Home About us Contact | |||
Endothelial Function (endothelial + function)
Kinds of Endothelial Function Selected AbstractsDO PLASMA NON-ESTERIFIED FATTY ACIDS AND INSULIN RESISTANCE CONTRIBUTE TO IMPAIRED ENDOTHELIAL FUNCTION IN NEPHROTIC SYNDROME?NEPHROLOGY, Issue 1 2002G. Dogra [source] ENDOTHELIAL FUNCTION OF CONDUIT AND RESISTANCE ARTERIES IN NEPHROTIC RANGE PROTEINURIANEPHROLOGY, Issue 3 2000G. Dogra OBJECTIVE: To test the hypothesis that endothelial dysfunction occurs in nephrotic range proteinuria primarily as a consequence of dyslipidaemia. METHODS: Brachial artery and forearm microcirculatory endothelial function was compared among patients with nephrotic range proteinuria (NRP, n = 14 ), primary hyperlipidaemia (HL, n = 15) and normal controls (NC, n = 16). Endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) of the brachial artery using high resolution ultrasonography. Endothelium-independent, glyceryl trinitrate (GTN) mediated brachial artery vasodilatation was also measured. Basal and post-ischaemic blood flow of the forearm microcirculation was measured using venous-occlusion strain gauge plethysmography. RESULTS: Serum creatinine was similar among groups. The proteinuric group had a mean albumin of 27.6g/L(1.8) and 24-hour urinary protein excretion of 6.3g(1.3). Plasma lipids and lipoproteins were not statistically different between the NRP and HL groups. Brachial artery FMD was significantly lower in the NRP and HL groups compared with the controls (NRP 4.7%(1.3)*, HL 4.9%(0.7)* and NC 8.3%(0.6), *p = 0.012 vs. NC); GTN mediated dilatation and basal and post-ischaemic forearm blood flow were not statistically different among the three groups. CONCLUSION: Patients with nephrotic range proteinuria have endothelial dysfunction of conduit arteries in the peripheral circulation, similar to that observed in patients with primary hyperlipidaemia. This suggests dyslipoproteinaemia is the principal cause of endothelial dysfunction of conduit arteries in nephrotic range proteinuria. Confirmation of this should be sought with an intervention trial of lipid-regulating therapy. [source] LIPID-LOWERING IMPROVES ENDOTHELIAL FUNCTION IN NEPHROTIC RANGE PROTEINURIANEPHROLOGY, Issue 3 2000G. Dogra OBJECTIVE: To determine whether lipid-modifying therapy with atorvastatin improves impaired endothelial function in patients with nephrotic range proteinuria (NRP). METHODS: A sequential, open-label study of the effects of atorvastatin on dyslipidaemia and endothelial dysfunction in 9 patients with NRP. Endothelial function was assessed at baseline, after 12 weeks of atorvastatin treatment and after an 8 week wash-out period. Brachial artery endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) using ultrasonography. Endothelium- independent, glyceryl trinitrate (GTN) mediated vasodilatation was also measured. RESULTS: At baseline, median serum albumin was 31g/L (range 20-40) and 24 hour protein excretion was 4.7g (1.0-16.23). There was no significant change in serum creatinine and 24 hour protein excretion during the study. Total cholesterol (TC) and triglycerides (TG) were significantly lower following treatment with atorvastatin 20mg (20-40): TC 8.1mmol/L (5.9-14.9) vs. 5.2 (4.0-8.6), TG 2.9mmol/L (1.3-15.0) vs. 1.6 (1.0-3.5), both p < 0.05. Brachial artery FMD improved significantly following atorvastatin treatment: 2.1% (-1.2- 5.2%) to 4.7% (0.8-16.3%), p < 0.05. At the end of the 8 week wash-out, FMD had significantly deteriorated to 3.2% (-2.8-8.2), p < 0.05 vs. week 12 FMD, and was similar to pre-treatment values. GTN mediated dilatation was unchanged through the study. CONCLUSION: Atorvastatin significantly reduced the hyperlipidaemia of NRP. This was associated with improved conduit artery endothelial function after 12 weeks of treatment. This is consistent with the hypothesis that dyslipoproteinaemia is the primary cause of endothelial dysfunction in NRP. [source] PRETREATMENT WITH INTRAVENOUS ASCORBIC ACID PRESERVES ENDOTHELIAL FUNCTION DURING ACUTE HYPERGLYCAEMIA (R1)CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2005Brian A Mullan SUMMARY 1.,Acute hyperglycaemia may impair endothelial function. Ascorbic acid (AA), administered intra-arterially, has been reported to improve endothelium-dependent vasodilatation during a forearm hyperglycaemic clamp. Using a randomized, double-blind, placebo-controlled, cross-over study, we investigated the potential for intravenous ascorbic acid to modify the endothelial response to acute systemic hyperglycaemia in humans. 2.,Nine healthy male volunteers were recruited from the hospital staff. Endothelial function was determined by measuring the forearm blood flow responses to intrabrachial infusions of endothelium-dependent (ED) and endothelium-independent (EID) vasodilators. The endothelial function index (EFI) was derived from the ratio of ED and EID vasodilatation. Haemodynamic and endothelial function measurements were performed at baseline and then repeated 2 h after a systemic hyperglycaemic clamp (14 mmol/L). The subjects, studied on two separate occasions, were randomized to placebo or 2 g intravenous ascorbic acid prior to the initiation of hyperglycaemia. 3.,After systemic hyperglycaemia with placebo pretreatment, the EFI fell from 1.08 ± 0.21 to 0.74 ± 0.13 (difference (95% confidence interval): 0.34 (0.20, 0.47); P < 0.001). When subjects were pretreated with ascorbic acid, the EFI was not affected by hyperglycaemia (1.11 ± 0.21 to 1.12 ± 0.17; P = 0.938). This difference between placebo and ascorbic acid was significant (P < 0.001). Plasma ascorbate concentrations decreased during hyperglycaemia and correlated directly with the reduction in the EFI (r = 0.798; P < 0.001). 4.,Pretreatment with an intravenous bolus of ascorbic acid can prevent endothelial dysfunction during acute systemic hyperglycaemia. Therefore, ascorbic acid may have potential therapeutic use in clinical situations where acute hyperglycaemia may be a complication. [source] Acute and Chronic Oral Magnesium Supplementation: Effects on Endothelial Function, Exercise Capacity, and Quality of Life in Patients With Symptomatic Heart FailureCONGESTIVE HEART FAILURE, Issue 1 2006Johanna C. Fuentes MD Endothelial dysfunction is an important pathophysiologic mechanism in the progression of heart failure. The objective of the present study was to determine the effects of acute and chronic oral magnesium supplementation on endothelial function in patients with symptomatic heart failure. Twenty-two symptomatic chronic heart failure patients were randomized to receive 800 mg oral magnesium oxide daily or placebo for 3 months. Data collected included large and small arterial elasticity/compliance, hemodynamic parameters, exercise capacity, and quality-of-life score at baseline, 1 week, and 3 months. Patients who received magnesium had improved small arterial compliance at 3 months from baseline compared with placebo. This study suggests that chronic supplementation with oral magnesium is well tolerated and could improve endothelial function in symptomatic heart failure patients. [source] "Supranormal" Cardiac Function in Athletes Related to Better Arterial and Endothelial FunctionECHOCARDIOGRAPHY, Issue 6 2010Maria Florescu M.D. Objective: Athlete's heart is associated with left ventricular (LV) hypertrophy (LVH), and "supranormal" cardiac function, suggesting that this is a physiological process. Hypertrophy alone cannot explain increase in cardiac function, therefore, other mechanisms, such as better ventriculo-arterial coupling might be involved. Methods: We studied 60 male (21 ± 3 years) subjects: 27 endurance athletes, and a control group of 33 age-matched sedentary subjects. We assessed global systolic and diastolic LV function, short- and long-axis myocardial velocities, arterial structure and function and ventriculo-arterial coupling, endothelial function by flow-mediated dilatation, and amino-terminal pro-brain natriuretic peptide (NT-proBNP) and biological markers of myocardial fibrosis and of oxidative stress. Results: Athletes had "supranormal" LV longitudinal function (12.4 ± 1.0 vs 10.1 ± 1.4 cm/s for longitudinal systolic velocity, and 17.4 ± 2.6 vs 15.1 ± 2.4 cm/s for longitudinal early diastolic velocity, both P < 0.01), whereas ejection fraction and short-axis function were similar to controls. Meanwhile, they had better endothelial function (16.7 ± 7.0 vs 13.3 ± 5.3%, P < 0.05) and lower arterial stiffness (pulse wave velocity 7.1 ± 0.6 vs 8.8 ± 1.1 m/s, P = 0.0001), related to lower oxidative stress (0.259 ± 0.71 vs 0.428 ± 0.88 nmol/mL, P = 0.0001), with improved ventriculo-arterial coupling (37.1 ± 21.5 vs 15.5 ± 13.4 mmHg.m/s3× 103, P = 0.0001). NT-proBNP and markers of myocardial fibrosis were not different from controls. LV longitudinal function was directly related to ventriculo-arterial coupling, and inversely related to arterial stiffness and to oxidative stress. Conclusions: "Supranormal" cardiac function in athletes is due to better endothelial and arterial function, related to lower oxidative stress, with optimized ventriculo-arterial coupling; athlete's heart is purely a physiological phenomenon, associated with "supranormal" cardiac function, and there are no markers of myocardial fibrosis. (Echocardiography 2010;27:659-667) [source] Association between Endothelial Function and Chronotropic Incompetence in Subjects with Chronic Heart Failure Receiving Optimal Medical TherapyECHOCARDIOGRAPHY, Issue 3 2010M.D., Timothy J. Vittorio M.S. Objective: Impairment of flow-mediated, endothelium-dependent vasodilatation (FMD) of the brachial artery identifies peripheral endothelial dysfunction in subjects with chronic congestive heart failure (CHF) and is associated with increased morbidity and mortality. To further elucidate the interaction of peripheral and central mechanisms in the syndrome of CHF, we examined the association between endothelial function and chronotropic incompetence, an emerging prognostic marker in CHF. Methods: Thirty subjects with stable New York Heart Association (NYHA) functional class II,III CHF were studied. A vascular ultrasound study was performed to measure brachial artery FMD. The percentage of age-adjusted maximal predicted heart rate (MPHR) reached during cardiopulmonary exercise tolerance testing (CPETT) was used to assess the degree of chronotropic competence. All patients received ACE inhibitors and ,-adrenoceptor blockers. Results: Brachial artery FMD averaged 1.3 ± 2.4% and age-adjusted % MPHR 74.1 ± 11.7%. FMD correlated with % MPHR among all patients (r = 0.60, P = 0.01). FMD and resting heart rate (RHR) did not significantly correlate (r = 0.13, P = 0.55). Conclusions: FMD, a measure of peripheral endothelial dysfunction, and % MPHR, a central determinant of cardiac output, are moderately correlated in heart failure patients receiving optimal medical therapy. Whether a cause-effect relationship underlies this association remains to be investigated. (Echocardiography 2010;27:294-299) [source] Evaluation of Peripheral Vascular Endothelial Function with a Portable Ultrasound DeviceECHOCARDIOGRAPHY, Issue 8 2006Alawi A. Alsheikh-Ali M.D. Endothelial function can be assessed noninvasively by imaging the brachial artery with ultrasound before and during reactive hyperemia. However, the standard ultrasound equipment typically used for this purpose is limited by size and expense of the machinery. In this study, we compared the ability of a portable ultrasound device to standard ultrasound equipment to visualize the brachial artery for purposes of assessing peripheral vascular endothelial function. The portable device provided comparable imaging of the brachial artery at rest and during hyperemia to that of standard ultrasound technology. These findings support the feasibility of noninvasive evaluation of peripheral endothelial function in the ambulatory setting. [source] Endothelial Function in Patients With Migraine During the Interictal PeriodHEADACHE, Issue 1 2007Federico A. Silva MD Objectives.,The aim of this study is to evaluate endothelial function in migraineur subjects during the asymptomatic period. Background.,Migraine has been proposed as a risk factor for cerebrovascular events. The underlying mechanisms that relate these 2 pathologies are unknown. Nitric oxide (NO) has been proposed as the final causative molecule of migraine. Increased NO metabolites concentrations have been reported in migraineur subjects during acute migraine attacks, but there is no evidence indicating alterations in endothelial NO release during the symptom free period in theses subjects. Design and Methods.,Fifty migraineur subjects and 25 healthy subjects matched by gender and age were included. Every subject underwent a complete examination that included medical history, physical examination, resting electrocardiogram, forearm flow-mediated vasodilation (FMD), blood determinations of fasting nitrates and nitrites (NO2,+ NO3,), glucose, lipid profile, creatinine, C-reactive protein, and blood cell count. Results.,No differences in FMD or NO2,+ NO3, were detected among groups. The only difference between migraineurs and control subjects was a higher mean blood pressure 92.1 (8.8) mmHg versus 86.7 (8.2) mmHg P= .01. Conclusion.,The endothelial function is not altered during the interictal period in migraineur subjects. [source] Effect of Postconditioning on Coronary Blood Flow Velocity and Endothelial Function and LV Recovery After Myocardial InfarctionJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 5 2006XIAOJING MA Objective: Postconditioning is a novel approach to myocardial protection during ischemia reperfusion. Our study observed the effect of postconditioning on coronary blood flow velocity and endothelial function in patients who underwent emergency percutaneous coronary intervention (PCI). Methods: Ninety-four patients with their first acute myocardial infarction who underwent revascularization within 12 hours of onset by primary PCI were recruited in the study. All the patients were randomized to two groups, IR group (PCI without postconditioning) and Postcond group (PCI with postconditioning). Corrected TIMI frame count (CTFC) was used to evaluate velocity of coronary blood after PCI. Creatine phosphokinase (CK), CK-MB, and malondialdehyde (MDA) were measured before and after PCI. Arterial endothelial function was studied noninvasively by examination of brachial artery responses to endothelium-dependent and endothelium-independent stimuli by echo Doppler technique. Wall motion score index (WMSI) was assessed by two-dimensional echocardiography before and 8 weeks after angioplasty. Results: There were no significant differences between the two groups with regard to age, sex, presence of angiographically visible collaterals, and elapsed time from the onset of symptoms until perfusion. Patients with postconditioning had much faster CTFC than patients without postconditioning (25.38 ± 5.35 vs 29.23 ± 5.54). After 8 weeks, the WMSI improved significantly in both groups, but the ,WMSI in Postcond group was significantly larger than that of IR group (1.20 ± 0.30 vs 1.04 ± 0.36, P < 0.05). There was a significant negative correlation between ,WMSI and CTFC in IR group and Postcond group (r =,0.9032, P < 0.01; r =,0.7884, P < 0.01). The peaks of CK and CK-MB of Postcond group were much lower than that of IR group (1236.57 ± 813.21 U/L vs 1697.36 ± 965.74 U/L; 116.92 ± 75.83 U/L vs 172.41 ± 92.64 U/L), and MDA-reactive products were significantly lower than that in the IR group at any same time after PCI. All patients with acute myocardial infarction had a depressed endothelium-dependent vasodilation function, while the endothelium-dependent vasodilation function was improved in Postcond group. Conclusion: Postconditioning is a simple, operative procedure for salvaging the coronary endothelial function and cardiomyocyte. It could be used widely in clinic and to better the prognosis of acute myocardial infarction. [source] Influence of Glucose Control and Improvement of Insulin Resistance on Microvascular Blood Flow and Endothelial Function in Patients with Diabetes Mellitus Type 2MICROCIRCULATION, Issue 7 2005THOMAS FORST ABSTRACT Objective: The study was performed to investigate the effect of improving metabolic control with pioglitazone in comparison to glimepiride on microvascular function in patients with diabetes mellitus type 2. Methods: A total of 179 patients were recruited and randomly assigned to one treatment group. Metabolic control (HbA1c), insulin resistance (HOMA index), and microvascular function (laser Doppler fluxmetry) were observed at baseline and after 3 and 6 months. Results: HbA1c improved in both treatment arms (pioglitazone: 7.52 ± 0.85% to 6.71 ± 0.89%, p < .0001; glimepiride: 7.44 ± 0.89% to 6.83 ± 0.85%, p < .0001). Insulin-resistance decreased significantly in the pioglitazone group (6.15 ± 4.05 to 3.85 ± 1.92, p < .0001) and remained unchanged in the glimepiride group. The microvascular response to heat significantly improved in both treatment groups (pioglitazone 48.5 [15.2; 91.8] to 88.8 [57.6; 124.1] arbitrary units [AU], p < .0001; glimepiride 53.7 [14.1; 91.9] to 87.9 [52.9, 131.0] AU, p < .0001, median [lower and upper quartile]). Endothelial function as measured with the acetylcholine response improved in the pioglitazone group (38.5 [22.2; 68.0] to 60.2 [36.9; 82.8], p = .0427) and remained unchanged in the glimepiride group. Conclusions: Improving metabolic control has beneficial effects in microvascular function in type 2 diabetic patients. Treatment of type 2 diabetic patients with pioglitazone exerts additional effects on endothelial function beyond metabolic control. [source] Testing Endothelial Function of Brachial and Cavernous Arteries in Patients with Erectile DysfunctionTHE JOURNAL OF SEXUAL MEDICINE, Issue 2 2006Evsey Mazo MD ABSTRACT Introduction., There is considerable clinical and scientific evidence that endothelial dysfunction may be an important clinical link connecting erectile dysfunction (ED) with cardiovascular diseases. Aims., To modify the method of assessment of endothelial function of cavernosal arteries, to develop a new algorithm for evaluating its results, and to investigate the relationship between postocclusive changes in the diameter of brachial and cavernous arteries. Methods., The study participants were 212 patients presenting to our department complaining of ED and 40 healthy volunteers without sexual problems, which formed the control group. All patients with ED underwent complex evaluation and ultrasound assessment of postocclusive changes in the diameter of cavernosal arteries modified by us and standard ultrasound assessment of endothelium-dependent flow-mediated dilation of the brachial artery. Main Outcome Measures., As the main outcome measure, the percent of increase of the cavernosal arteries diameter (PICAD) was recorded. Results., In the patients with arteriogenic ED, PICAD values were significantly less than in other groups (P < 0.001 for pairs of comparison). At the same time there were no differences between the control group and groups of patients with psychogenic and organic nonarterial ED. The sensitivity and specificity of a PICAD value of 50% in diagnosis of arteriogenic ED were 100% and 98.2%, respectively. In all groups and in the entire sample of patients studied we did not find a correlation between PICAD and postocclusive changes in the diameter of brachial arteries. Conclusion., The method of ultrasound assessment of postocclusive changes in the diameter of cavernosal arteries is, reliable and, a, highly informative tool for diagnosis of arteriogenic ED. It cannot be substituted by techni-cally simpler method of ultrasound examination of brachial arteries, while results of the latter could help to define the necessity of performing an examination of cavernous arteries. Mazo E, Gamidov S, Anranovich S, and Iremashvili V. Testing endothelial function of brachial and cavernous arteries in patients with erectile dysfunction. J Sex Med 2006;3:323,330. [source] State of the Art IV: ED as a Marker of Endothelial Dysfunction: L3: Is Lifestyle Modification an Efficacious Treatment Strategy for Endothelial Function and ED?THE JOURNAL OF SEXUAL MEDICINE, Issue 2004Robert Ross PhD [source] Nutraceuticals in Cardiovascular Prevention: Lessons from Studies on Endothelial FunctionCARDIOVASCULAR THERAPEUTICS, Issue 4 2010Cinzia Zuchi An "unhealthy" diet is considered as a main cause of increased atherosclerotic cardiovascular disease in the industrialized countries. There is a substantial interest in the potential cardiovascular protective effects of "nutraceuticals," that is food-derived substances that exert beneficial health effects. The correct understanding of cardiovascular effects of these compounds will have important implications for cardiovascular prevention strategies. Endothelial dysfunction is thought to play an important role in development and progression of atherosclerosis, and the characterization of the endothelial effects of several nutraceuticals may provide important insights into their potential role in cardiovascular prevention. At the same time, the analysis of the endothelial effects of nutraceuticals may also provide valuable insights into mechanisms of why certain nutraceuticals may not be effective in cardiovascular prevention, and it may aid in the identification of food-derived substances that may have detrimental cardiovascular effects. These findings further support the notion that nutraceuticals do need support from large clinical outcome trials with respect to their efficacy and safety profile for cardiovascular prevention, before their widespread use can be recommended. In fact, the term nutraceutical was coined to encourage an extensive and profound research activity in this field, and numerous large-scale clinical outcome trials to examine the effects of nutraceuticals on cardiovascular events have now been performed or are still ongoing. Whereas it is possible that single nutraceuticals may be effective in cardiovascular prevention, this field of research provides also valuable insights into which food components may be particularly important for cardiovascular prevention, to further advice the composition of a particularly healthy diet. The present review summarizes recent studies on the endothelial effects of several nutraceuticals, that have been intensely studied. [source] Alcohol And Endothelial Function: A Brief ReviewCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2001IB Puddey SUMMARY 1. In spite of the dose-related effects of alcohol consumption to increase blood pressure, regular light to moderate alcohol intake appears to confer protection against both coronary artery disease and ischaemic stroke. In contrast, heavy alcohol consumption increases the risk of coronary artery disease and the risk of both haemorrhagic and ischaemic stroke. 2. Effects of alcohol consumption on endothelial cell function may be relevant to these disparate effects on cardiovascular outcomes. In in vitro animal studies, low doses of alcohol have been demonstrated to increase release of nitric oxide and augment endothelium-mediated vasodilatation, whereas higher doses impair endothelium-dependent relaxation responses. In contrast, chronic administration of alcohol to rats has generally been associated with tolerance to the acute inhibitory effects of alcohol on endothelium-mediated vasodilatation and may even result in augmentation of such responses. 3. The few human studies to date that have examined the effects of alcohol on endothelial function have focused on postischaemic flow-mediated dilation of the brachial artery (FMD). Although blunted FMD responses have been reported in alcoholic subjects, acute administration of alcohol or short-term interventions to reduce alcohol intake have had no effect to either improve or impair FMD. 4. Further studies in humans assessing acute and longer term dose-related effects of alcohol on endothelial function in both conduit and resistance vessels will be necessary if the relevance of the findings from in vitro and in vivo animal studies are to be understood in the context of the complex interrelationships of alcohol with cardiovascular disease. [source] Effect Of Anti-Oxidant Treatment And Cholesterol Lowering On Resting Arterial Tone, Metabolic Vasodilation And Endothelial Function In The Human Forearm: A Randomized, Placebo-Controlled StudyCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2001Stephen J Duffy SUMMARY 1. The aim of the present study was to determine whether anti-oxidant therapy with vitamin E and/or cholesterol-lowering therapy with simvastatin would augment resting forearm blood flow (FBF) and metabolic vasodilation in response to exercise and improve endothelial function in young patients with hypercholesterolaemia. 2. Endothelium-dependent and -independent, nitric oxide (NO)-mediated vasodilation have been shown to be impaired in young, otherwise healthy subjects with hypercholesterolaemia. Recent experimental and clinical studies suggest that vascular function may be improved with anti-oxidant or cholesterol- lowering therapy, although these treatments may be synergistic. 3. We compared FBF at rest, in response to isotonic exercise, the endothelium-dependent vasodilator acetylcholine (ACh), the endothelium-independent vasodilator sodium nitroprusside (SNP) and the NO synthase inhibitor NG -monomethyl- L -arginine (L -NMMA) in 26 young, otherwise healthy volunteers (mean (±SD) age 29±7 years; 14 female, 12 male) with hypercholesterolaemia, before and after 6 months treatment with vitamin E, simvastatin and/or placebo. Treatment was randomized, double-blinded in a 2 × 2 factorial design. Forearm blood flow was measured using venous occlusion plethysmography. 4. Vitamin E therapy increased plasma ,-tocopherol from 39.5±9.6 to 75.7±33.8 ,mol/L (P < 0.001). Simvastatin reduced total cholesterol from 6.9±1.7 to 4.9±0.8 mmol/L and low- density lipoprotein (LDL) from 4.8±1.7 to 3.0±0.7 mmol/L (both P < 0.001), although total and LDL,cholesterol also decreased slightly in the placebo group. Vitamin E increased resting FBF from 2.1±0.3 to 2.4±0.3 mL/100 mL per min (P = 0.04) and decreased resting forearm vascular resistance from 42.1±4.2 to 36.1±3.4 units (P = 0.01), but the reduction in resting FBF with L -NMMA was not affected. Vasodilation in response to isotonic exercise, ACh and SNP was similar before and after treatment in the placebo, vitamin E, simvastatin and in the combined vitamin E,simvastatin groups. NG -Monomethyl- L -arginine infusion reduced resting FBF and functional hyperaemia in response to exercise and these responses were not altered by treatment. 5. These data suggest that while vitamin E therapy augments resting FBF and reduces forearm vascular resistance in young hypercholesterolaemic subjects, these effects may not be via NO-dependent pathways. Metabolic vasodilation and responses to the NO-mediated vasodilators ACh and SNP were not favourably affected by anti-oxidant or cholesterol-lowering therapy, either alone or in combination. [source] Effect of Tai Chi on Endothelial FunctionCLINICAL CARDIOLOGY, Issue 3 2007Tsung O. Cheng M.D Professor of Medicine No abstract is available for this article. [source] Evaluation of Peripheral Vascular Endothelial Function with a Portable Ultrasound DeviceECHOCARDIOGRAPHY, Issue 8 2006Alawi A. Alsheikh-Ali M.D. Endothelial function can be assessed noninvasively by imaging the brachial artery with ultrasound before and during reactive hyperemia. However, the standard ultrasound equipment typically used for this purpose is limited by size and expense of the machinery. In this study, we compared the ability of a portable ultrasound device to standard ultrasound equipment to visualize the brachial artery for purposes of assessing peripheral vascular endothelial function. The portable device provided comparable imaging of the brachial artery at rest and during hyperemia to that of standard ultrasound technology. These findings support the feasibility of noninvasive evaluation of peripheral endothelial function in the ambulatory setting. [source] A diet enriched with mackerel (Scomber scombrus),derived products improves the endothelial function in a senior population (Prevención de las Enfermedades Cardiovasculares: Estudio Santoña , PECES project)EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2009J. R. De Berrazueta ABSTRACT Background, Regular consumption of fish reduces cardiovascular risks. Here, we investigate if the consumption of products with mackerel (Scomber scombrus) with 8·82 g of eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) content per 100 g of product improves parameters of endothelial function in a controlled population. Materials and methods, Subjects maintained a 12-week diet with products with mackerel. The population consisted of 58 senior subjects (12 withdrawals, 25 women), aged 82·08 ± 8·13 years (Group A). Twenty-three senior subjects (13 women) on a regular diet were used as the control group (Group B). Subjects of Group A received 57 portions throughout 12 weeks (four to five portions a week of products with a mean EPA + DHA content of 2·5 g a day). A continuous follow-up and a final evaluation were performed to determine the level of consumption. Plasma samples were stored at ,70 °C for a biochemical study. Endothelial function was analysed by reactive hyperemia with a mercury strain gauge plethysmography with measurement of blood flow in the forearm, both baseline and at the end of the 12-week diet. Results, Endothelium-dependent vasodilatation significantly increased in Group A subjects (P < 0·001). No changes were found in Group B. The subgroup analyses showed that improvements were produced in Group A subjects without cardiovascular disease (P < 0·001). Nitrites/nitrates and von Willebrand factor plasma concentrations were higher in participants after the 12-week diet. Conclusions, The consumption of mackerel meat products improves endothelium-dependent, flow-mediated vasodilatation in a senior population. This finding might explain some of the cardioprotective effects of fish consumption. [source] CD31+/Annexin V+ microparticles in healthy offsprings of patients with coronary artery diseaseEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2009D. Bulut ABSTRACT Background, First-degree relatives of patients with premature coronary artery disease (CAD) develop endothelial dysfunction even in the case they are apparently healthy. In this study we wanted to clarify whether reduced blood levels of circulating endothelial progenitor cells (EPCs), an endogenous repair mechanism to replace dysfunctional endothelium, or elevated endothelial-derived microparticles (EMPs), an indicator and a mediator of increased endothelial cell damage/apoptosis, are an initial step in the pathogenesis of endothelial dysfunction in genetically predisposed subjects. Materials and methods, Fifty-six healthy young men (aged 23 to 31 years) from a fire brigade were enrolled, of which 20 subjects had a positive family history (FH) for premature CAD. Subjects with or without a positive FH did not differ with respect to age, body mass index, risk factors and C-reactive protein. Endothelial function was assessed by hyperaemia-mediated relaxation of the brachial artery, blood levels of EPCs (VEGFR2+CD34+ cells) and number of EMPs (CD31+(bright)/Annexin V+ particles) were analysed by flow cytometry. Results, Hyperaemia-mediated relaxation of the brachial artery was similar in both groups, and the blood levels of EPCs were comparable. However, the number of EMPs were significantly increased in subjects with a positive FH compared to those with a negative FH (neg. FH: 55·31 ± 4·88 vs. pos. FH: 70·37 ± 6·32 particles µL,1 platelet poor plasma; P < 0·05). Number of EMPs correlate inversely with the FMD response. Conclusions, These results suggest that increased plasma levels of EMPs may be an initial step in the development of endothelial dysfunction in genetically predisposed subjects. [source] International conference on the healthy effect of virgin olive oilEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2005Summary 1Ageing represents a great concern in developed countries because the number of people involved and the pathologies related with it, like atherosclerosis, morbus Parkinson, Alzheime's disease, vascular dementia, cognitive decline, diabetes and cancer. 2Epidemiological studies suggest that a Mediterranean diet (which is rich in virgin olive oil) decreases the risk of cardiovascular disease. 3The Mediterranean diet, rich in virgin olive oil, improves the major risk factors for cardiovascular disease, such as the lipoprotein profile, blood pressure, glucose metabolism and antithrombotic profile. Endothelial function, inflammation and oxidative stress are also positively modulated. Some of these effects are attributed to minor components of virgin olive oil. Therefore, the definition of the Mediterranean diet should include virgin olive oil. 4Different observational studies conducted in humans have shown that the intake of monounsaturated fat may be protective against age-related cognitive decline and Alzheimer's disease. 5Microconstituents from virgin olive oil are bioavailable in humans and have shown antioxidant properties and capacity to improve endothelial function. Furthermore they are also able to modify the haemostasis, showing antithrombotic properties. 6In countries where the populations fulfilled a typical Mediterranean diet, such as Spain, Greece and Italy, where virgin olive oil is the principal source of fat, cancer incidence rates are lower than in northern European countries. 7The protective effect of virgin olive oil can be most important in the first decades of life, which suggests that the dietetic benefit of virgin olive oil intake should be initiated before puberty, and maintained through life. 8The more recent studies consistently support that the Mediterranean diet, based in virgin olive oil, is compatible with a healthier ageing and increased longevity. However, despite the significant advances of the recent years, the final proof about the specific mechanisms and contributing role of the different components of virgin olive oil to its beneficial effects requires further investigations. [source] Endothelial function and dysfunctionINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 5 2004Graham Jackson [source] High dietary methionine plus cholesterol stimulates early atherosclerosis and late fibrous cap development which is associated with a decrease in GRP78 positive plaque cellsINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 3 2009Anthony Zulli Summary The role of homocysteine, or its precursor methionine, in the formation of fibrous caps and its association with endoplasmic reticulum (ER) stress is unclear. Homocysteine can stimulate collagen accumulation and upregulate the ER stress chaperone glucose regulated protein 78 (GRP78). The aim of this study was to determine if high dietary methionine would increase fibrous caps, and that removal of an atherogenic diet would decrease the amount of ER stressed cells. New Zealand white rabbits were fed for 2, 4, or 12 weeks an atherogenic diet [1% methionine + 0.5% cholesterol (2MC, 4MC or 12MC)]; for 4 or 12 weeks a 0.5% cholesterol diet (4Ch, 12Ch); and to study plaque regression, an MC diet for 2 or 4 weeks accompanied by 10 weeks of a normal diet (2MCr, 4MCr). Endothelial function, atherosclerosis and GRP78 positive cells were studied. Endothelial function was abolished in 4MC and atherosclerosis increased 17-fold (P < 0.05) compared with 4Ch. Fibrous caps composed 48% of total plaque area in 12MC vs. 10% in 12Ch (P < 0.01), and 12MC expressed less GRP78 plaque cells vs. 12Ch (P < 0.01). Four MCr had less plaque GRP78 cells than 12MC (P < 0.05) and less endothelial GRP78 cells (P < 0.01). In addition, GRP78 positive cells were the highest in 4MC, but decreased in all other groups (P < 0.01). GRP78 positive cells within the fibrous cap inversely correlated with cap size (r2 = 0.9). These studies suggest that high dietary methionine could be beneficial for plaque stabilisation, and a normal diet also stabilises plaque and decreases the number of stressed plaque cells. [source] Raloxifene, conjugated oestrogen and endothelial function in postmenopausal womenJOURNAL OF INTERNAL MEDICINE, Issue 1 2003E. J. J. Duschek Abstract., Duschek EJJ, Stehouwer CDA, de Valk-de Roo GW, Schalkwijk CG, Lambert J, Netelenbos C (VU University Medical Center, Amsterdam; Sophia Hospital, Zwolle; The Netherlands). Raloxifene, conjugated oestrogen and endothelial function in postmenopausal women. J Intern Med 2003; 254: 85,94. Objectives., To study the long-term effects of raloxifene, a potential designer oestrogen, and oestrogen monotherapy on endothelial function in healthy postmenopausal women. Design., A 2-year double-blind, randomized and placebo-controlled study in an Academic Medical Center. Fifty-six hysterectomized but otherwise healthy postmenopausal women randomly received raloxifene hydrochloride 60 mg day,1 (n = 15) or 150 mg day,1 (n = 13), conjugated equine oestrogen (CEE) 0.625 mg day,1 (n = 15), or placebo (n = 13). Main outcome measures., Endothelial function as estimated from brachial artery flow-mediated, endothelium-dependent vasodilation and nitroglycerine-induced endothelium-independent vasodilation, and plasma levels of the endothelium-derived regulatory proteins, von Willebrand factor (vWF) and endothelin (ET). Results., Raloxifene 60 mg did not significantly affect endothelial function. As compared with placebo, at 6 months of therapy, raloxifene 150 mg and CEE were associated with a mean increase in vWF of 25.5% point (95% CI 3.6,47.3) and 26.6% point (95% CI 6.9,46.3), respectively. At 24 months of therapy, raloxifene 150 mg was associated with a mean decrease in ET of 0.96 pg mL,1 (95% CI ,1.57 to ,0.36). Raloxifene nor CEE significantly affected endothelium-dependent and/or -independent vasodilation. Conclusions., Our results suggest that long-term therapy with raloxifene or oral CEE does not affect endothelium-dependent vasodilation in healthy postmenopausal women. Raloxifene 150 mg day,1 might have both positive and negative effects on endothelium. The clinical significance of these findings remains to be investigated. [source] Influence of Glucose Control and Improvement of Insulin Resistance on Microvascular Blood Flow and Endothelial Function in Patients with Diabetes Mellitus Type 2MICROCIRCULATION, Issue 7 2005THOMAS FORST ABSTRACT Objective: The study was performed to investigate the effect of improving metabolic control with pioglitazone in comparison to glimepiride on microvascular function in patients with diabetes mellitus type 2. Methods: A total of 179 patients were recruited and randomly assigned to one treatment group. Metabolic control (HbA1c), insulin resistance (HOMA index), and microvascular function (laser Doppler fluxmetry) were observed at baseline and after 3 and 6 months. Results: HbA1c improved in both treatment arms (pioglitazone: 7.52 ± 0.85% to 6.71 ± 0.89%, p < .0001; glimepiride: 7.44 ± 0.89% to 6.83 ± 0.85%, p < .0001). Insulin-resistance decreased significantly in the pioglitazone group (6.15 ± 4.05 to 3.85 ± 1.92, p < .0001) and remained unchanged in the glimepiride group. The microvascular response to heat significantly improved in both treatment groups (pioglitazone 48.5 [15.2; 91.8] to 88.8 [57.6; 124.1] arbitrary units [AU], p < .0001; glimepiride 53.7 [14.1; 91.9] to 87.9 [52.9, 131.0] AU, p < .0001, median [lower and upper quartile]). Endothelial function as measured with the acetylcholine response improved in the pioglitazone group (38.5 [22.2; 68.0] to 60.2 [36.9; 82.8], p = .0427) and remained unchanged in the glimepiride group. Conclusions: Improving metabolic control has beneficial effects in microvascular function in type 2 diabetic patients. Treatment of type 2 diabetic patients with pioglitazone exerts additional effects on endothelial function beyond metabolic control. [source] ENDOTHELIAL FUNCTION OF CONDUIT AND RESISTANCE ARTERIES IN NEPHROTIC RANGE PROTEINURIANEPHROLOGY, Issue 3 2000G. Dogra OBJECTIVE: To test the hypothesis that endothelial dysfunction occurs in nephrotic range proteinuria primarily as a consequence of dyslipidaemia. METHODS: Brachial artery and forearm microcirculatory endothelial function was compared among patients with nephrotic range proteinuria (NRP, n = 14 ), primary hyperlipidaemia (HL, n = 15) and normal controls (NC, n = 16). Endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) of the brachial artery using high resolution ultrasonography. Endothelium-independent, glyceryl trinitrate (GTN) mediated brachial artery vasodilatation was also measured. Basal and post-ischaemic blood flow of the forearm microcirculation was measured using venous-occlusion strain gauge plethysmography. RESULTS: Serum creatinine was similar among groups. The proteinuric group had a mean albumin of 27.6g/L(1.8) and 24-hour urinary protein excretion of 6.3g(1.3). Plasma lipids and lipoproteins were not statistically different between the NRP and HL groups. Brachial artery FMD was significantly lower in the NRP and HL groups compared with the controls (NRP 4.7%(1.3)*, HL 4.9%(0.7)* and NC 8.3%(0.6), *p = 0.012 vs. NC); GTN mediated dilatation and basal and post-ischaemic forearm blood flow were not statistically different among the three groups. CONCLUSION: Patients with nephrotic range proteinuria have endothelial dysfunction of conduit arteries in the peripheral circulation, similar to that observed in patients with primary hyperlipidaemia. This suggests dyslipoproteinaemia is the principal cause of endothelial dysfunction of conduit arteries in nephrotic range proteinuria. Confirmation of this should be sought with an intervention trial of lipid-regulating therapy. [source] LIPID-LOWERING IMPROVES ENDOTHELIAL FUNCTION IN NEPHROTIC RANGE PROTEINURIANEPHROLOGY, Issue 3 2000G. Dogra OBJECTIVE: To determine whether lipid-modifying therapy with atorvastatin improves impaired endothelial function in patients with nephrotic range proteinuria (NRP). METHODS: A sequential, open-label study of the effects of atorvastatin on dyslipidaemia and endothelial dysfunction in 9 patients with NRP. Endothelial function was assessed at baseline, after 12 weeks of atorvastatin treatment and after an 8 week wash-out period. Brachial artery endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) using ultrasonography. Endothelium- independent, glyceryl trinitrate (GTN) mediated vasodilatation was also measured. RESULTS: At baseline, median serum albumin was 31g/L (range 20-40) and 24 hour protein excretion was 4.7g (1.0-16.23). There was no significant change in serum creatinine and 24 hour protein excretion during the study. Total cholesterol (TC) and triglycerides (TG) were significantly lower following treatment with atorvastatin 20mg (20-40): TC 8.1mmol/L (5.9-14.9) vs. 5.2 (4.0-8.6), TG 2.9mmol/L (1.3-15.0) vs. 1.6 (1.0-3.5), both p < 0.05. Brachial artery FMD improved significantly following atorvastatin treatment: 2.1% (-1.2- 5.2%) to 4.7% (0.8-16.3%), p < 0.05. At the end of the 8 week wash-out, FMD had significantly deteriorated to 3.2% (-2.8-8.2), p < 0.05 vs. week 12 FMD, and was similar to pre-treatment values. GTN mediated dilatation was unchanged through the study. CONCLUSION: Atorvastatin significantly reduced the hyperlipidaemia of NRP. This was associated with improved conduit artery endothelial function after 12 weeks of treatment. This is consistent with the hypothesis that dyslipoproteinaemia is the primary cause of endothelial dysfunction in NRP. [source] Involvement of the renin,angiotensin system in the development of vascular damage in a rat model of arthritis: Effect of angiotensin receptor blockersARTHRITIS & RHEUMATISM, Issue 5 2010Takeo Sakuta Objective To explore the involvement of the renin,angiotensin system (RAS) in the development of vascular damage in adjuvant-induced arthritis (AIA) in rats. Methods Angiotensin II (Ang II; 0.25 or 1.0 mg/kg/day) was infused in control rats and rats with AIA for 21 days, and the impact of systemic inflammation on Ang II,induced hypertension, endothelial dysfunction, and vascular hypertrophy was evaluated. Expression of angiotensin II type 1 receptor (AT1R) and angiotensin-converting enzyme (ACE) in the aortas of rats with AIA were examined by real-time polymerase chain reaction (PCR) and Western blot analyses. Losartan (3 mg/kg/day) or irbesartan (5 mg/kg/day), both of which are AT1R blockers, was administered orally to rats with AIA for 21 days. In situ superoxide production in aortas was assessed according to the fluorogenic oxidation of dihydroethidium to ethidium. The expression and activity of NAD(P)H oxidases in aortas were examined by real-time PCR analysis and lucigenin chemiluminescence assay. Endothelial function in rats with AIA treated in vivo or ex vivo with AT1R blockers was also determined. Results The Ang II,induced hypertensive response, endothelial dysfunction, and vascular hypertrophy were exacerbated in rats with AIA. Expression of AT1R and ACE was increased in the aortas of rats with AIA. Both losartan and irbesartan decreased the levels of superoxide and the expression and activity NAD(P)H oxidases in the aortas of rats with AIA. The endothelial dysfunction in AIA was improved by the in vivo or ex vivo treatment with AT1R blockers. Conclusion The locally activated RAS is involved in the increased vascular oxidative stress and endothelial dysfunction in AIA. Our findings have important implications for clinical approaches to the reduction of cardiovascular risk in patients with rheumatoid arthritis. [source] PRETREATMENT WITH INTRAVENOUS ASCORBIC ACID PRESERVES ENDOTHELIAL FUNCTION DURING ACUTE HYPERGLYCAEMIA (R1)CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2005Brian A Mullan SUMMARY 1.,Acute hyperglycaemia may impair endothelial function. Ascorbic acid (AA), administered intra-arterially, has been reported to improve endothelium-dependent vasodilatation during a forearm hyperglycaemic clamp. Using a randomized, double-blind, placebo-controlled, cross-over study, we investigated the potential for intravenous ascorbic acid to modify the endothelial response to acute systemic hyperglycaemia in humans. 2.,Nine healthy male volunteers were recruited from the hospital staff. Endothelial function was determined by measuring the forearm blood flow responses to intrabrachial infusions of endothelium-dependent (ED) and endothelium-independent (EID) vasodilators. The endothelial function index (EFI) was derived from the ratio of ED and EID vasodilatation. Haemodynamic and endothelial function measurements were performed at baseline and then repeated 2 h after a systemic hyperglycaemic clamp (14 mmol/L). The subjects, studied on two separate occasions, were randomized to placebo or 2 g intravenous ascorbic acid prior to the initiation of hyperglycaemia. 3.,After systemic hyperglycaemia with placebo pretreatment, the EFI fell from 1.08 ± 0.21 to 0.74 ± 0.13 (difference (95% confidence interval): 0.34 (0.20, 0.47); P < 0.001). When subjects were pretreated with ascorbic acid, the EFI was not affected by hyperglycaemia (1.11 ± 0.21 to 1.12 ± 0.17; P = 0.938). This difference between placebo and ascorbic acid was significant (P < 0.001). Plasma ascorbate concentrations decreased during hyperglycaemia and correlated directly with the reduction in the EFI (r = 0.798; P < 0.001). 4.,Pretreatment with an intravenous bolus of ascorbic acid can prevent endothelial dysfunction during acute systemic hyperglycaemia. Therefore, ascorbic acid may have potential therapeutic use in clinical situations where acute hyperglycaemia may be a complication. [source] Functional Capillary Rarefaction in Mild Blood Pressure ElevationCLINICAL AND TRANSLATIONAL SCIENCE, Issue 1 2008Cynthia Cheng Abstract Capillary rarefaction is described in patients with moderate-to-severe hypertension. The study objective was to determine if structural and/or functional capillary rarefaction is detectable and associated with endothelial dysfunction in patients with mild blood pressure elevation (HBP: Systolic blood pressure 130,160 mm Hg). Capillary density was quantified by direct capillaroscopy in 110 nondiabetic black and non-black subjects. Endothelial function was quantified by plethysmographic measures of flow-mediated vasodilation. Compared to normotensives (NBP: N = 90), functional capillary rarefaction was detected in HBP (N = 20; p < 0.001). Functional capillary density measures correlated with endothelial function (p < 0.001). Functional, but not structural, capillary rarefaction is detectable and associated with endothelial dysfunction in both black and non-black individuals with mild blood pressure elevation. [source] |