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Nutrition Part I
Published in Mark C Houston, The Truth About Heart Disease, 2023
The DASH diets provide various mechanisms for the improvement of all the cardiovascular risk factors and CHD risks including the following:Increased nitric oxide and increased plasma nitrate.Increased kidney excretion of salt and water, like a diuretic.Decreased oxidative stress and increased oxidative defense.Reduced oxidative stress.Improved endothelial function.Decreased arterial stiffness.
Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Treatment of atherosclerosis includes serious modifications of risk factors, designed to slow down disease progression and cause existing plaques to regress. Today, it is recommended to lower LDL to as much as possible, not only to certain target levels. Lifestyle changes and medications can improve endothelial function, reduce inflammation, and improve the prognosis. Patients must greatly decrease intake of saturated fat, refined or processed carbohydrates, and increase the types of carbohydrates that contain fiber: Fruits and vegetables. These dietary changes are required for all patients. Caloric intake must be limited to keep weight gain in a normal range. Fat intake must be limited to no more than 20 grams per day. This must consist of 6–10 g of polyunsaturated fat with equal proportions of omega-3 and omega-6 fatty acids. There must be 2 g or less of saturate fat, and the remainder must be monounsaturated fat. All sources of trans fats must be avoided.
The cardiovascular system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Mary N Sheppard, C. Simon Herrington
Oxidized LDL is toxic to endothelial cells and causes endothelial dysfunction. This leads to increased stiffness of large arteries and raises the blood pressure by deficient nitric oxide release. Endothelial function is improved by administration of antioxidants. Oxidized LDL is chemotactic for monocytes and their recruitment could contribute to plaque growth. There is therefore substantial evidence that, in the vessel wall, oxidized LDL mediates some of the atherogenicity of raised blood LDL.
Generation of a novel ex-vivo model to study re-endothelialization
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Siti Sarah Azman, Muhammad Dain Yazid, Nur Azurah Abdul Ghani, Raja Zahratul Azma Raja Sabudin, Mohd Ramzisham Abdul Rahman, Nadiah Sulaiman
Endothelial dysfunction begins with an initial injury or damage to the endothelial cells, which lead to changes in the endothelial function. These changes include impaired vasodilation, increased adhesion of leukocytes and platelets, increased vascular permeability and reduced production of nitric oxide [2]. In addition, the dysfunction triggers a phenotypic switch in SMC at the media layer leading to its proliferative state. The activated SMC start to proliferate and migrated to the intimal layer leading to IH, which results in the formation of a thickened neointima layer [7,8]. This condition contributes to the narrowing of the vessel lumen, leading to stenosis. The thickened intimal layer and altered vessel architecture due to IH can exacerbate endothelial dysfunction and perpetuate the cycle of vascular injury, inflammation and proliferation [9]. If the condition persists, it can lead to the development of several cardiovascular pathologies such as atherosclerosis, hypertension or vessel restenosis [10,11].
A controlled chamber study of effects of exposure to diesel exhaust particles and noise on heart rate variability and endothelial function
Published in Inhalation Toxicology, 2022
Leo Stockfelt, Yiyi Xu, Anders Gudmundsson, Jenny Rissler, Christina Isaxon, Jonas Brunskog, Joakim Pagels, Patrik T. Nilsson, Margareta Berglund, Lars Barregard, Mats Bohgard, Maria Albin, Inger Hagerman, Aneta Wierzbicka
Heart rate variability (HRV) and endothelial function are attractive as intermediate outcomes for cardiovascular risk since they react rapidly and can be measured non-invasively with user-independent methods, and both decreased HRV and endothelial dysfunction are known risk factors for cardiovascular morbidity and mortality (Tsuji et al. 1996; Patel et al. 2017). HRV is a biological signal that mirrors ANS-mediated alterations in cardiovascular reactivity. The outflow from the sympathetic and parasympathetic branches of ANS, together with baroreceptor activity of the vascular system modulates the heart rate and its variability. HRV can be assessed by several different metrics, mainly divided into time-domain and frequency-domain measures. Time-domain measures quantify the amount of HRV observed during monitoring periods and are suitable for sustained recording periods; frequency-domain measures calculate the absolute or relative amount of signal energy within component bands and are considered more reliable for short recording periods (Evrengül et al. 2005; Shaffer and Ginsberg 2017). The term endothelial function includes several mechanisms of which the hallmark is endothelium-dependent vasodilation, i.e. the blood vessels capacity to dilate in response to ischemia (Sun et al. 2019).
Uremic serum induces prothrombotic changes in venous endothelial cells and inflammatory changes in aortic endothelial cells
Published in Renal Failure, 2021
Patrycja Sosińska-Zawierucha, Andrzej Bręborowicz
Evaluation of endothelial function in vivo is based on indirect methods, mainly measurement of the flow-mediated dilation of the arteries, which reflects the vasodilatory action of the endothelium [4]. Another approach is the measurement in blood concentration of biomarkers reflecting endothelial dysfunction, such as soluble vascular adhesion molecule-1, soluble E-selectin, or von Willebrand factor (vWF) [5]. Finally, the cytotoxicity of uremic serum toward endothelial cells can be studied ex vivo on human endothelial cells maintained in in vitro culture. Such experiments are performed mainly with human umbilical venous endothelial cells (VEC) [6–8]. It is well known that the morphology and functional properties of venous and arterial endothelial cells are totally different [9,10]. Aortic endothelial cells (AEC) are more active, as reflected by protein synthesis, whereas venous cells are larger and more pleomorphic [9]. Venous endothelial cells produce more prostacyclin than aortic cells, when studied in vitro under static conditions or in a mechanically active environment imitating shear stress [11]. One can expect that the effect of various noxious factors such as uremia on these cells may be different.