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Results for “Endothelial function”

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PubMed2002

The effect of the Interleukin-6-174G > C promoter gene polymorphism on endothelial function in healthy volunteers.

AIMS: Atherosclerosis is a chronic inflammatory condition, manifest in its early stages by endothelial dysfunction. Interleukin-6 (IL6) plays a key role in driving this process through stimulation of acute phase protein synthesis. We have examined the effect of the IL6 gene -174G > C promoter polymorphism on endothelial function in a group of healthy subjects. METHODS: 248 adults aged 20-28 years participated. Polymerase chain reaction was performed for the -174G > C polymorphism. Brachial artery diameter was measured at rest and after forearm cuff occlusion by high-resolution ultrasound. Responses were represented as absolute flow mediated dilatation (FMDA). RESULTS: Overall there was a trend towards greater FMDA for genotype CC, P = 0.14. No effect was seen in women; however, in men, following multivariate analysis, there was a significant association between genotype and FMDA, P = 0.04. In addition, a significant detrimental effect of smoking on FMDA was only seen in males of genotype CC (P < 0.05) when compared to nonsmokers of the same genotype. CONCLUSION: IL6-174G > C promoter polymorphism influences endothelial function in healthy male subjects. The detrimental effect of smoking on endothelial function is most clearly seen in men of genotype -174 CC, suggesting a genotype-specific interaction with smoking.

Adult↗

PubMed2003

Comparison of forearm endothelial function between premenopausal and postmenopausal women with or without hypercholesterolemia.

We sought to determine whether menopausal status or postmenopausal hypercholesterolemia affects forearm resistance artery endothelial function. We studied the forearm resistance artery endothelial function in 75 Japanese women: 25 premenopausal volunteers, 25 postmenopausal women with normal serum low-density lipoprotein (LDL) cholesterol concentrations, and 25 hypercholesterolemic postmenopausal women. Excluded from the study were patients with hypertriglyceridemia, hypertension, or diabetes, cigarette smokers. The forearm blood flow (FBF) during reactive hyperemia and after sublingual nitroglycerin (NTG) administration was measured by strain-gauge plethysmography. The serum concentrations of lipoprotein (a) [Lp(a)] were significantly higher in the hypercholesterolemic postmenopausal group than in the other two groups (P<0.01). These lipid parameters were similar between the premenopausal and postmenopausal women with normal cholesterol. The FBF responses to reactive hyperemia were significantly lower in the postmenopausal hypercholesterolemic women than in the other two groups (P<0.01). The reactive hyperemia also was impaired in the postmenopausal group with normal cholesterol as compared with the premenopausal group (P<0.01). Increases in FBF after NTG were similar between the three groups. By stepwise multivariate analysis, menopausal status and serum LDL cholesterol was the significant predictor of forearm endothelial function. These findings suggest that reactive hyperemia is impaired in forearm resistance arteries after menopause, especially in postmenopausal women with hypercholesterolemia.

Adult↗

PubMed2005

Endothelial function and weight loss in obese humans.

BACKGROUND: Obesity is a major risk factor for the development of endothelial dysfunction. We explored the effect of different degrees of body mass on endothelial function, lipids, systemic inflammation and glucose homeostasis and the effect of surgically-induced weight loss on endothelial function in severely obese humans. METHODS: A cross-sectional study of healthy subjects across a wide range of body fatness was performed to characterize the effect of obesity on flow-mediated dilatation (FMD), systemic inflammation, blood pressure and insulin sensitivity. A longitudinal study was performed to assess the effect of bariatric surgery induced weight loss on these parameters. 73 healthy subjects across a wide range of body mass were recruited; of these, 8 underwent bariatric surgery (median BMI 52.2 kg/m2, interquartile range 50.355.9). Endothelial dependent vasodilatation was measured using the brachial artery vasodilatory response to forearm hyperemia assessed using highresolution ultrasonography. RESULTS: Obese subjects were characterised by a complex collection of abnormalities, with hypertension, impaired glucose homeostasis, systemic inflammation and reduced FMD. BMI < or =25 kg/m2 (median FMD 9.7%, interquartile range 6.8-12.2), BMI >30 kg/m2 (median FMD 6.7% 4.8-7.5), P=0.01 comparing FMD in lean and obese subjects. A mean reduction in weight of 23.4 (4.6) kg produced an improvement in FMD from 5.3% (3.87.0) to 10.2% (7.6-13.3), P=0.01. CONCLUSIONS: Even moderate obesity leads to endothelial dysfunction. In severely obese subjects, FMD is normalized by weight loss. This improvement in FMD is associated with a decline in inflammatory markers, blood pressure and insulin. The improvement in FMD occurred despite patients remaining significantly obese. These results suggest that an integrated approach to improving endothelial function in obese humans may be necessary.

Adult↗

PubMed2002

Endothelial function. From vascular biology to clinical applications.

The endothelium, by releasing nitric oxide (NO), promotes vasodilation and inhibits inflammation, thrombosis, and vascular smooth muscle cell proliferation. These biological actions of NO make it an important component in the endogenous defense against atherosclerosis and its overt clinical complications. Loss of the functional integrity of the endothelium, as seen commonly in the milieu of cardiovascular risk factors, plays an integral role in all stages of atherosclerosis from lesion initiation to plaque rupture. A number of established techniques can assess endothelial function in human vascular beds. The outcome of endothelial testing has profound prognostic implications and is an independent predictor of atherosclerosis disease progression and cardiovascular event rates. The large clinical benefit of statins and angiotensin-converting enzyme inhibitors in patients with atherosclerosis involves favorable effects of endothelial function. Studies of endothelial function represent a prime example of a successful application of insights derived from vascular biology at the bedside.

Coronary Artery Disease↗

PubMed2004

Spironolactone impairs endothelial function and heart rate variability in patients with type 2 diabetes.

AIMS/HYPOTHESIS: Aldosterone blockade has followed in the footsteps of ACE inhibition in reducing mortality in patients with heart failure. This is associated with its beneficial effects on endothelial function and heart rate variability. Diabetes is another area, where angiotensin II withdrawal has proven to be of particular value. We postulated that aldosterone blockade with spironolactone might also have beneficial effects on the prognostic markers of endothelial function and heart rate variability in diabetic patients. METHODS: We assessed endothelial function by forearm venous occlusion plethysmography in 42 patients with type 2 diabetes mellitus after 1 month of treatment with spironolactone or placebo allocated in a randomised double-blind trial. Of the 42 patients, 20 were on ACE inhibitor therapy. We also assessed heart rate variability, HbA1c and plasma angiotensin II levels at the end of each treatment period. RESULTS: Compared to placebo, spironolactone decreased forearm blood flow response to acetylcholine by 44.56+/-14.56% (p=0.003) in the group as a whole and by 57.61+/-15.56% (p<0.001) in the 20 patients on ACE inhibition. Spironolactone also worsened heart rate variability parameters, with root mean squared standard deviation decreased by 1.99+/-0.93 ms (p=0.03), low-frequency normalised power increased by 2.00+/-0.91 normalised units (nu) (p=0.03), high-frequency normalised power decreased by 1.98+/-0.94 nu (p=0.04) and the low frequency : high frequency ratio increased by 0.40+/-0.19 (p=0.04). HbA1c and angiotensin II increased during treatment with spironolactone by 0.26+/-0.07% (p=0.001) and 8.12+/-1.94 pg/ml (p=0.001) respectively. CONCLUSIONS/INTERPRETATION: Spironolactone worsened endothelial function and heart rate variability in patients with type 2 diabetes. These findings are possibly due to the worsening of glycaemic control and increase in plasma angiotensin II that were seen with spironolactone treatment. Thus the prescription of spironolactone to diabetic patients without heart failure does not seem to be justified.

Adult↗

PubMed2001

Mediterranean and low-fat diets improve endothelial function in hypercholesterolemic men.

BACKGROUND: The regulatory function of the endothelium is altered in hypercholesterolemia, and the subsequent endothelial dysfunction plays a central role in the development of atherosclerosis. OBJECTIVE: To determine whether endothelial function in hypercholesterolemic patients is affected by replacing a saturated fat-enriched diet with a low-fat, low-saturated fat diet (the U.S. National Cholesterol Education Program stage 1 [NCEP-1] diet) or a diet rich in monounsaturated fat (such as that common in Mediterranean countries). DESIGN: Intervention dietary study with a baseline phase and two randomized crossover dietary periods. SETTING: Hospital Universitario Reina Sofía, Córdoba, Spain. PATIENTS: 22 hypercholesterolemic men. INTERVENTION: Patients followed a diet high in saturated fat, then were assigned in a crossover design to the NCEP-1 diet or a Mediterranean diet. Each dietary period lasted 28 days. MEASUREMENTS: Plasma P-selectin levels, lipid concentrations, and endothelial function. RESULTS: Compared with the saturated fat diet, flow-mediated dilatation increased during the Mediterranean diet but not during the NCEP-1 diet. In addition, levels of plasma cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, and P-selectin decreased during the NCEP-1 and Mediterranean diets. CONCLUSION: In hypercholesterolemic men, diets low in fat (especially saturated fat) and diets rich in monounsaturated fats improve endothelial function.

Adolescent↗

PubMed2003

Impaired endothelial function in the brachial artery after Kawasaki disease and the effects of intravenous administration of vitamin C.

BACKGROUND: Previous studies in patients with a history of Kawasaki disease have focused on vascular endothelial function in coronary arteries, and the endothelial function of systemic arteries is not fully understood. Furthermore the effect of vitamin C on systemic endothelial function after Kawasaki disease has not been elucidated. OBJECTIVES: We attempted to analyze endothelium-dependent vasodilatation in the brachial artery after Kawasaki disease by using high resolution ultrasonography and to investigate whether the acute administration of vitamin C could restore such systemic endothelial dysfunction. METHODS: We compared 39 patients (7.1 +/- 2.7 years) 1.0 to 9.6 years after acute Kawasaki disease with 17 matched healthy subjects (7.0 +/- 3.1 years) as controls. Using high resolution vascular ultrasound, we measured brachial artery responses to reactive hyperemia (with increased flow causing endothelium-dependent dilatation) and sublingual nitroglycerin (causing endothelium-independent dilatation). RESULTS: The percent change in diameter of the brachial artery induced by reactive hyperemia in the patients with a history of Kawasaki disease (6.2 +/- 3.9%) was significantly lower than that in the control group (14.1 +/- 6.8%; P < 0.0001). No significant difference could be found in percent change in diameter induced by sublingual administration of nitroglycerin between the control (33.2 +/- 13.7%) and the patients with a history of Kawasaki disease (30.6 +/- 9.2%; P = 0.49). There was no significant difference in percent change in diameter of the brachial artery induced by reactive hyperemia between the patients who received gamma-globulin (6.0 +/- 4.0%) and those who did not receive gamma-globulin (7.9 +/- 3.3%; P = 0.33). Intravenous infusion of vitamin C significantly increased the percent change in diameter of brachial artery induced by reactive hyperemia in 19 patients with history of Kawasaki disease (6.6 +/- 3.5 to 13.0 +/- 5.5%; P < 0.0001), whereas no significant increase was seen in the percent change in diameter of brachial artery induced by reactive hyperemia in 20 patients with history of Kawasaki disease after placebo administration (6.5 +/- 4.5 to 7.3 +/- 4.9%; P = 0.20). CONCLUSIONS: Our study showed decreased percent change in diameter of the brachial artery induced by reactive hyperemia in patients with history of Kawasaki disease compared with the healthy children, indicating that systemic endothelial dysfunction exits after Kawasaki disease. Although such systemic endothelial dysfunction after Kawasaki disease is not influenced by early treatment with high dose gamma-globulin in the acute stage of Kawasaki disease, it can be restored by the acute intravenous administration of vitamin C.

Adolescent↗

PubMed2003

Altered myocardial flow reserve and endothelial function late after Kawasaki disease.

OBJECTIVES: Coronary arterial lesions after Kawasaki disease (KD) may cause coronary endothelial dysfunction as the result of intimal hypertrophy. Our purpose was to assess myocardial flow reserve (MFR) and endothelial function in various myocardial regions after KD by using positron emission tomography. STUDY DESIGN: Twenty-seven patients, 17.2 +/- 3.2 years of age, who had KD at 1.9 +/- 1.4 years, and 12 normal healthy subjects, 26.5 +/- 3.4 years of age, were evaluated by means of myocardial blood flow (MBF) with (15)O-water positron emission tomography. MFR was estimated by MBF changes under adenosine triphosphate infusion and endothelial function by MBF changes under cold pressor testing. The left ventricle was divided into three coronary territories. Ten stenotic regions, 20 aneurysmal regions, 30 regressed aneurysmal regions, and 21 regions without coronary arterial lesions were compared with 36 control regions of the normal volunteers. RESULTS: MBF at rest was similar in each region. Hyperemic blood flow and MFR in each region after KD was significantly lower than those in the regions of normal volunteers. MBF during cold pressor testing was significantly reduced in each region after KD, as compared with no change in the control regions. CONCLUSIONS: Our study indicates impaired MFR and endothelial function regardless of coronary artery status after KD.

Adenosine Triphosphate↗

PubMed1997

Xanthine oxidase inhibition prevents mesenteric blood flow deficits after resuscitated hemorrhagic shock by preserving endothelial function.

To determine the contribution of xanthine oxidase-mediated endothelial dysfunction to the blood flow deficits seen in the mesenteric circulation after resuscitated hemorrhagic shock, rats were prepared for intravital microscopic study then bled to 50% of baseline blood pressure for 60 min. Treatment animals received a 50 mg/kg bolus and a 25 mg/kg/hr infusion of the xanthine oxidase inhibitor allopurinol (allo) after shock but before resuscitation with shed blood and an equal volume of Ringer's lactate. A similarly resuscitated group (Std Res) and a nonhemorrhage group served as controls. Endothelial function was quantified at baseline, 30 min (R30), and 90 min (R90) postresuscitation as a change in mesenteric vessel diameter after topical application of acetylcholine (Ach), an endothelial-dependent vasodilator. Resuscitation restored cardiac output and blood pressure in both groups. First-order arteriolar blood flow (A1) remained depressed in the Std Res group but was restored to baseline in the group treated with allo. A1 arterioles demonstrated a 22 and a 27% reduction in ability to dilate to Ach at R30 and R90 after Std Res. V1 venules demonstrated a 39 and a 36% reduction in ability to dilate to Ach at R30 and R90 after Std Res. Endothelial-dependent vasodilation and blood flow were preserved in the group receiving Std Res plus allo. The preservation of endothelial function correlated with the restoration of microvascular blood flow postresuscitation. These data suggest that xanthine oxidase-mediated ischemia-reperfusion injury contributes to endothelial dysfunction and blood flow deficits in the mesenteric microcirculation after resuscitated hemorrhagic shock, the effect of which can be attenuated by the addition of the xanthine oxidase inhibitor allopurinol to standard resuscitation.

Acetylcholine↗

PubMed2000

Impaired endothelial function in arterial hypertension and hypercholesterolemia: potential mechanisms and differences.

This review focuses on the role of impaired endothelial function for the development of atherosclerosis in human arterial hypertension and hypercholesterolemia in vivo. Potential mechanisms underlying impaired endothelial function and decreased bioavailability of nitric oxide under these clinical conditions are discussed and potential differences in these mechanisms between arterial hypertension and hypercholesterolemia are outlined. It further addresses therapeutic strategies aiming to improve the bioavailability of nitric oxide in these patients. The overall conclusion is that the bioavailability of nitric oxide is probably impaired not by a single defect, but by various mechanisms affecting nitric oxide synthesis as well as nitric oxide breakdown. In both diseases, increased superoxide anion production and oxidative stress represents a major mechanism. However, potential differences in the underlying mechanisms of superoxide production or nitric oxide synthesis are evident between arterial hypertension and hypercholesterolemia. Decreased bioavailability of nitric oxide does not only impair endothelium-dependent vasodilation, but also activates other mechanisms that play an important role in the pathogenesis of atherosclerosis. Thus, therapeutic strategies should aim to restore bioavailability of nitric oxide, which has been demonstrated for lipid-lowering therapy in hypercholesterolemia. The mechanisms by which nitric oxide bioavailability can be improved by any drug therapy remain to be elucidated and may provide further insights into the mechanisms that are involved in impaired endothelial function and atherogenesis.

Animals↗

PubMed2005

Oral contraceptives improve endothelial function in amenorrheic athletes.

Athletic amenorrhea has been associated with endothelial dysfunction and unfavorable lipid profile. Estrogen substitution may reverse these metabolic consequences. The aim of this study was to evaluate the effects of oral contraceptives (OCs) on endothelial function measured as flow-mediated dilatation (FMD) of the brachial artery, the lipid profile, and blood markers of endothelial activation (inflammation) in amenorrheic athletes. Age- and body mass index-matched groups of young endurance athletes with amenorrhea (n = 11), regularly cycling athletes (n = 13), and sedentary controls (n = 12) were examined before and after 9 months of treatment with a low dose, monophasic, combined OC (30 mug ethinyl estradiol and 150 mug levonorgestrel). The amenorrheic athletes displayed the lowest FMD at baseline and the largest increase after OC treatment. FMD also increased in the control group, but not in the regularly menstruating athletes, who had the highest values of FMD before treatment. All three groups, particularly the controls, showed moderate unfavorable changes in the lipid profile in accordance with previous known effects of a second generation OC. Furthermore, there was an overall increase in some inflammatory markers (high sensitive C-reactive protein and TNF-alpha) and a decrease in one of the markers (vascular cell adhesion molecule-1). We conclude that amenorrheic athletes benefit from treatment with OC with respect to endothelial function. OC treatment is also associated with some modest alterations in the lipid profile and in markers of inflammation.

Adolescent↗

PubMed2005

Low high-density lipoprotein cholesterol is associated with impaired endothelial function in Asian Indians.

This study was designed to assess the relationship between plasma lipid levels and endothelial function in Asian Indians without cardiovascular risk factors living in the United States. While traditional risk factors do not account for the increased incidence of coronary heart disease (CHD) in Asian Indians, low high-density lipoprotein (HDL) cholesterol, elevated triglycerides, elevated lipoprotein (a), and insulin resistance are consistently found in Asian Indians with CHD. Endothelial function was measured in 86 healthy Asian Indians (mean age 33 years) free of cardiac risk factors with LDL levels<160 mg/dL. Subjects were divided into two groups on the basis of HDL levels (low HDL<40 mg/dL and normal HDL-40 mg/dL). Endothelial function during reactive hyperemia was significantly impaired in Asian Indians in the low HDL group. After covariate adjustment, NTG-induced brachial vasodilation was not different between patients in the two HDL groups. These data indicate that low HDL is associated with endothelial dysfunction in this population.

Adult↗

PubMed2005

Metformin reduces blood pressure and restores endothelial function in aorta of streptozotocin-induced diabetic rats.

Effect of metformin treatment on blood pressure, endothelial function and oxidative stress in streptozotocin (STZ)-induced diabetes in rats was studied. In vitro effect of metformin on vascular reactivity to various agonist in the presence of metformin in untreated nondiabetic and STZ-diabetic rats were also studied. Sprague-Dawley rats were randomized into nondiabetic and STZ-diabetic groups. Rats were further randomized to receive metformin (150 mg/kg) or vehicle for 4 weeks. Metformin treatment reduced blood pressure without having any significant effect on blood glucose level in STZ-diabetic rats. Enhanced phenylephrine (PE)-induced contraction and impaired acetylcholine (Ach)-induced relaxation in STZ-diabetic rats were restored to normal by metformin treatment. Enhanced Ach-induced relaxation in metformin-treated STZ-diabetic rats was blocked due to pretreatment with 100 microM of Nomega-nitro-L-arginine-methyl ester (L-NAME) or 10 microM of methylene blue but not 10 microM of indomethacin. Metformin treatment significantly increased antioxidant enzymes and reduced lipid peroxidation in STZ-diabetic rats. In vitro studies in aortic rings of untreated nondiabetic and STZ-diabetic rats showed that the presence of higher concentration of metformin (1 mM and 10 mM) significantly reduced PE-induced contraction and increased Ach-induced relaxation. Metformin per se relaxed precontracted aortic rings of untreated nondiabetic and STZ-diabetic rats in a dose-dependent manner. Pretreatment with L-NAME or removal of endothelium blocked metformin-induced relaxation at lower concentration (up to 30 microM) but not at higher concentration (above 30 microM). Metformin-induced relaxation was blocked in the presence of 1 mM of 4-aminopyridine, or 1 mM of tetraethylammonium but not in the presence of 100 microM of barium ion or 10 microM of glybenclamide. The restored endothelial function along with direct effect of metformin on aortic rings and reduced oxidative stress contributes to reduced blood pressure in STZ-diabetic rats. From the present study, it can be concluded that metformin administration to STZ-diabetic rats lowers blood pressure, and restores endothelial function.

4-Aminopyridine↗

PubMed2003

Vitamin C improves endothelial function in healthy estrogen-deficient postmenopausal women.

OBJECTIVE: Estrogen deficiency is associated with increased cardiovascular risk and endothelial dysfunction. Improvements in endothelial function with antioxidants, including vitamin C, have been reported. We aimed to determine the acute effect of vitamin C on endothelial function in healthy women with established menopause. SUBJECTS: Subjects (aged 47-59 years) were at least 1 year postmenopause. Ten (serum estradiol < 50 pmol/l) were not receiving hormone replacement therapy, while eight hysterectomized subjects received subcutaneous estradiol. DESIGN: Forearm blood flow (FBF; strain-gauge plethysmography) responses to intrabrachial artery infusions of incremental doses of acetylcholine (endothelium-dependent vasodilation) and sodium nitroprusside (endothelium-independent vasodilation) were determined at baseline, and following 1.5 g vitamin C given intravenously. RESULTS: At baseline, estrogen-treated subjects had a lower index of insulin resistance (homeostasis model assessment, HOMA) and lower fibrinogen than those of estrogen deficient subjects. There was a trend towards higher baseline FBF and larger baseline FBF response to acetylcholine in estrogen-treated subjects. FBF responses to acetylcholine were significantly enhanced after vitamin C in estrogen-deficient subjects (area under the dose-response curve (AUC): estrogen-deficient 9.9 +/- 2.6 vs. 15.1 +/- 3.2 (mean +/- SEM), p = 0.02; estrogen-treated 17.0 +/- 2.9 vs. 21.0 +/- 3.2, p = 0.07). Resting FBF and response to sodium nitroprusside were unchanged in either group by vitamin C. Plasminogen activator inhibitor-1 levels fell after vitamin C in the estrogen-deficient group (17.0 +/- 1.6 vs. 14.7 +/- 0.9 IU/ml, p = 0.03). CONCLUSIONS: These results indicate that endothelial function may be improved acutely by antioxidant treatment in postmenopausal women with established estrogen deficiency.

Acetylcholine↗

PubMed2005

Effects of maternal hypoxia or nutrient restriction during pregnancy on endothelial function in adult male rat offspring.

Compromised fetal growth impairs vascular function; however, it is unclear whether chronic hypoxia in utero affects adult endothelial function. We hypothesized that maternal hypoxia (H, 12% O2, n= 9) or nutrient restriction (NR, 40% of control, n= 7) imposed from day 15-21 pregnancy in rats would impair endothelial function in adult male offspring (relative to control, C, n= 10). Using a wire myograph, endothelium-dependent relaxation in response to methacholine was assessed in small mesenteric arteries from 4- and 7-month-old (mo) male offspring. Nitric oxide (NO) mediation of endothelium-dependent relaxation was evaluated using N(omega)-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor). Observed differences in the NO pathway at 7 months were investigated using exogenous superoxide dismutase (SOD) to reduce NO scavenging, and sodium nitroprusside (SNP; NO donor) to assess smooth muscle sensitivity to NO. Sensitivity to methacholine-induced endothelium-dependent relaxation was reduced in H offspring at 4 months (P < 0.05), but was not different among groups at 7 months. L-NAME reduced methacholine sensitivity in C (P < 0.01), H (P < 0.01) and NR (P < 0.05) offspring at 4 months, but at 7 months L-NAME reduced sensitivity in C (P < 0.05), tended to in NR (P= 0.055) but had no effect in H offspring. SOD did not alter sensitivity to methacholine in C, but increased sensitivity in H offspring (P < 0.01). SNP responses did not differ among groups. In summary, prenatal hypoxia, but not nutrient restriction impaired endothelium-dependent relaxation at 4 months, and reduced NO mediation of endothelial function at 7 months, in part through reduced NO bio-availability. Distinct effects following reduced maternal oxygen versus nutrition suggest that decreased oxygen supply during fetal life may specifically impact adult vascular function.

Aging↗

PubMed2000

Automated ultrasonic measurement of human arteries for the determination of endothelial function.

AIM: Brachial artery ultrasonography is used to measure flow-mediated dilatation (FMD) as a marker of endothelial function in patients at risk for atherosclerosis. Major disadvantages are the time-consuming manual readings and the high within- and between-observer variability. The authors hypothesize that the ultrasound-based determination of endothelial function can be simplified and refined by an automated analysis system. METHODS AND RESULTS: FMD was quantified by a 7.5 MHz linear transducer following 5 minutes of ischemia of the proximal forearm in 8 healthy volunteers on two occasions. Brachial artery diameter was comparatively assessed 1. manually from the video signal and 2. by a PC-based analyzing system. For the manual readings the mean differences for the FMD were 2.5 +/- 2.3% between-reader, 2.0 +/- 0.9% within-reader and 2.1 +/- 1.5% for scans on different days in contrast to 0.8 +/- 0.4 (between-reader), 0.8 +/- 0.6 (within-reader) and 1.3 +/- 0.9% (day-to-day) for the computerized system. The coefficient of variability for the measurement of arterial diameter was 1.34% for manual readings and 0.78% for the automated analysis system. The mean time for manual readings from S-VHS tapes was 35 minutes in contrast to 9 minutes for the PC-based analysis system. CONCLUSIONS: The new automated analysis system for the boundary detection of the vascular wall reduces the variability and greatly increases the speed of the measurements to determine endothelial function. In future, these advantages will help to screen larger numbers of individuals for endothelial dysfunction, particularly for follow-up and intervention trials, and to reduce the variability between different laboratories.

Adult↗

PubMed2006

Comparative effects of enzogenol and vitamin C supplementation versus vitamin C alone on endothelial function and biochemical markers of oxidative stress and inflammation in chronic smokers.

Chronic smoking is associated with endothelial dysfunction and inflammation, with oxidative stress contributing to both these processes. In this study, we investigated the effect of combined antioxidant treatment with Enzogenol, a flavonoid extract from the bark of Pinus radiata and vitamin C, over and above vitamin C alone, on endothelial function, plasma markers of inflammation and oxidative stress, blood pressure (BP) and anthropometrics. Forty-four chronic smokers without established cardiovascular disease were assigned randomly to receive either 480 mg Enzogenol and 60 mg vitamin C, or 60 mg vitamin C alone daily for 12 weeks. Endothelial function in the brachial artery was assessed by flow-mediated vasodilation (FMD). FMD improved in both treatment groups (p < 0.001), with no significant difference between the two groups (p = 0.84). In the group receiving Enzogenol and vitamin C, protein carbonyl levels were significantly reduced compared to the group taking vitamin C alone (p = 0.03). Enzogenol and vitamin C resulted in a significant reduction in fibrinogen levels in heavy smokers compared with vitamin C alone (p < 0.009). These findings demonstrated that co-supplementation with Enzogenol and vitamin C in smokers conferred no additional beneficial effect on macrovascular endothelial function over and above that seen in the vitamin C alone group. However, Enzogenol did demonstrate additional favourable effects on protein oxidative damage and fibrinogen levels.

Adult↗

PubMedDate not supplied

Endothelial function in mesenteric resistance arteries from the genetically hypertensive rat.

1. Endothelial function in mesenteric resistance arteries (MRA) from male 12-week-old New Zealand genetically hypertensive (GH) rats and their normotensive control strain (N) was compared in vessels mounted on a wire myograph and by the production of intracellular cGMP. In parallel experiments, MRA from the spontaneously hypertensive (SHR) rat strain, in which there is an endothelial defect, and from GH rats, in which an endothelial defect was induced by chronic nitric oxide synthase (NOS) inhibition with Nomega-nitro-L-arginine methyl ester (L-NAME), were studied. 2. Contractile responses to potassium (124 mmol/L) depolarization and to NA (10(-8) to 10(-4) mol/L) were similar in GH and N rats; however, in SHR, enhanced contractile responses were found (P < 0.05). The endothelium-dependent relaxation induced by acetylcholine (ACh; 10(-9) to 10(-4) mol/L) and endothelium- independent relaxation induced by sodium nitroprusside (SNP; 10(-9) to 10(-4) mol/L) were identical in preparations from GH and N. A significantly attenuated (P < 0.01) vasodilator response to ACh was observed in preparations from SHR. 3. Levels of intracellular cGMP were similar in untreated small mesenteric arterial trees from GH, N and SHR rats. Acetylcholine (10-5 mol/L) significantly (P < 0.001) increased the cGMP content in both GH and N rats. A non-significant increase occurred in cGMP content in preparations from SHR. 4. In GH rats given L-NAME (10 mg/kg per day for up to 5 weeks), an attenuated (P < 0.01) endothelium-dependent relaxation to ACh and an enhanced (P < 0.01) endothelium- independent relaxation to SNP were observed. Lower basal cGMP levels were found in preparations from L-NAME-treated GH rats and ACh (10-5 mol/L) failed to significantly elevate the cGMP content in these preparations. 5. These experiments failed to show evidence of reduced endothelial function in GH rats, although an endothelial defect in SHR rats and after NOS inhibition in GH rats could be demonstrated.

Animals↗