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Omega-3 Fatty Acids and NO from Flax Intervention in Atherosclerosis and Chronic Systemic Inflammation
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
Atherosclerosis is a life-threatening predominantly asymptomatic pandemic condition, a known health hazard that is responsible for more annual deaths in the United States than COVID-19. It is the thickening, and therefore hardening, of the arteries caused by a buildup of plaque in the blood vessel wall. A lipoprotein-driven disease, it leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis and calcification. It is said to lead to hypertension, heart disease and peripheral vascular disease.
Arterial Wave Reflections
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
The arterial tree is made up of a system of distensible tubes along which pressure and flow waves, generated by the heart, are transmitted and reflected. Since the PWV of these waves is in meters/second, it is obvious that in one cardiac cycle the generated wave has sufficient time to travel to the periphery and back. If the reflected waves were damped out completely, the pressure and flow waves generated by the heart would be identical in contour. Reflection of pressure waves has been discussed in considerable detail in the literature (McDonald and Taylor, 1956; McDonald, 1974; O'Rourke, 1982a, 1982b; Milnor, 1989; O'Rourke and Hashimoto, 2007), but the physiological and clinical importance of reflected flow waves was not emphasized until more recently (Westerhof et al., 1972; Nichols et al., 1993; Westerhof and O'Rourke, 1995; O'Rourke et al., 2013; Townsend et al., 2015; O'Rourke et al., 2016; Townsend et al., 2016; O'Rourke et al., 2017, 2018). The analysis of wave reflections and their influence on pressure and flow waveforms are outlined next.
Atherosclerosis
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
The effect of hypertension on vascular complications may include disturbances in flow pattern, causing endothelial injury.425 High levels of catecholamines and other vasoactive substances increase endothelial permeability and mediate the entry of lipids and other plasma constituents into the arterial wall. The production of prostaglandins is associated with hypertension.671 Moreover, the induction of high blood pressure in rats and rhesus monkeys causes significant increase of arterial smooth muscle lysosomal hydrolases, which reverted to normal when the blood pressure was restored to normal. The lysosomal changes are probably secondary to the mechanical actions of hypertension. Significant rise in pressure and rheologic and metabolic consequences in the arterial tree constitute the dominant factors in hypertension-related atherosclerotic lesions.
Angiography derived assessment of the coronary microcirculation: is it ready for prime time?
Published in Expert Review of Cardiovascular Therapy, 2022
Jinying Zhou, Yoshinobu Onuma, Scot Garg, Nozomi Kotoku, Shigetaka Kageyama, Shinichiro Masuda, Kai Ninomiya, Yunlong Huo, Johan H.C. Reiber, Shengxian Tu, Jan J. Piek, Javier Escaned, Divaka Perera, Christos Bourantas, Hongbing Yan, Patrick W. Serruys
The coronary arterial tree can be divided into four serial vascular compartments: epicardial arteries (>400 µm), pre-arterioles (100–400 µm), arterioles (40–100 µm), and capillaries (<10 µm) (Figure 1(c)) [15]. The epicardial arteries have a primary role in flow conductance and distribution of blood to different myocardial territories, abide by the hemodynamic laws of Poiseuille and Bernoulli, and offer minimal vascular resistance under normal conditions. Complementary to the conductance function of epicardial arteries, pre-arterioles, and arterioles regulate flow resistance to adjust myocardial blood supply to myocardial oxygen demands through multiple mechanisms, including neuro-humoral, metabolic, endothelial, and intrinsic myogenic responses, which are globally termed autoregulation [16,17], although the concept is frequently simplified to the absence of flow variation despite changes in driving pressure. Finally, capillaries are the predominant site of metabolic exchange, with the metabolic needs of the myocardium determining the actual blood supply that reaches the capillaries, and acting as a feedback signal to autoregulate the coronary blood supply [17]. Capillaries account for most of intravascular coronary volume. By lacking medial and adventitial layers, capillaries are particularly sensitive to extravascular compression by intracavitary or intramyocardial pressure, which may be elevated in specific pathological conditions.
The emerging significance of circadian rhythmicity in microvascular resistance
Published in Chronobiology International, 2022
Jeffrey T. Kroetsch, Darcy Lidington, Steffen-Sebastian Bolz
The mechanisms that drive rhythmic changes in TPR are not well understood. TPR rhythms persist under conditions of systemic alpha- and beta-adrenergic receptor blockade (Talan and Engel 1989); MAP rhythms persist in adrenalectomized patients (van der Steen et al. 1995) and are independent of catecholamines, sympathetic outflow and cardiac or renal function (Shea et al. 2011). Collectively, these observations indicate that TPR rhythm originates from a local microvascular mechanism, rather than being centrally controlled. This necessitates shifting our focus to the resistance arteries, arteries <300 μm in diameter that prominently control vascular resistance. Resistance arteries are the regulatory hotspots in the cardiovascular system that (i) serve as the gateway between the high-pressure conductive segment of the arterial tree and the lower-pressure capillary perfusion network; (ii) protect fragile capillary structure and prevent hydrostatic edema formation; and (iii) maintain constant flow, independent of incoming MAP (Schubert et al. 2008).
Exaggerated blood pressure response to exercise is associated with subclinical vascular impairment in healthy normotensive individuals
Published in Clinical and Experimental Hypertension, 2021
Nobuyuki Miyai, Maki Shiozaki, Kazufumi Terada, Tatsuya Takeshita, Miyoko Utsumi, Kazuhisa Miyashita, Mikio Arita
A significant positive association between an exaggerated BP response to exercise and the baPWV was found in a multiple adjusted regression model. Arterial stiffness reflects systemic arteriosclerosis at various sites in the vascular tree (22). An increase in the pulse wave velocity is often associated with high pulse pressure amplification in the arteries, which may stimulate hypertrophy, remodeling, or rarefaction in microcirculation (23). This causes the blood vessels to become unresponsive to the demand for changing blood flow, and such vascular alterations may affect the function of peripheral vasculature to appropriately vasodilate and allow peripheral runoff of increased blood flow (10,24). Alternatively, a reduction in aortic compliance will decrease the ability of the arterial tree to buffer the increased arterial pressure generated by the left ventricular ejection (25) and could also contribute to an excessive increase in BP during exercise.