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Arterial Wave Reflections
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
In addition to serving as a conduit that delivers blood to peripheral vascular beds, the function of the elastic arteries (aorta, carotid, iliac etc.) is to cushion flow pulsations from the ventricle so that the heart may function most efficiently. Efficient function is apparent as a small pulse pressure in the ascending aorta, with average pressure during systole being only slightly greater (by about 5 mmHg) than mean cycle pressure and average pressure during diastole only slightly less (by about 3 mmHg). Design of the normal arterial system is such that pressure rise during systole is minimized (so that myocardial oxygen demands are minimized), and pressure is maintained as high as possible during diastole (so that coronary blood flow may be maintained). In adolescent humans, and in most experimental animals (but not all), wave reflection is seen to be so timed as to enhance pressure during diastole without boosting systolic pressure. Appropriately timed wave reflection is thus an important factor in minimizing myocardial oxygen requirements and maximizing the capacity for myocardial blood flow (Figure 8.20).
The respiratory system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The normal pulmonary vasculature is a low-pressure system. Pulmonary arteries are divided into three groups. Elastic arteries are >500 μm in diameter and have multiple elastic laminae and smooth muscle. Muscular arteries are between 80 μm and 500 μm in diameter, with internal and external elastic laminae, between which is a thin media, reflecting the low-pressure system. Pulmonary arterioles, <80 μm in diameter, lose their media with decreasing calibre and have a single elastic lamina. Pulmonary veins contain muscle, collagen, and elastic fibres, the last forming an internal elastic lamina. The alveolar capillaries lie within the alveolar walls and have a single layer of endothelium resting on a continuous basal lamina.
Cardiovascular System and Muscle
Published in George W. Casarett, Radiation Histopathology: Volume II, 2019
The elastic arteries are conducting arteries in which the elastic tissue expands to absorb some of the pulse beat of the heart and temporarily store some of the energy involved. In the return of the stretched walls during refilling of the heart, the elastic tissue releases kinetic energy and maintains a more constant pressure and a smoother, less interruptive flow of blood. The muscular arteries are distributing arteries which, under the nervous control of their muscular medial layers, can regulate the quantities of blood brought to various organs and tissues according to need by contracting or dilating. The arterioles, with their relatively thick muscular walls and narrow lumen, play a prime role in controlling the local flow of blood in tissues and in controlling systemic blood pressure, being responsible for most of the fall in blood pressure within tissues and organs.
Assessment of hypertension-mediated organ damage in children and adolescents with hypertension
Published in Blood Pressure, 2023
Michał Pac, Łukasz Obrycki, Jan Koziej, Krzysztof Skoczyński, Anna Starnawska-Bojsza, Mieczysław Litwin
Arterial hypertension (HT) is one of the main potentially reversible factors determining increased cardiovascular risk. Appropriate diagnostic management in children and adolescents with elevated blood pressure (BP) values enables not only confirmation of the disease [after exclusion of a white coat hypertension (WCH)], but also assessment of hypertension-mediated organ damage (HMOD). Presence of HMOD affects the decision about the optimal antihypertensive (anti-HT) treatment, either non-pharmacological or pharmacological. HMOD is a structural or/and functional alteration of arteries and target organs such as heart, central nervous system and kidneys, caused by elevated BP. In the vascular bed the unfavourable process can affect a wide spectrum of arteries – especially large, elastic arteries, arterioles, and microcirculation. Some forms of HMOD can be reversible after BP normalisation, however, not in a case of long-lasting exposure to increased BP and concomitant immune-metabolic abnormalities which lead to persistent damage, persisting even after successful achievement of normotension.
More than a matter of the heart: the concept of intravascular multimorbidity in cardiac rehabilitation
Published in Expert Review of Cardiovascular Therapy, 2020
Chueh-Lung Hwang, Ahmed Elokda, Cemal Ozemek, Ross Arena, Shane A. Phillips
Another common feature associated with atherosclerosis is the stiffening of large elastic arteries, such as the aorta. The aorta serves as a reservoir and buffer to attenuate pulsatile flow, prevents excessive pulsatile energy into the periphery, and maintains coronary perfusion during diastole [12]. Stiffening of the aorta causes hemodynamic changes including excessive pulsatile load and early return of reflected waves from the periphery to the heart during systole [12]. The early wave reflection results in reduced coronary perfusion, as well as augments systolic blood pressure and increases heart afterload and thus wasted energy [12]. These hemodynamic alterations may cause endothelial damages and increase the risk of developing CAD. It is not clear whether arterial stiffening is a cause or consequence of atherosclerosis [13]. The etiology of atherosclerosis, including vascular calcification, plaque formation, collagen disposition, and endothelial dysfunction, also contributes to arterial stiffening [14].
Inhibitory effect of recombinant human CXCL8(3-72)K11R/G31P on atherosclerotic plaques in a mouse model of atherosclerosis
Published in Immunopharmacology and Immunotoxicology, 2019
Yuanhua Qin, Weifeng Mao, Lingmin Pan, Yunliang Sun, Fushun Fan, Ying Zhao, Ying Cui, Xiaoqing Wei, Kazuhiro Kohama, Fang Li, Ying Gao
The development of atherosclerosis is a complex process, in which the abnormal proliferation and migration of VSMCs play a vital role in this process [32]. We have previously demonstrated that G31P inhibits the proliferation and migration of VSMCs, and therefore inhibits the development of hyperlipidemic conditions [33]. In this study, we investigated the roles of G31P in development of atherosclerosis. Through histochemistry analysis, we found that G31P inhibited the formation of atherosclerotic plaques in the coronary artery. However, G31P did not induce a significant difference in plaque formation in the aortic root. The elastic arteries contain fewer VSMC than muscular arteries [34]. G31P competes with IL-8 for binding to the IL-8R on smooth muscle cells, thereby G31P may inhibit proliferation and migration of VSMC, further suppress the atherosclerotic plaques.