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NO from Flaxseed Enhances Sexual Function
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
As previously noted, the endothelium is a thin layer of cells lining the interior surface of blood vessels. It shields the vessel wall from circulating blood in the vessel inner cavity through which blood flows called the lumen. Endothelial cells line the entire circulatory system from the heart to the smallest capillary. They reduce the turbulence of blood flowing through the vessel, allowing it to be pumped farther. These cells also function in vasoconstriction and vasodilation, and hence they control blood flow and pressure.
The Arteries, the Endothelium, Endothelial Dysfunction, Glycocalyx, Glycocalyx Dysfunction, Nitric Oxide, and CHD
Published in Mark C Houston, The Truth About Heart Disease, 2023
The endothelium is one of the most important parts of the artery, and its role in protecting us from CHD is crucial. It is like the air traffic control tower that communicates to all the substances and the blood cells in the lumen as well as to the arterial muscle (1–13). It works in direct communication with the glycocalyx. The endothelium is a thin layer of cells (Figure 5.9) that separates the blood from the muscle of the artery (the media) (Figure 5.1). The left-side panel in Figure 5.9 is a normal endothelium, and the right-side panel presents a damaged endothelium. There are many things that can damage the endothelium, such as hypertension, high cholesterol, high blood sugar, diabetes mellitus, smoking, obesity, high homocysteine, and more. Both the structure and function of the endothelium are changed in the right panel of Figure 5.9. These changes are abnormal and cause the endothelium to not function in its usual fashion. The medical term for this is endothelial dysfunction (ED). The endothelium serves as a barrier (like a solid plank fence) to prevent things in the blood from crossing over into the subendothelial layer and the arterial muscle (1–13). However, just as a damaged fence allows undesired passage from one side to the other, when the endothelium is damaged, some of the endothelial cells become separated and the membrane will start to leak substances from the blood (see the right-side panel in Figure 5.9).
Other Complications of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Primary ED is present when attaining or sustaining an erection has never been possible. Psychologic causes of primary ED include fear of intimacy, guilt, anxiety, or depression. Secondary ED is acquired later in life after previously having had normal function. It is the most common form, with more than 90% of cases having an organic etiology. Reactive psychologic difficulties may later develop, worsening the condition. Causes may be related to performance anxiety, stress, or depression. Psychogenic ED may involve a certain place, time, or partner. Organic causes of ED are usually vascular or neurologic disorders, often due to diabetes or atherosclerosis. Atherosclerosis of the cavernous arteries of the penis is highly common. Endothelial dysfunction is due to diabetes, smoking, and low testosterone levels. Neurologic causes include diabetic neuropathy. One of the most common causes of retrograde ejaculation is prostate surgery for noncancerous prostate enlargement. Other common causes include diabetes, certain drugs, spinal cord injuries, and major abdominal or pelvic surgery. Aside from diabetes, decreased vaginal lubrication may be due to hormonal changes related to menopause, pregnancy, or breastfeeding. It is also caused by irritation from contraceptive creams and foams, fear, and anxiety about sexual intimacy, OTC antihistamines, oral contraceptives, and reduced estrogen levels because of aging.
Endothelial function in patients with COPD: an updated systematic review of studies using flow-mediated dilatation
Published in Expert Review of Respiratory Medicine, 2023
Anouk W. Vaes, Patrick De Boever, Frits M.E. Franssen, Nicole H.M.K. Uszko-Lencer, Lowie E.G.W. Vanfleteren, Martijn A. Spruit
The endothelium plays a significant role in regulating vascular tone, controlling tissue blood flow and inflammatory responses, and maintaining blood fluidity. Nitric oxide (NO) is the primary mediator of endothelial function, ensuring a balanced response between vasoconstrictive and vasodilatory stimuli [8,9]. An imbalance in NO production is an essential mechanism of endothelial dysfunction [9]. Also, it has been recognized that endothelial dysfunction is an early, potentially reversible precursor of vascular disease [8]. Important risk factors for endothelial dysfunction are smoking, aging, family history of early cardiovascular diseases, elevated triglycerides, elevated low-density lipoprotein cholesterol and reduced high-density lipoprotein cholesterol, hyperglycemia, hypertension, physical inactivity, obesity, and systemic inflammation [8–10].
Endothelial dysfunction: a therapeutic target in bacterial sepsis?
Published in Expert Opinion on Therapeutic Targets, 2021
Jean-Louis Vincent, Can Ince, Peter Pickkers
In conclusion, there is a huge potential for the prevention and/or restoration of endothelial function to improve organ function and outcomes in patients with sepsis. It is unlikely that a single molecule will be identified as a magic bullet for endothelial dysfunction in all patients. It is more likely that a subgroup of patients may benefit and that a combination of several compounds will be needed to ensure protection and facilitate restoration of endothelial function. There are many pathways and factors involved in endothelial dysfunction and many potential therapeutic strategies have already been identified. However, the lack of techniques to provide theragnostic feedback and the need to rely instead on ineffective surrogates of endothelial (dys)function has resulted in ineffective measures of therapeutic efficacy. Many questions therefore remain including which agents or combinations of agents may be effective in which patients and how this effect should best be monitored.
Chicoric acid attenuates hyperglycemia-induced endothelial dysfunction through AMPK-dependent inhibition of oxidative/nitrative stresses
Published in Journal of Receptors and Signal Transduction, 2021
Xiaojuan Ma, Junli Zhang, Zejie Wu, Xia Wang
Diabetes, a chronic metabolic disease, is characterized by hyperglycemia and it is also a profound risk factor for cardiovascular disorders [1]. Cardiovascular complications are a leading cause of mortality and morbidity in diabetic individuals [2]. Endothelial cell dysfunction is a key physiological feature in the development of diabetes, eventually leading to cardiovascular events [3]. The damage in micro- and macrovascular endothelial cells may facilitate the initiation of heart failure and worsen the clinical outcome of cardiovascular ailments, thus threatening or shortening life expectancy [4]. Chronic hyperglycemia, glucose, and lipid metabolism disorders result in impaired nitric oxide (NO) bioavailability, elevated production of reactive oxygen species (ROS), and inflammatory factors in endothelial cells, which eventually causes endothelial cell apoptosis and damage [5]. The excessive ROS react with NOx may cause the inactivation of NO and the generation of cytotoxic molecule peroxynitrite (nitrative stress), which plays an important role in the pathogenesis of diabetic angiopathy [6,7]. Accumulative evidence suggests that oxidative/nitrative stresses are closely associated with endothelial cell injury in diabetes [8,9]. As a consequence, therapeutic strategies against endothelial dysfunction may be helpful to reduce the risk of cardiovascular diseases. It is greatly desired to identify novel therapeutic targets or drugs.