OBJECTIVES: A progressive decline in endothelium-dependent vasodilation (EDV) in the human forearm with age has previously been reported. The aim of this study was to evaluate the interplay between age, gender and metabolic factors on EDV in healthy subjects in a population-based study. SETTING: Tertiary university hospital. SUBJECTS AND DESIGN: Thirty-six healthy men and 30 women, aged 20-69 years, underwent measurements of forearm blood flow (FBF) at rest and during local infusions of 2 and 4 microg min-1 of metacholine (evaluating EDV) and 5 and 10 microg min-1 of sodium nitroprusside (evaluating endothelium-independent vasodilation, EIDV) and during reactive hyperaemia by venous occlusion plethysmography. RESULTS: Age was inversely related to EDV (r = - 0.41, P , 0.05 in men; r = - 0.61, P , 0.01 in women) and maximal FBF during reactive hyperaemia in both men and women. EIDV was significantly related to age in an inverse way in women only. EDV was more pronounced in females than in males ...
The present study demonstrates that long-term cigarette smoking is associated with impaired endothelium-dependent coronary vasodilation regardless of the presence or absence of atherosclerotic wall thickening. These findings extend previous observations obtained in the brachial artery to coronary arteries, suggesting that smoking is associated with a generalized endothelial vasodilator dysfunction. Most importantly, even in the presence of atherosclerotic wall thickening, smokers exhibited further impairment in flow-dependent coronary arterial dilation indicative of an additive adverse effect on endothelium-dependent coronary vasodilator function. Vasodilation in response to increased blood flow in conductance vessels was shown to be strictly dependent on an intact, normally functioning endothelium18 19 and is mediated by the signal of shear stress on the endothelial cell layer20 to release vasoactive factors like endothelium-derived relaxing factor (EDRF), believed to be nitric oxide or a ...
TY - JOUR. T1 - Impaired endothelium-mediated vasodilation in the peripheral vasculature of patients with congestive heart failure. AU - Katz, Stuart D.. AU - Biasucci, Luigi. AU - Sabba, Carlo. AU - Strom, Joel A.. AU - Jondeau, Guillaume. AU - Galvao, Marie. AU - Solomon, Steven. AU - Nikolic, Srdjan D.. AU - Forman, Robert. AU - LeJemtel, Thierry H.. PY - 1992/4. Y1 - 1992/4. N2 - Impaired endothelial-dependent vasodilation has been demonstrated in two animal models of congestive heart failure and in the coronary circulation of patients with idiopathic dilated cardiomyopathy. To determine whether this impairment contributes to the abnormal peripheral vasomotor tone in patients with congestive heart failure, the local vascular response to intraarterial infusions of graded concentrations (10-8 M to 10-5 M) of acetylcholine (an endothelial-dependent vasodilator) and nitroglycerin (a direct-acting vasodilator) was studied in the superficial femoral artery of 19 patients with congestive heart ...
TY - JOUR. T1 - Endothelium removal augments endothelium-independent vasodilatation in rat mesenteric vascular bed. AU - Iwatani, Y.. AU - Kosugi, K.. AU - Isobe-Oku, S.. AU - Atagi, S.. AU - Kitamura, Yoshihisa. AU - Kawasaki, H.. PY - 2008/5. Y1 - 2008/5. N2 - Background and purpose: The vascular endothelium regulates vascular tone by releasing various endothelium-derived vasoactive substances to counteract excess vascular response. We investigated whether the vascular endothelium regulates vasodilatation via released endothelium-derived contracting factors (EDCFs), by examining the effect of endothelium removal on responses to periarterial nerve stimulation (PNS) and various vasodilator agents. Experimental approach: The rat mesenteric vascular bed was perfused with Krebs solution. Vasodilator responses to PNS and 5 min perfusion of vasodilator agents in preparations with endothelium were compared with those in the same preparations without endothelium. The endothelium was removed by 30 s ...
In acute ischaemia, glucose-insulin-potassium administration reduces mortality and β-adrenoceptor antagonists have favourable effects on the outcome of ischaemic heart disease. The present study was designed to investigate whether insulin (1.4×10−7 M) and the β-adrenoceptor antagonist, propranolol (10−5 M), increase hypoxic vasodilation in correspondence with changes in glycolysis. Porcine coronary arteries, precontracted with 10−5 M prostaglandin F2α, were mounted in a pressure myograph and a microdialysis catheter was inserted in the tunica media. Hypoxic vasodilation, interstitial lactate/pyruvate ratio and interstitial glucose were measured at low (2 mM) and high (20 mM) glucose concentrations. Hypoxia (60 min) caused vasodilation and doubled the lactate/pyruvate ratio. Treatment with insulin quadrupled the lactate/pyruvate ratio during hypoxia, but did not change hypoxic vasodilation. Propranolol blocked isoprenaline-evoked vasodilation, but hypoxic increases in lactate/pyruvate ...
Background: Several studies have shown that both early and late effects of ischemic preconditioning (IPC) protect against myocardial injury following ischemic reperfusion. Recently, we have shown that repetition of IPC stimulus augments endothelium-dependent vasodilation in forearm circulation of healthy subjects through increases in nitric oxide (NO) production and number of endothelial progenitor cells (EPCs) under a local condition. The purpose of this study was to evaluate the late effects of IPC on endothelial function in smokers.. Methods and Results: Late phase of IPC was induced by upper limb ischemia (cuff inflation of over 200 mmHg for 5 minutes) six times a day for one month. We evaluated forearm blood flow (FBF) responses to acetylcholine (ACh) and to sodium nitroprusside (SNP) before and after IPC stimulus in 15 male smokers (27±7 yr) and 15 male non-smokers (26±5 yr). FBF was measured using a strain-gauge plethysmography. The IPC stimulus significantly increased plasma ...
Endothelial cells line the inner walls of all the arteries, where they release substances that can cause vasodilation and lower the blood pressure. The loss of endothelium-dependent vasodilation increases vascular resistance and blood pressure in cardiovascular disorders. Thus, strategies to target the loss of endothelium-dependent vasodilation may have therapeutic benefit in cardiovascular disorders.. Under normal conditions, endothelium-dependent vasodilation is driven by increases in intracellular calcium. My laboratory studies the activity of individual calcium entry events in endothelial cells and their signaling targets under normal and disease conditions. We focus on two life-threatening disorders that are commonly associated with the loss of endothelial function- obesity and pulmonary hypertension. New findings reveal that calcium influx through TRPV4 ion channels, a key calcium entry pathway in endothelial cells, is drastically reduced in rodent models of obesity or pulmonary ...
Synonyms for vasodilation in Free Thesaurus. Antonyms for vasodilation. 2 words related to vasodilation: dilatation, dilation. What are synonyms for vasodilation?
Percent change in coronary blood flow, coronary vascular resistance and coronary epicardial diameter in response to (A) endothelium-dependent vasodilation with acetylcholine and (B) endothelium-independent vasodilation with sodium nitroprusside. (C) Percent change in coronary blood flow and coronary vascular resistance in response to adenosine. Overweight and obese subjects (BMI ≥ 25 kg/m2) in dark columns and normal weight subjects (BMI , 25kg/m2) in open columns. Results expressed as mean ± SEM. Probability values by students t-test ...
This study aimed to examine the effects of aerobic training on endothelium-dependent vasorelaxation induced by acetylcholine and the expression of enzymes controlling NO bioavailability in the aorta of hypertensive rats.. We confirmed findings from previous reports showing that compared with the WKYsd group, the SHRsd group exhibits higher BP and impaired maximal vasorelaxation 24,25. Moreover, the relative endothelium-dependent vasorelaxation induced by 10-4 M ACh was lower in the SHRsd group than in WKY and showed paradoxical vasoconstriction in SHR. These results clearly reveal endothelial dysfunction in the aorta of SHR 24,32. Acetylcholine activates smooth muscle muscarinic receptors and evokes endothelium-dependent contractions in the aortas of SHR, but not WKY 33.. When aorta samples were incubated with L-NAME, differences in maximal vasorelaxation were not observed, but the relative endothelium-dependent vasorelaxation induced by ACh (10-4 M) remained different between the SHRsd and ...
To test the hypothesis that activation of protein kinase C impairs vascular reactivity in patients with diabetes.. A major cause of death and disability in patients with diabetes mellitus is atherosclerosis. Endothelial dysfunction is an important, if not primary, factor in atherogenesis. Nitric oxide is an important substance made and released by the endothelium. Many prior studies in animals and humans have shown that the ability of the blood vessel to dilate is impaired in diabetes. This process of vasodilation is mediated by a substance, nitric oxide, which is thought to be highly susceptible to destruction by oxidant molecules. In previous studies, we found that acute administration of the antioxidant, vitamin C, improves endothelium-dependent vasodilation in blood vessels of patients with type 1 and type 2 diabetes. This suggests that by scavenging oxidants, such as superoxide, vitamin C may reduce the destruction of nitric oxide and thereby preserve endothelial function. Additional ...
Cardiovascular dysfunction is usually a primary indie predictor of age-related morbidity and mortality. Strategies To be able to evaluate the function of IL-10 in maintenance of vascular function, power stress myography was useful to gain access to ex-vivo endothelium reliant vasorelaxation in vessels isolated from IL-10 knockout IL-10(tm/tm) and control mice. Pulse influx speed ((PWV), index of rigidity) of vasculature was assessed using ultrasound and blood circulation pressure was assessed using the tail cuff technique. Echocardiography was utilized to elucidated framework and functional adjustments in the center. Outcomes Mean arterial stresses were considerably higher in IL-10(tm/tm) mice when compared with C57BL6/outrageous type (WT) handles. PWV was elevated in IL-10(tm/tm) indicating stiffer vasculature. GMCSF Endothelial unchanged aortic bands isolated from IL-10(tm/tm) mice confirmed impaired vasodilation at low acetylcholine dosages and vasoconstriction at higher dosages whereas ...
This medical exhibit provides an overview of the venous circulatory system. It also illustrates the process of vasodilation and subsquent shock.
MOA: AT1-receptor antagonists. Block the activation of angiotensin II AT1 receptor on vessels which directly causes vasodilatation, reduces secretion of vasopressin, reduces production and secretion of ...
The principal finding of this study is that IC inhibits NO-mediated endothelium-dependent and -independent vasodilation in rat aortic vascular smooth muscle. IC inhibited both receptor- and non-receptor-mediated endothelium-dependent vasodilation induced by ACh, histamine, and A23187 and endothelium-independent vasodilation induced by SNP. Agents like ACh, histamine, and A23187 produce vasodilation through the endothelial synthesis and release of NO, which activates vascular smooth muscle soluble guanylyl cyclase to produce an increase of cGMP concentration.15 16 19 SNP produces vasodilation by activation of soluble guanylyl cyclase after its breakdown to NO.24 Thus, the site of action for NO is soluble guanylyl cyclase, whether it is released endogenously from endothelial cell activation by receptor-mediated (ACh, histamine) or non-receptor-mediated (A23187) agents or is produced intracellularly in the smooth muscle cells from metabolism of the nitrovasodilator SNP.24 Our findings that IC had ...
In the present article we report that deletion polymorphism in the ACE gene is associated with an impairment of endothelium-dependent vasodilation in a group of newly discovered, never-treated hypertensive patients. Our patients who were homozygous for deletion (DD) are characterized by significantly less endothelium-dependent vasodilation compared with subjects who were homozygous for insertion (II) and heterozygous (ID). Furthermore, the present data demonstrate that normotensive controls with a DD genotype had similar endothelium-dependent vascular responses when compared with these normotensive individuals with the non-DD genotype. Similarly, although the DD genotype among hypertensive patients was associated with further impairment of endothelium-dependent vasodilation, it must be noted that hypertensive patients with the non-DD genotype also had significantly impaired endothelium responses compared with normotensive controls. Thus, it is clear that it is hypertension and not the ACE ...
HIV-infected subjects on a stable protease inhibitor (PI) containing antiretroviral regimen with plasma HIV RNA ,500 copies/mL, who have LDL cholesterol levels ,130 mg/dL or fasting triglycerides levels ,200 mg/dL, will be randomized (1:1) to continue their current antiretroviral regimen or to switch the PI to atazanavir (ATV). Brachial artery reactivity will be measured before (at entry) and 12 and 24 weeks after subjects are randomized.. ARM A: Switch current PI to atazanavir 400 mg once daily plus current , 2 nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) for 24 weeks.. Subjects currently on ritonavir (RTV) (400 mg BID or greater) or RTV-boosted PI (,400 mg/day) , or tenofovir (TDF) as backbone NRTI therapy, will switch to ATV 300 mg boosted with RTV 100mg once daily.. ARM B: Continue current antiretroviral regimen (single or RTV-boosted PI plus , 2 NRTIs) for 24 weeks. Brachial artery reactivity in response to two vasoactive stimuli (increased forearm blood flow and ...
BACKGROUND: Some studies have demonstrated beneficial effects of L-arginine as a substrate for nitric oxide synthesis, and diclofenac as an inhibitor of cyclooxygenase (COX)-derived vasoconstrictive agents on vascular responses in humans during several pathological conditions. The aim of the present study was to investigate the acute effects of L-arginine and diclofenac on endothelium-dependent vasodilatation (EDV) and endothelium-independent vasodilatation (EIDV) in patients with chronic renal failure (CRF).. METHODS: Effects of L-arginine and diclofenac on EDV and EIDV were measured in 15 patients with CRF and in 15 healthy controls by means of forearm blood flow measurements with venous occlusion plethysmography during local intra-arterial infusions of methacholine (2 and 4 micro g/min evaluating EDV) and sodium nitroprusside (5 and 10 micro g/min evaluating EIDV).. RESULTS: L-Arginine infusion increased methacholine-induced vasodilatation both in patients with CRF and healthy controls. ...
The findings of the present study show that endothelium-dependent vasodilation was preserved in young untreated subjects with BH, in whom their BP elevation had persisted over a period of 4 to 5 years. However, BH subjects had a nonspecific attenuation of the vasodilatory response to the NO donor SNP. The observation that the relative vascular response to MCh over SNP was even greater in BH subjects supports the interpretation that the reduced FBF response was not due to a dysfunction of the endothelium per se. Rather, it appears that the functional impairment of the vasorelaxant response may be related to some as-yet-undefined ineffective action of NO on the vascular smooth muscle cells or to structural changes in the vasculature. To test this hypothesis, we also investigated the postischemic vasodilatory capacity, which may reflect structural vascular changes and/or reduced production or action of endogenous vasodilator release during tissue ischemia. However, BH subjects had no evidence of ...
BACKGROUND: While recent reports suggest that both flow-mediated vasodilation (FMD) in the brachial artery (BA), endothelium-dependent vasodilatation, and intima media thickness (IMT) in the carotid artery correlate with the extent of coronary artery
BACKGROUND Impaired arterial dilatation response to nitroglycerin has been observed in adults with risk factors for atherosclerosis and in patients with established atherosclerotic disease. This defect parallels changes in vascular endothelial function and may be attributed to increased oxidative stress. Because atherosclerosis begins in childhood, we examined the correlates of nitrate-mediated dilatation (NMD) in children, including brachial artery endothelial function, oxidized LDL, and carotid artery intima-media thickness (IMT). METHODS AND RESULTS Brachial artery flow-mediated endothelium-dependent dilatation (FMD) and nitrate-mediated smooth muscle function, IMT of the carotid bulb, and brachial artery and oxidized LDL were measured in 142 children (mean age, 11 years; range, 8 to 17 years), including 87 healthy children, 41 diabetic children, and 14 children with familial hypercholesterolemia. NMD correlated directly with FMD (r=0.46, P|0.001) and inversely with brachial artery baseline
TY - JOUR. T1 - Endothelium-derived hyperpolarizing factor(s). T2 - Species and tissue heterogeneity. AU - Triggle, C. R.. AU - Dong, H.. AU - Waldron, G. J.. AU - Cole, W. C.. PY - 1999/1/1. Y1 - 1999/1/1. N2 - 1. Endothelium-derivcd relaxing factor is almost universally considered to be synonymous with nitric oxide (NO); however, it is now well established that at least two other chemically distinct species (prostacyclin (PGI2) and a hyperpolarizing factor) may also contribute to endothelium-dependent relaxation. 2. Only relatively few studies have provided definitive evidence that an endothelium-derived hyperpolarizing factor (EDHF), which is neither NO nor PGI2, exists as a chemical mediator. 3. There is a lack of agreement as to the likely chemical identity of this putative factor. Some evidence suggests that EDHF may be a cytochrome P450-derived arachidonic acid product, possibly an epoxyeicosatrienoic acid (EET); conflict-ing evidence supports an endogenous cannabinoid as the mediator and ...
Markus Juonala;Costan G. Magnussen;Alison Venn;Seana Gall;Mika Kähönen;Tomi Laitinen;Leena Taittonen;Terho Lehtimäki;Eero Jokinen;Cong Sun;Jorma S.A. Viikari;Terence Dwyer;Olli T. Raitakari ...
Flow-mediated, endothelium-dependent vasodilation in response to transient arterial occlusion was determined with ultrasonographic imaging of the brachial artery with an 11 MHz linear array ultrasound transducer connected to an ATL Apogee 800 plus duplex ultrasound machine (Advanced Technology Laboratories, Bothell, Washington) adapted from previously published methods (15,16). The axial resolution of the 11 MHz transducer is capable of detection of changes in brachial artery diameter of ,0.1 mm. Arterial diameter (cm) was determined as the internal dimension of the vessel wall, from trailing edge to leading edge of the anterior and posterior intimal markings, respectively (to confirm full alignment of the ultrasound beam with the maximum anterior-posterior diameter of the brachial artery in its long axis). Brachial artery blood flow velocity was determined with a 1.2 mm pulsed Doppler ultrasound sampling volume placed in the center of the image of the vessel lumen with internal software ...
The proposed mechanistic link between the age-related attenuation in vascular function and free radicals is an attractive hypothesis; however, direct evidence of free radical attenuation and a concomitant improvement in vascular function in the elderly is lacking. Therefore, this study sought to test the hypothesis that ascorbic acid (AA), administered intra-arterially during progressive handgrip exercise, improves brachial artery (BA) vasodilation in a nitric oxide (NO)-dependent manner, by mitigating free radical production. BA vasodilation (Doppler ultrasound) and free radical outflow [electron paramagnetic resonance (EPR) spectroscopy] were measured in seven healthy older adults (69 ± 2 yr) during handgrip exercise at 3, 6, 9, and 12 kg (∼13-52% of maximal voluntary contraction) during the control condition and nitric oxide synthase (NOS) inhibition via N(G)-monomethyl-L-arginine (L-NMMA), AA, and coinfusion of l-NMMA + AA. Baseline BA diameter was not altered by any of the treatments, while L
TY - JOUR. T1 - Effect of cigar smoking on endothelium-dependent brachial artery dilation in healthy young adults. AU - Santo-Tomas, Minerva. AU - Lopez-Jimenez, Francisco. AU - Machado, Humberto. AU - Aldrich, Harry R.. AU - Lamas, Gervasio A.. AU - Lieberman, Eric H.. PY - 2002. Y1 - 2002. N2 - Background: Cigar smoking has become a quickly growing trend among teenagers, women, and young adults. The objective was to explore whether cigar smoking affects flow-mediated vasodilation in healthy, non-smoking young adults. Methods: This was a prospective randomized trial with open design. It was performed in a cardiology teaching program in a private community hospital that serves as a major referral center within the greater Miami area. Apparently healthy, non-smoking young adult cardiology trainees and staff between the ages of 20 and 45 years were randomly assigned to a cigar smoking group (n = 15) or a control group (n = 14). The main outcome measures were the difference in percent diameter ...
Looking for cold-induced vasodilation? Find out information about cold-induced vasodilation. A sequence of vasoconstriction followed by vasodilation that acts as a protective mechanism to prevent cold weather injury to the extremities Explanation of cold-induced vasodilation
This study demonstrated that treatment with a single dose of commonly used antihypertensive and antianginal medication lowers blood pressure and heart rate, but has no effect on resting brachial artery size, FMD, NMD, and the reproducibility of FMD. These results were obtained when healthy patients received single doses of specific agents for the first time and when patients on chronic therapy for CAD are studied before and after receiving their clinically prescribed medications. These findings suggest that acute alterations in systemic hemodynamics and/or local resting arterial tone induced by these medications do not alter the capacity of the brachial artery to respond to endothelium-derived and exogenous vasodilators.. No previous study examined the specific question addressed in the current study. In most prior studies of endothelial function in human subjects, all vasoactive medications were withheld for at least 24 h, and a recent paper recommended withholding medications for four ...
We fed 10 healthy, normolipidemic subjects five meals containing 900 kcal and 50 g fat. Three meals contained different fat sources: olive oil, canola oil, and salmon. Two olive oil meals also contained antioxidant vitamins (C and E) or foods (balsamic vinegar and salad). We measured serum lipoproteins and glucose and brachial artery flow-mediated vasodilation (FMD), an index of endothelial function, before and 3 h after each meal ...
The purpose of this study was to determine the association between vascular diameters and amount of magnification and to assess the influence of the magnification media on the microanastomosis quality and permeability. Sixty arterial microanostomoses
Vasodilation is where blood vessels widen.[1] It results from relaxation of muscle cells within blood vessel walls. The process is essentially the opposite of vasoconstriction, which is the narrowing of blood vessels.. When vessels widen, blood flow is increased. This in turn decreases blood pressure. Drugs that cause vasodilation are called vasodilators.. ...
Nicotinic acid, known as vitamin B3, is an effective lipid lowering drug and intense cutaneous vasodilator. This study reports the effect of 2-(1-adamantylthio)nicotinic acid (6) and its amide 7 and nitrile analog 8 on phenylephrine-induced contraction of rat thoracic aorta as well as antioxidative activity. It was found that the tested thionicotinic acid analogs 6-8 exerted maximal vasorelaxation in a dose-dependent manner, but their effects were less than acetylcholine (ACh)-induced nitric oxide (NO) vasorelaxation. The vasorelaxations were reduced, apparently, in both NG-nitro-L-arginine methyl ester (L-NAME) and indomethacin (INDO). Synergistic effects were observed in the presence of L-NAME plus INDO, leading to loss of vasorelaxation of both the ACh and the tested nicotinic acids. Complete loss of the vasorelaxation was noted under removal of endothelial cells. This infers that the vasorelaxations are mediated partially by endothelium-induced NO and prostacyclin. The thionicotinic acid analogs all
TY - JOUR. T1 - Role of angiotensin II and α-adrenergic receptors during estrogen-induced vasodilation in ewes. AU - Davis, L. E.. AU - Magness, R. R.. AU - Rosenfeld, C. R.. PY - 1992/1/1. Y1 - 1992/1/1. N2 - Estradiol-17β (E2β) produces uterine and systemic vasodilation in nonpregnant ewes without altering mean arterial pressure (MAP). Mechanisms responsible for maintaining MAP and thus uterine blood flow (UBF) may include activation of the renin-angiotensin and/or adrenergic systems. We therefore investigated the effects of systemic blockade of angiotensin II (ANG II) and/or α-adrenergic receptors in nonpregnant, castrated ewes, using saralasin (Sar) and/or phentolamine (Phen) in the presence or absence of intravenous E2β (1.0 μg/kg). In nonestrogenized ewes neither antagonist alone had substantial cardiovascular effects; however, Sar + Phen decreased systemic vascular resistance (SVR) 20 ± 7.4% (SE) and increased heart rate (HR) 50 ± 19% (P , 0.01); MAP and UBF were unaffected. ...
Although we found that the vasoconstrictor response to l-NMMA was lower in blacks, we did not examine effects of other nonspecific vasoconstrictors to investigate whether this is a reflection of reduced sensitivity of the vascular smooth muscle to vasoconstrictors. However, the fact that the constrictor response to TEA was similar to whites suggests that the response to l-NMMA is specific for reduced NO bioavailability. The reduced sensitivity to exogenous NO (sodium nitroprusside) complicates the interpretation of the reduced dilator responses observed with acetylcholine and bradykinin in blacks. However, because basal NO and the contribution of NO during exercise is lower in blacks, it is likely that in addition to reduced sensitivity, there is also an endothelial defect in NO release in blacks.. l-NMMA and TEA are competitive inhibitors, and thus our results may underestimate the physiological contribution of both NO and K+Ca channels to vasodilation. Our investigation was conducted on a ...
The purpose of this study was to investigate if myogenic responses of isolated coronary arterioles were dependent on an intact, functional endothelium. Arterioles were located in situ by intracoronary perfusion with india ink-gelatin solution and then dissected and cannulated at both ends with glass micropipettes. Intraluminal pressure was initially set at 60 cm H2O; then the pressure was altered in steps of 20 cm H2O over a range of 20-140 cm H2O. Arterioles developed spontaneous tone and exhibited a significant myogenic response in physiological saline solution (36 degrees -37 degrees C). Arteriolar dilation and constriction were observed at lower (20-60 cm H2O) and higher (60-140 cm H2O) pressures, respectively. The presence of a functional and automatically intact endothelium was confirmed by relaxation to the endothelium-dependent vasodilator bradykinin and by transmission electron microscopy, respectively. After mechanical denudation of the endothelium with a specially designed abrasive ...
Forty-seven papers on the mechanisms whereby natural regulatory phenomena and synthetic vasodilator agents effect vasodilation. Outlines the complexity of the physiologic regulation of vascular smooth muscle tone and provides different points of view on debated issues. From a symposium, Mechanisms of Vasodilation, held July 1980 in Belgium. Five sections: neurohumoral regulation, local regulation, cellular mechanisms, the blood-vessel wall in hypertension, and vasodilator agents. ...
We found that Nrf2 KO mice show an impaired left ventricular diastolic function as assessed by high resolution ultrasound. Accordingly, isolated perfused Nrf2 KO hearts showed an impaired response to β adrenergic stimulation by isoproterenol, while systolic left ventricular function was preserved. Surprisingly, blood pressure in Nrf2 KO mice was significantly decreased, and endothelial function of arterial conductance and coronary resistive vessels was preserved. This is consistent with an increased maximal dilation after vascular occlusion of the arteria iliaca externa, which indicates a fully preserved vascular and endothelial function in these mice. Mice lacking the endothelial nitric oxide synthase (eNOS KO) showed no dilatatory response to shear stress, confirming that flow-mediated-dilation response mainly depends on eNOS-dependent vasodilatory pathways. The circulating NO pool analysed by HPLC and chemiluminescence showed no differences between Nrf2 KO mice and WT littermates. However, ...
In the current study, we found that type 2 diabetes impaired the ability of mesenteric arteries to remodel and improve NO-dependent dilation in response to a chronic increase in blood flow. Indeed, AGEs and RAGEs were overexpressed, whereas eNOS level and MMP activity were reduced in arteries from ZDF rats. Ongoing treatment with the AGE-breaker ALT-711 restored the ability of mesenteric arteries from ZDF rats to increase their diameter and improved endothelium-dependent dilation in response to a chronic rise in blood flow.. Physiologically, a chronic rise in blood flow in resistance arteries enlarges vascular diameter and improves endothelium-dependent dilation (9,19,34). This remodeling is essential to adjust organ perfusion during physiological processes, such as development (35), pregnancy (36), or exercise training (37), as well as during pathological processes (mainly ischemic diseases). A similar remodeling also occurs in response to vasodilator treatments (38,39). This remodeling plays a ...
... Online Course is designed to provide a comprehensive introduction to peripheral vascular sonography and has been designed to provide a strong foundation to perform and/or interpret vascular ultrasound examinations.
Endothelium plays a critical role in maintaining healthy homeostatic properties of the vasculature. Endothelial dysfunction promotes atherosclerosis by creating a vasospastic, prothrombotic, and proinflammatory milieu. Therefore, the assessment of endothelial function as a surrogate marker of arterial health has gained significant interest for clinical risk assessment beyond the risk conveyed by a structural impediment to flow (1). Furthermore, the observation that cardiovascular events may occur remotely from the site in which the endothelial dysfunction is detected prompted clinical studies in search for peripheral vascular endothelial dysfunction as a predictor of cardiovascular events.. Endothelial dysfunction is characterized by a paradoxical vasoconstriction or attenuated dilation due to reduced endothelium-dependent nitric oxide (NO) release. In earlier studies, the response of the epicardial arteries to infused acetylcholine was measured invasively to assess endothelial function in the ...
With the worlds elderly population expected to double by 2050, understanding how aging affects the body is an important focus for researchers globally. Cardiovascular disease, the No. 1 cause of death worldwide, often is associated with aging arteries that restrict blood flow. Now, University of Missouri researchers have identified an age-related cause of arterial dysfunction, a finding that could lead to future treatments for some forms of vascular disease., With the worlds elderly population expected to double by 2050, understanding how aging affects the body is an important focus for researchers globally. Cardiovascular disease, the No. 1 cause of death worldwide, often is associated with aging arteries that restrict blood flow. Now, University of Missouri researchers have identified an age-related cause of arterial dysfunction, a finding that could lead to future treatments for some forms of vascular disease.
OBJECTIVE: To search for determinants of endothelial dysfunction in type 2 diabetes. RESEARCH DESIGN AND METHODS: We performed a comprehensive analysis of cardiovascular risk markers and measured blood flow responses to endothelium-dependent (acetylcholine [ACh] and NG-monomethyl-L-arginine) and -independent (sodium nitroprusside [SNP]) vasoactive agents in 30 nonsmoking men with type 2 diabetes (age 51 +/- 1 years, BMI 27.8 +/- 0.4 kg/m2, HbA1c 7.4 +/- 0.3%) and 12 matched normal control men. RESULTS: ACh-induced vasodilation was 37% lower in type 2 diabetic (6.1 +/- 0.5) than in normal subjects (9.7 +/- 1.5 ml.dl-1.min-1, P , 0.01), while flows during SNP were similar (9.1 +/- 0.6 vs. 9.9 +/- 1.3 ml.dl-1.min-1, NS). The ratio of endothelium-dependent vs. -independent flow (ACh:SNP ratio) was 31% lower in type 2 diabetic (0.70 +/- 0.05) than in normal subjects (1.10 +/- 0.18, P , 0.01). Total (2.2 +/- 0.4 vs. 1.3 +/- 0.2 mmol/l, P , 0.05), VLDL, and intermediate-density lipoprotein ...
In the present study, the role of reactive oxygen species and the contribution of antioxidant defence in the time course of changes in acetylcholine-stimulated endothelium-dependent and sodium nitroprusside-stimulated endothelium-independent relaxation were investigated in aortic rings isolated from 6-month streptozotocin-diabetic and age-matched control rats. Although there were no significant differences in the degree of the peak relaxations produced by a single administration of acetylcholine (1 μM) or sodium nitroprusside (0.01 μM) between control and diabetic rings, the endothelium-dependent and -independent relaxant responses were more transient and the time required to reach a peak relaxation after addition of acetylcholine was shorter in diabetic vessels. Pretreatment of diabetic vessels with superoxide dismutase (100 U/ml) normalized the recovery phases of endothelium-dependent and -independent relaxations, but had no effect on the peak responses to acetylcholine and sodium ...
Did you know that dark circles under your eyes are a result of the influence of histamine on vasodilation. Histamines dilate blood vessels (vasodilate). So if you are having an allergic reaction that is filling up your histamine bucket, you probably have dark circles under your eyes. I can attest to this. Ever since I…
Focused ultrasound (FUS) in combination with microbubbles temporally and locally increases the permeability of the blood-brain barrier (BBB) for facilitating drug delivery. However, the temporary effects of FUS on the brain microstructure and microcirculation need to be addressed. We used label-free optical coherence tomography (OCT) and OCT angiography (OCTA) to investigate the morphological and microcirculation changes in mouse brains due to FUS exposure at different power levels. Additionally, the recovery progress of the induced effects was studied. The results show that FUS exposure causes cerebral vessel dilation and can be identified and quantitatively analyzed via OCT/OCTA. Micro-hemorrhages can be detected when an excessive FUS exposure power is applied, causing the degradation of OCTA signal owing to strong scattering by leaked red blood cells (RBCs) and weaker backscattered intensity from RBCs in vessels. The vessel dilation effect due to FUS exposure was found to abate in several ...
Cardiovascular agentsCardiovascular agents: In humans, L-arginine caused decreased blood pressure and improved endothelium-dependent dilation (EDD) and acetylcholine- and nitroglycerin-mediated vasodilation (125; 126; 127; 91; 128; 129; 130; 131; 132; 93; 133; 134; 115; 95; 229; 135; 145) and has resulted in hypotension or additive effects when used with antihypertensives (136; 137; 138; 145); it also decreased the need for hypotensive agents (177). In a systematic review, select trials reported a lack of significant improvement in blood pressure and EDD (145). In a human study, hypertensive exacerbation was noted in one subject following a heart transplant (179). Also, in humans, arginine caused hyperkalemia (84; 85) and so should be used cautiously with agents that increase potassium, including beta-blockers and alpha-blockers. In humans, arginine caused hyperkalemia (84; 85) and so should be used cautiously with agents that may increase potassium, including digitalis. Theoretically, ...
Video articles in JoVE about cardiovascular diseases include Hydra, a Computer-Based Platform for Aiding Clinicians in Cardiovascular Analysis and Diagnosis, An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause, Near-infrared Fluorescence Imaging of Abdominal Aortic Aneurysms, Blood Pressure Measurement, Invertebrate Lifespan Quantification, Simultaneous Isolation of High Quality Cardiomyocytes, Endothelial Cells, and Fibroblasts from an Adult Rat Heart, Intracellular Staining and Flow Cytometry to Identify Lymphocyte Subsets within Murine Aorta, Kidney and Lymph Nodes in a Model of Hypertension, Glycoproteomics of the Extracellular Matrix: A Method for Intact Glycopeptide Analysis Using Mass Spectrometry, Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice, Electrophysiological Analysis of human Pluripotent Stem Cell-derived Cardiomyocytes (hPSC-CMs) Using Multi-electrode
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Premier Surgical Associates in Knoxville has a team or 9 registered Vascular Ultrasound Technologists who are well-trained and experienced.
The AngioDefender system technology takes various readings during the test and converts them to an AngioDefender Score based on flow-mediated dilation (%FMD) of your brachial artery. Your healthcare provider interprets this score along with other factors, including age and lifestyle, to paint a comprehensive picture of your hearts health and future risk of CVD.. How is the AngioDefender system data saved? ...