effect on the overall mechanical response of the tissues. The arterial tissue was a composite structure composed of three relevant layers with different mechanical properties. A mixture of ECM components, particularly elastin and collagen, collectively contribute to mechanical behavior [85]. Collagen provides strength and elastin provides elastic recoil. The elastin fibers contained in the elastic lamellae of media of elastic arteries are circumferentially oriented, and of the internal and external elastic lamina (IEL and EEL) are longitudinally oriented [86]. Collagen fiber alignment analyzed by second harmonic generation microscopy revealed that the collagen fibers were mainly oriented circumferentially in the outer adventitia and media [87]. The collagen fibers that were distributed near the regions of internal and external elastic lamina were mainly longitudinally oriented similar to the elastin fibers [87]. Thus, the uniaxial tensile properties were performed on both longitudinal and circumferential directions.