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At least 1,315 records · Page 73Linked to original sources
PubMed2001

Iron chelation improves endothelial function in patients with coronary artery disease.

BACKGROUND: Some epidemiological studies have shown that increased iron stores are associated with increased cardiovascular events. Redox-active iron may contribute to lipid peroxidation, endothelial cell activation, and generation of reactive oxygen species (especially hydroxyl radical, via Fenton chemistry). Increased oxidative stress is associated with impaired action of endothelium-derived nitric oxide in patients with atherosclerosis. METHODS AND RESULTS: To test the hypothesis that reducing vascular iron stores would reverse endothelial dysfunction, we examined the effects of the iron chelator deferoxamine (500 mg intra-arterially over 1 hour) on vasomotor function in forearm resistance vessels of patients with coronary artery disease by venous occlusion plethysmography. Patients with coronary artery disease had impaired endothelium-dependent vasodilation in response to methacholine compared with healthy control subjects (P<0.001). Deferoxamine infusion decreased serum iron levels (P<0.001). Deferoxamine improved the blood flow response to methacholine in patients with coronary artery disease (P<0.01 by 2-way repeated-measures ANOVA) but had no effect on the response to sodium nitroprusside. In normal volunteers, deferoxamine had no effect on the response to methacholine. The nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine abolished augmentation of the methacholine response associated with deferoxamine. The hydroxyl radical scavenger mannitol had no effect on the methacholine response. CONCLUSIONS: Deferoxamine improved nitric oxide-mediated, endothelium-dependent vasodilation in patients with coronary artery disease. These results suggest that iron availability contributes to impaired nitric oxide action in atherosclerosis.

Adult↗
PubMed1997

Identification of functional endothelial protein C receptor in human plasma.

The endothelial cell protein C receptor (EPCR) binds protein C and facilitates activation by the thrombin-thrombomodulin complex. EPCR also binds activated protein C (APC) and inhibits APC anticoagulant activity. In this study, we detected a soluble form of EPCR in normal human plasma. Plasma EPCR appears to be approximately 43, 000 D, and circulates at approximately 100 ng/ml (98.4+/-27.8 ng/ml, n = 22). Plasma EPCR was purified from human citrated plasma using ion exchange, immunoaffinity, and protein C affinity chromatography. Flow cytometry experiments demonstrated that plasma EPCR bound APC with an affinity similar to that previously determined for recombinant soluble EPCR (Kdapp = 30 nM). Furthermore, plasma EPCR inhibited both protein C activation on an endothelial cell line and APC anticoagulant activity in a one-stage Factor Xa clotting assay. The physiological function of plasma EPCR is uncertain, but if the local concentrations are sufficiently high, particularly in disease states, the present data suggest that the soluble plasma EPCR could attenuate the membrane-bound EPCR augmentation of protein C activation and the anticoagulant function of APC.

Anticoagulants↗
PubMed1999

[The ultrasonic measurement of the endothelial function of the brachial artery in suspected coronary heart disease].

BACKGROUND AND OBJECTIVE: A positive correlation between the presence of coronary artery disease (CAD) and peripheral endothelial dysfunction (ED) of the brachial artery has been shown in several studies. Aim of the present study was to evaluate whether the non-invasive determination of ED could also be used as a screening test in patients suspected of having CAD. PATIENTS AND METHODS: 122 patients were included. 112 had an exercise-ECG before hospital admission. Preceding coronary angiography, FMD% was measured by high-resolution ultrasound (13 Mhz). Longitudinal scans of the brachial artery were done at rest, during reactive hyperemia and after the sublingual administration of nitroglycerin. RESULTS: In 101 of the 122 patients the presence of CAD was diagnosed by angiography, whereas 21 patients had normal coronary arteries. The extent of the vasodilation (FMD%) was found to be largely independent of the resting vessel diameters (FMD%/vessel diameter at rest: r = -0.32767 p = 0.0002). FMD% was significantly higher in patient without CAD than in the CAD group (7.01 +/- 3.5% vs. 3.73 +/- 4.11%, p < 0.001). Comparison of sensitivity and specificity to predict the presence of CAD between FMD% [sensitivity 71.3%, specificity 81%] and exercise-ECG [sensitivity 82.4%, specificity 57.1%] gave similar results. No correlation was found between the degree of the impairment of FMD% and the severely of CAD. CONCLUSION: The determination of peripheral ED was found to be a sensitive and specific measure for predicting the presence of CAD in our cohort. Since this approach is non-invasive, non-radioactive and cost-effective it warrants further evaluation of its role as an additional screening test in patients clinically suspected of having CAD.

Aged↗
PubMed1998

Tetrahydrobiopterin and endothelial function.

Tetrahydrobiopterin is an essential co-factor required for catalytic activity of nitric oxide synthases. A close link between tetrahydrobiopterin and nitric oxide synthesis has been recently demonstrated in a number of different cell types, including endothelial cells. The precise role of tetrahydrobiopterin in regulation of nitric oxide synthase activity is not completely understood; however, it may function as both an allosteric and redox co-factor. In peripheral and cerebral arteries, administration of tetrahydrobiopterin can stimulate production of nitric oxide. By contrast, in arteries depleted of tetrahydrobiopterin, nitric oxide production is impaired. Evidence indicates that, under certain pathological conditions, decreased availability of tetrahydrobiopterin may be responsible for a dysfunction of nitric oxide synthase leading to a shift in the balance between the production of protective nitric oxide and deleterious oxygen-derived free radicals. This concept may have important implications in understanding the mechanisms of endothelial dysfunction and oxidative vascular injury described in a number of vascular diseases, including atherosclerosis. This review will discuss the complex interaction between tetrahydrobiopterin and nitric oxide synthase and its role in the control of vascular tone.

Animals↗
PubMed1999

Thiazolidinediones down-regulate plasminogen activator inhibitor type 1 expression in human vascular endothelial cells: A possible role for PPARgamma in endothelial function.

The effect of peroxisome proliferator-activated receptor (PPAR) gamma activators, thiazolidinediones, on plasminogen activator type 1 (PAI-1) was examined in cultured human umbilical vein endothelial cells (HUVEC). Tumor necrosis factor alpha (TNF-alpha) enhanced PAI-1 secretion and mRNA expression by approximately 2-fold. The thiazolidinediones, troglitazone and pioglitazone, decreased basal and TNF-alpha-stimulated PAI-1 secretion and mRNA expression in HUVEC in a dose-dependent fashion. PPARgamma mRNA in HUVEC could be detected by reverse transcriptase-polymerase chain reaction using specific primers. These results suggest that PPARgamma may regulate PAI-1 expression in HUVEC and that thiazolidinediones have a therapeutic potential for improving endothelial dysfunction observed in insulin resistance.

Base Sequence↗
PubMed1997

The link among nitric oxide synthase activity, endothelial function, and aortic and ventricular hypertrophy in hypertension.

The adaptive changes that occur in the left ventricle (LV) and vessels in response to hypertension, namely, muscle hypertrophy/hyperplasia, endothelial dysfunction, and extracellular matrix increase, do not depend solely on blood pressure elevation. These changes are in fact, maladaptive since they are forerunners of cardiac failure, stroke, and renal failure. Nitric oxide, an endogenous vasodilator and inhibitor of vascular smooth muscle cell growth, is synthesized in the endothelium by constitutive nitric oxide synthase (cNOS). We investigated the relationships among LV and aortic cNOS activity (conversion of [14C] L-arginine to [14C] L-citrulline), with LV hypertrophy (LV weight/body weight), and (2) aortic hypertrophy (aortic weight/ length) in spontaneously hypertensive rats (SHR) and Dahl salt-sensitive (DS) rats matched for blood pressure (219 +/- 12 versus 211 +/- 7 mm Hg, P = NS) and age. Compared with their normotensive counterparts, aortic cNOS activity was increased 106% in SHR but reduced by 73% in DS rats. The correlation between blood pressure and aortic cNOS activity was positive (r = .74, P < .01) in SHR and negative (r = -.82, P < .01) in DS rats, LV cNOS activity was increased 73% in SHR compared with normotensive Wistar-Kyoto rats (P < .01). On the other hand, LV cNOS activity was not increased in hypertensive DS rats compared with normotensive DS rats. In SHR, aortic hypertrophy did not increase significantly and LV hypertrophy increased only 15%, whereas in hypertensive DS rats the aorta and LV hypertrophied 36% and 88%, respectively (both P < .01). Moreover, in DS rats there was a negative correlation between cNOS activity and aortic hypertrophy (r = -.70, P < .01). In DS rats, antihypertensive therapy consisting of an angiotensin-converting enzyme inhibitor, perindopril, and a diuretic, indapamide, normalized blood pressure, aortic cNOS activity, and LV hypertrophy and reduced aortic hypertrophy. Our studies imply that upregulation of vascular cNOS activity has a protective cardiovascular homeostatic role in hypertension. Clinically, the variable end-organ disease observed in individuals with similar severity of hypertension may be explained, at least in part, by genetically conditioned differences in vascular cNOS activity in response to hypertension.

Animals↗
PubMed2005

Reduction in visceral adiposity is highly related to improvement in vascular endothelial dysfunction among obese women: an assessment of endothelial function by radial artery pulse wave analysis.

Because obesity is frequently complicated by other cardiovascular risk factors, the impact of a reduction in visceral adiposity on vascular endothelial dysfunction (VED) in obese patients is difficult to determine. In the present study, we evaluated the impact of a reduction in visceral adiposity on VED in obese women. Thirty-six premenopausal obese women (BMI >/= 25 kg/m2) without complications were enrolled in the study. VED was evaluated by determining the augmentation index (AIx) from radial artery pulse waves obtained by applanation tonometry. Changes in AIx in response to nitroglycerin- induced endothelium-independent vasodilatation (DeltaAIx-NTG) and in response to salbutamol administration (DeltaAIx-Salb) were determined before and after weight reduction. After a 12-week weight reduction program, the average weight loss was 7.96 +/- 3.47 kg, with losses of 21.88 +/- 20.39 cm2 in visceral fat areas (p < 0.001). Pulse wave analysis combined with provocative pharmacological testing demonstrated preserved endothelium-independent vasodilation in healthy premenopausal obese women (DeltaAIx-NTG: 31.36 +/- 9.80% before weight reduction vs. 28.25 +/- 11.21% after weight reduction, p > 0.1) and an improvement in endothelial-dependent vasodilation following weight reduction (DeltaAIx-Salb: 10.03 +/- 6.49% before weight reduction vs. 19.33 +/- 9.28% after reduction, p < 0.001). A reduction in visceral adipose tissue was found to be most significantly related to an increase in DeltaAIx-Salb (beta=-0.57, p < 0.001). A reduction in visceral adiposity was significantly related to an improvement in VED. This finding suggests that reduction of visceral adiposity may be as important as the control of other major risk factors in the prevention of atherosclerosis in obese women.

Adipose Tissue↗
PubMed1997

Albumin microbubble adherence to human coronary endothelium: implications for assessment of endothelial function using myocardial contrast echocardiography.

OBJECTIVES: We hypothesized that sonicated 5% human albumin microbubbles (Albunex) adhere to disrupted vascular endothelium and that this interaction is a marker of endothelial integrity. This study sought to identify sites and determinants of Albunex-endothelial cell (EC) attachment. BACKGROUND: Under normal conditions, Albunex microbubbles used in myocardial contrast echocardiography (MCE) pass unimpeded through the coronary microcirculation. During pathophysiologic states associated with endothelial dysfunction, however, microbubbles linger in the myocardium despite normal flow. The sites and conditions regulating microbubble adhesion are unknown. METHODS: Coverslips with cultured human coronary artery ECs were mounted in a parallel plate perfusion system and perfused with a suspension of fluorescein-labeled Albunex in culture medium, followed by a bubble-free wash at a wall shear rate of 100 s-1. To create inflammatory ECs, phorbol myristate acetate was added 4.5 h before perfusion, and flow cytometry was used to confirm an inflammatory response. Perfusions were performed under normal and inflammatory conditions using surfaces of confluent and subconfluent ECs and isolated extracellular matrix. Bubble adherence was quantified in 20 random fields per cover-slip using epifluorescent video microscopy. RESULTS: No microbubbles adhered to normal confluent ECs, although small numbers adhered to inflamed ECs (0.03 +/- 0.01 bubbles/cell, p < 0.01 vs. normal cells). Fever microbubbles attached to normal versus inflamed matrix of both partially exposed (1,800 +/- 520 vs. 4,100 +/- 1,000 bubbles/mm2, p = 0.05) and completely denuded (2,700 +/- 1,300 vs. 7,200 +/- 1,100 bubbles/ mm2, p < 0.03) endothelium. CONCLUSIONS: Albunex microbubbles preferentially adhere to inflammatory endothelial extracellular matrix. These data suggest that MCE can be used to noninvasively study endothelial integrity and may have implications for the assessment of preclinical atherosclerotic heart disease.

Adhesiveness↗
PubMed1998

Endothelin ETA receptor blockade restores NO-mediated endothelial function and inhibits atherosclerosis in apolipoprotein E-deficient mice.

This study investigated whether endothelin-1 (ET-1), a potent vasoconstrictor, which also stimulates cell proliferation, contributes to endothelial dysfunction and atherosclerosis. Apolipoprotein E (apoE)-deficient mice and C57BL/6 control mice were treated with a Western-type diet to accelerate atherosclerosis with or without ETA receptor antagonist LU135252 (50 mg/kg/d) for 30 wk. Systolic blood pressure, plasma lipid profile, and plasma nitrate levels were determined. In the aorta, NO-mediated endothelium-dependent relaxation, atheroma formation, ET receptor-binding capacity, and vascular ET-1 protein content were assessed. In apoE-deficient but not C57BL/6 mice, severe atherosclerosis developed within 30 wk. Aortic ET-1 protein content (P < 0.0001) and binding capacity for ETA receptors was increased as compared with C57BL/6 mice. In contrast, NO-mediated, endothelium-dependent relaxation to acetylcholine (56 +/- 3 vs. 99 +/- 2%, P < 0.0001) and plasma nitrate were reduced (57.9 +/- 4 vs. 93 +/- 10 micromol/liter, P < 0.01). Treatment with the ETA receptor antagonist LU135252 for 30 wk had no effect on the lipid profile or systolic blood pressure in apoE-deficient mice, but increased NO-mediated endothelium-dependent relaxation (from 56 +/- 3 to 93 +/- 2%, P < 0.0001 vs. untreated) as well as circulating nitrate levels (from 57.9 +/- 4 to 80 +/- 8.3 micromol/liter, P < 0.05). Chronic ETA receptor blockade reduced elevated tissue ET-1 levels comparable with those found in C57BL/6 mice and inhibited atherosclerosis in the aorta by 31% without affecting plaque morphology or ET receptor-binding capacity. Thus, chronic ETA receptor blockade normalizes NO-mediated endothelial dysfunction and reduces atheroma formation independent of plasma cholesterol and blood pressure in a mouse model of human atherosclerosis. ETA receptor blockade may have therapeutic potential in patients with atherosclerosis.

Acetylcholine↗
PubMed2006

Epigallocatechin gallate preserves endothelial function by reducing the endogenous nitric oxide synthase inhibitor level.

Asymmetric dimethylarginine (ADMA), the endogenous nitric oxide synthase inhibitor, is thought to be a key factor contributing to endothelial dysfunction. Tea catechins can cause an endothelium-dependent vasorelaxation. The present study examined the effect of epigallocatechin gallate (EGCG), the major component of tea catechins, on endothelial dysfunction induced by native low density lipoprotein (LDL) in rats and oxidized LDL (ox-LDL) in cultured endothelial cells, and whether the protective effect of EGCG is related to reduction of ADMA level. A single injection of LDL (4 mg x kg(-1), i.v.) markedly reduced endothelium-dependent relaxation and the serum nitrite/nitrate (NO) level, and increased serum concentrations of ADMA, malondialdehyde (MDA), and tumor necrosis factor-alpha (TNF-alpha). EGCG (10 or 50 mg x kg(-1), i.p.) significantly attenuated the inhibition of vasodilator response to acetylcholine and the decreased serum nitrite/nitrate level, and reduced the elevated levels of ADMA, MDA, and TNF-alpha. Exposure of endothelial cells to ox-LDL (100 microg x mL(-1)) for 24 h markedly increased the medium levels of lactate dehydrogenase (LDH), ADMA, TNF-alpha, and MDA, and decreased the level of nitrite/nitrate in the medium and the activity of dimethylarginine dimethylaminohydrolase (DDAH) in the endothelial cells. EGCG (10 and 100 microg x mL(-1)) significantly decreased the levels of LDH, ADMA, TNF-alpha, and MDA, and increased the level of nitrite/nitrate and the activity of DDAH. These results suggest that EGCG protects endothelial dysfunction induced by native LDL in vivo or by ox-LDL in endothelial cells, and the protective effect of EGCG on the endothelium is related to decrease in ADMA level via increasing of DDAH activity.

Animals↗
PubMed2005

Oxidized LDL and small LDL particle size are independently predictive of a selective defect in microcirculatory endothelial function in type 2 diabetes.

AIM: To explore the associations of LDL (low-density lipoprotein) particle size and oxidized LDL with endothelium-dependent function of the forearm microcirculation in diabetes. METHODS: Endothelium-dependent function was examined in 43 middle-aged men and women with type 2 diabetes and 10 age-matched controls. All received aspirin to inhibit endothelial cyclo-oxygenase. Forearm blood flow (FBF) was measured using venous occlusion plethysmography with separate administration of acetylcholine (ACh) and bradykinin (BK) into the brachial artery. Endothelium-independent function was assessed using sodium nitroprusside (SNP). N(G)-monomethyl-L-arginine (L-NMMA) was co-infused with ACh (ACh + L-NMMA) and BK (BK + L-NMMA) to assess non-NO-mediated contributions to endothelium-dependent function. RESULTS: Subjects with diabetes had impaired endothelium-dependent and endothelium-independent function compared with controls (p < 0.01 for ACh, BK and SNP). In multivariate regression analysis, LDL size (r = 0.41 and p = 0.007), oxidized LDL (r = -0.41 and p = 0.007) and duration of diabetes (r = -0.37 and p = 0.02) predicted FBF response to ACh independently of age, gender and systolic blood pressure. There were no associations between LDL size, oxidized LDL, duration of diabetes and FBF response to BK, SNP, ACh + L-NMMA or BK + L-NMMA. CONCLUSION: In type 2 diabetes, small dense LDL particles, duration of diabetes and oxidized LDL may independently contribute to endothelial dysfunction of the microcirculation. These disturbances may occur via a selective defect, because ACh and BK activate endothelial NO synthase via different G-protein signal transduction pathways.

Acetylcholine↗
PubMed2000

Effect of nitrite on endothelial function in isolated lung.

Nitrated tyrosine, implicated in protein dysfunction, is increased in various tissues in association with diverse pathological processes. Angiotensin converting enzyme (ACE) is a luminal vascular endothelial enzyme whose dysfunction is an early sign of endothelial injury. ACE contains a tyrosine critical for its enzymatic activity. Others have shown that nitrite exacerbates the ACE dysfunction of cultured endothelial cells in contact with activated polymorphonuclear neutrophils (PMN). We hypothesized that exogenous nitrite would enhance endothelial ACE dysfunction associated with PMN activation in the isolated lung. Rats received lipopolysaccharide (LPS) 2 h prior to isolated lung perfusion with Ficoll containing buffer. Either formyl-Met-Leu-Phe (fMLP, 10(-7) M) or phorbol myristate acetate (PMA, 10(-7) M) was used to activate PMN in lungs treated or not treated with 300-microM nitrite. A first pass indicator dilution method and first order reaction kinetics were used to determine ACE activity, while lung Ficoll content served as an index of vascular permeability. Both fMLP and PMA decreased endothelial ACE activity and increased pulmonary artery pressure, edema and vascular permeability. Exogenous nitrate did not potentiate the decrease in ACE activity, the lung injury or nitrotyrosine immunoreactivity of lung homogenates. In contrast to observations in cultured endothelial cells, our findings in the whole lung are compatible with the speculation of others that the rat lung has an unidentified factor, which minimizes accumulation of nitrated proteins.

Animals↗
PubMed2003

Sleep apnea and markers of vascular endothelial function in a large community sample of older adults.

Clinical studies have suggested that sleep apnea is associated with impaired brachial artery flow-mediated dilation, a surrogate of endothelial dysfunction. We examined this question among older participants in the baseline examination of the Sleep Heart Health/Cardiovascular Health Study cohort (n = 1,037, age 68 years or older, 56% female). Indices of sleep apnea, derived from 12-channel home polysomnography, were the apnea-hypopnea index (average number of apneas/hypopneas per hour) and the hypoxemia index (percentage of time below 90% O2 saturation). Baseline arterial diameter and percentage of flow-mediated dilation were measured by ultrasound. Sleep apnea measures were associated with baseline diameter and the percentage of flow-mediated dilation, although these associations were weakened after adjustment for other cardiovascular risk factors, particularly body mass index. However, a statistically significant linear association between the hypoxemia index and baseline diameter was observed even after adjustment for body mass index and other confounders (p < 0.01). The associations were stronger among participants who were younger than 80 years and among those who with hypertension. This study adds to the growing body of evidence linking sleep apnea with vascular dysfunction in older subjects. Whether these relationships are entirely independent of obesity is unclear. This association might be one of the mechanisms explaining the relationship between sleep apnea, hypertension, and cardiovascular disease.

Age Factors↗
PubMed2000

Acute elevations of plasma asymmetric dimethylarginine and impaired endothelial function in response to a high-fat meal in patients with type 2 diabetes.

Asymmetric dimethylarginine (ADMA), a compound detectable in human plasma, is an endogenous inhibitor of NO synthase. Endothelial dysfunction is an early event in atherogenesis, and large-vessel atherosclerosis is a major cause of morbidity and mortality in patients with type 2 diabetes mellitus. Fifty patients with type 2 diabetes mellitus were studied at baseline and 5 hours after ingestion of a high-fat meal. Plasma ADMA measured by using high-performance liquid chromatography increased from 1.04+/-0.99 to 2.51+/-2.27 micromol/L (P:<0.0005). Brachial arterial vasodilation after reactive hyperemia, a NO-dependent function, measured by high-resolution ultrasound, decreased from 6.9+/-3.9% at baseline to 1.3+/-4.5% (P:<0.0001). These changes occurred in association with increased plasma levels of triglycerides and very low density lipoprotein triglycerides, with reduced low density lipoprotein cholesterol and high density lipoprotein cholesterol, and with no changes in total cholesterol. The increase in plasma ADMA in response to a high-fat meal was significantly and inversely related to the decrease in percent vasodilation. In 10 of the subjects studied with a similar protocol on another day, no significant changes in the brachial artery flow responses or in plasma ADMA were observed 5 hours after ingestion of a nonfat isocaloric meal. The data suggest that ADMA may contribute to abnormal blood flow responses and to atherogenesis in type 2 diabetics.

Adult↗
PubMed2006

Effects of pioglitazone on endothelial function, insulin sensitivity, and glucose control in subjects with coronary artery disease and new-onset type 2 diabetes.

OBJECTIVE: About one of five patients with coronary artery disease (CAD) suffers from previously unknown, predominantly postprandial type 2 diabetes. In the process of atherogenesis and the subsequent increased cardiovascular mortality of diabetic patients, endothelial dysfunction is suspected to play an important role, and it is observed in diabetic as well as insulin-resistant states. Thus, the aim of our study was to investigate the effect of pioglitazone on endothelial dysfunction, insulin sensitivity, and glucose control in newly detected type 2 diabetic patients with CAD. RESEARCH DESIGN AND METHODS: We investigated 42 patients (39 men and 3 women, age 60.25 +/- 7.5 years, HbA1c 6.1 +/- 0.5%) with manifest CAD and newly detected type 2 diabetes. A randomized, double-blind, placebo-controlled, parallel study with pioglitazone (30 mg/day for 12 weeks) was performed. At study entry and end, we performed an oral glucose tolerance test and measurements of endothelial dysfunction by photoplethysmographic pulse wave analysis. RESULTS: Endothelial dysfunction was severely impaired at baseline in both groups. After 12 weeks, endothelial dysfunction was significantly better in the pioglitazone group (change of reflection index 6.5 +/- 5.1 vs. 1.6 +/- 2.9%, P = 0.002) compared with placebo. Insulin sensitivity, as assessed by homeostasis model assessment (2.20 +/- 1.62 vs. 3.61 +/- 1.87, P = 0.01), or the change of insulin sensitivity index from baseline to study end (0.021 +/- 0.023 vs. -0.003 +/- 0.012 micromol x kg(-1) x min(-1) per pmol/l, P = 0.0001) and beta-cell function (57.42 +/- 49.86 vs. 21.78 +/- 18.54 mU/l per mmol/l, P = 0.0014) significantly improved in the pioglitazone group, with no change observed after placebo. CONCLUSIONS: Pioglitazone improves endothelial dysfunction independently from the observed benefits on insulin sensitivity and beta-cell function in patients with newly diagnosed type 2 diabetes and CAD.

Aged↗
PubMed2005

The role of virgin olive oil components in the modulation of endothelial function.

The endothelium is involved in many of the processes related to the development of atherosclerosis, which is considered an inflammatory disease. Actually, traditional risk factors for atherosclerosis predispose to endothelial dysfunction, which is manifested as an increase in the expression of specific cytokines and adhesion molecules. There are firm evidence supporting the beneficial effects of olive oil, the most genuine component of the Mediterranean diet. Although the effects of olive oil and other oleic acid-rich dietary oils on atherosclerosis and plasma lipids are well known, the roles of minor components have been less investigated. Minor components constitute only 1-2% of virgin olive oil (VOO) and are composed of hydrocarbons, polyphenols, tocopherols, sterols, triterpenoids and other components usually found in traces. Despite their low concentration, non-fatty acid constituents may be of importance because studies comparing monounsaturated dietary oils have reported different effects on cardiovascular disease. Most of these compounds have demonstrated antioxidant, anti-inflammatory and hypolipidemic properties. In this review, we summarize current knowledge on the effects of these compounds contained in VOO on vascular dysfunction and the mechanisms by which they modulate endothelial activity. Such mechanisms involve the release of nitric oxide, eicosanoids (prostaglandins and leukotrienes) and adhesion molecules, in most cases by activation of nuclear factor kappaB by reactive oxygen species.

Animals↗
PubMed2000

Omega-3 fatty acids alter soluble markers of endothelial function in coronary heart disease patients.

Several studies have indicated that omega-3 poly-unsaturated fatty acids in fish oil have protective effects on cardiovascular disease by reducing vascular endothelial inflammation in atherosclerosis. In a recent study, supplementation of patients with fish oil following coronary angioplasty elevated levels of lipid peroxides and two adhesion molecules in plasma suggesting a proinflammatory action of fish oil. However, decreases in several plasma markers of endothelial hemostatic activity indicated a healthier and better vasculature associated with fish oil supplementation.

Arteriosclerosis↗