SEARCH · PubMed Health

Results for “Endothelial function”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources

PubMed2006

Plant stanols do not restore endothelial function in pre-pubertal children with familial hypercholesterolemia despite reduction of low-density lipoprotein cholesterol levels.

OBJECTIVE: To examine the effect of plant stanols on lipids and endothelial function in pre-pubertal children with familial hypercholesterolemia (FH). STUDY DESIGN: Children with FH (n=42), aged 7-12 years, were enrolled in a double-blind crossover trial, in which they consumed 500 mL of a low-fat yogurt enriched with 2.0 g of plant stanols and 500 mL of a low-fat placebo yogurt for 4 weeks, separated by a 6-week washout period. Lipid profiles and endothelial function were assessed after both consumption periods. Endothelial function was measured as flow-mediated dilation (FMD) of the brachial artery. RESULTS: This daily intake of 2.0 g of stanols significantly decreased the levels of total cholesterol (TC) by 7.5% and low-density lipoprotein cholesterol (LDL-C) by 9.2% as compared with placebo. High-density lipoprotein cholesterol and triglyceride levels remained unaltered. The reduction of LDL-C levels did not improve FMD, which was 10.5%+/-5.1% after plant stanol consumption and 10.6%+/-5.0% after placebo consumption, respectively (P=.852). CONCLUSION: This study demonstrates that plant stanols reduce LDL-C levels in children with FH without improving endothelial function.

Anticholesteremic Agents↗

PubMedDate not supplied

The effect of PGI2 analogue on vascular endothelial function and platelet aggregation in patients with NIDDM.

The effect of the short-term administration of beraprost sodium, an analogue of prostaglandin I2 (PGI2), on the function of vascular endothelial cells and platelet in non-insulin-dependent diabetes mellitus (NIDDM) patients was investigated. Seven nonobese NIDDM patients with microalbuminuria were recruited for this study. They received a dose of 20 micrograms of beraprost sodium three times daily for 1 month. Before and after this treatment, various factors concerning functions of vascular endothelial cells and platelet were measured. Treatment with PGI2 analogue caused a decrease in basal levels of plasma lipoprotein (a) from 16.8 +/- 5.3 to 13.2 +/- 4.4 mg/dL (p < 0.05), immunoreactive-(i)endothelin from 2.4 +/- 0.3 to 1.6 +/- 0.2 pg/mL, and i-thrombomudulin from 9.3 +/- 3.7 to 7.9 +/- 3.0 FU/L, respectively, and caused a significant increase in basal plasma i-tissue type plasminogen activator (tPA) from 5.3 +/- 0.7 to 8.3 +/- 1.5 ng/mL (p < 0.01). This treatment also increased maximum response of i-tPA induced by desmopressin infusion. Platelet aggregation due to ADP was inhibited in five of six patients after this treatment. In conclusion, treatment with PGI2 analogue caused a decrease in the presumed promoting factors of angiopathy such as lipoprotein (a) and endothelin and an increase in the protecting endothelial factor of angiopathy, tissue type plasminogen activator in patients with NIDDM. And immunoreactive thrombomodulin levels which reflect the vascular endothelial cell injury tended to decrease with the treatment. Therefore, it is suggested that this treatment preserves the vascular endothelial function in diabetes.

Adult↗

PubMed2005

Preliminary results of the effect of treatment of hyperhomocysteinemia and its relationship with inflammation, coagulation status, and endothelial function after renal transplantation.

The aim of this study was to assess the relationship between total plasma homocysteine (tHC) and several markers of endothelial function, coagulation, and pro-inflammatory status in renal transplant recipients. Our own previous study demonstrated the efficacy of folic acid (FA) and vitamin B(12) (B(12)) treatment to reduce tHC. Using 70 stable recipients, 56 of whom showed hyperhomocisteinemia (HHC) (tHC > or = 14 micromol/L) and a control group (n = 14, tHC < 14 micromol/L), we treated 29 patients in the HHC group (10 mg FA and 500 mg B(12) daily) and determined their endothelial function, inflammatory activity, and coagulation status. We assessed plasma levels of von Willebrand Factor and fibrinogen as the prothrombotic profile and C-reactive protein and plasma albumin as inflammation markers. We performed Doppler sonography of the brachial artery to assess endothelial function. The mean value of plasma tHC of 19.05 +/- 3.70 micromol/L before treatment decreased to 13.45 +/- 3.25 micromol/L after 3 months of treatment (P < .001). The vWF was significantly correlated with tHC (P < .05) and was higher in the HHC patients (P < .05). The fibrinogen mean level was also significantly higher in HHC patients (P < .05). The C-reactive protein level was significantly higher and the albumin level was lower among patients with HHC. The endothelium-dependent dilation (EDD) correlated with baseline tHC (P < .05). In preliminary data we observed that homocysteine-lowering therapy may provide cardiovascular protection by enhancing endothelial function, limiting oxidative stress, and reducing procoagulation status.

Adult↗

PubMed2002

[Protective effect of Na(+)-H+ exchanger inhibitor cariporide on the injury of vascular endothelial function induced by hypercholesterolemia].

OBJECTIVE: To explore possible effects of cariporide, a new Na(+)-H+ exchanger (NHE-1) inhibitor, against injuries of vascular endothelial function induced by hypercholestrolemia. METHODS: Twenty-two healthy New Zealand rabbits were randomly divided into 3 groups: Six were fed with normal diet as the control; eight were fed with high cholesterol plus high fat diet (HCHF) as the injured control group; and the other eight were fed with HCHF plus cariporide orally (0.1 mg/kg.d-1) as the treated group. The animals were weighed and their blood was drawn from the central ear artery to analyze plasma cholesterol at the pre-experiment and in the 10th week of postexperiment. The animals were killed in the 10th week and the aortic artery was isolated to analyze vascular endothelial function. RESULTS: 1. The HCHF diet significantly attenuated endothelium-dependent relaxation (EDR) of rabbit aortic rings to acetylcholine (ACh), but cariporide significantly protected against HCHF diet-injured EDR of rabbit aortic rings. The dose-response curves elicited by ACh from HCHF diet rabbits were more significantly shifted to the right than those from HCHF diet plus HOE 642-treated rabbits. 2. The HCHF diet and cariporide did not significantly influence the endothelium-independent relaxation of the rabbit artery elicited by sodium nitroprusside (SNP). 3. There was no significant difference in the levels of total cholesterol and LDL-C between the HCHF diet and the HCHF diet plus cariporide rabbits. CONCLUSION: The Na(+)-H+ exchanger (NHE-1) inhibitor can protect against injuries of vascular endothelial function induced by hypercholesterolemia. The activized Na(+)-H+ exchangers of cellular membranes may be involved in injuries of vascular endothelial function induced by hypercholesterolemia.

Animals↗

PubMed1999

Impaired endothelial function following a meal rich in used cooking fat.

OBJECTIVES: The purpose of this study was to test the hypothesis that intake of used cooking fat is associated with impaired endothelial function. BACKGROUND: Diets containing high levels of lipid oxidation products may accelerate atherogenesis, but the effect on endothelial function is unknown. METHODS: Flow-mediated endothelium-dependent dilation and glyceryl trinitrate-induced endothelium-independent dilation of the brachial artery were investigated in 10 men. Subjects had arterial studies before and 4 h after three test meals: 1) a meal (fat 64.4 g) rich in cooking fat that had been used for deep frying in a fast food restaurant; 2) the same meal (fat 64.4 g) rich in unused cooking fat, and 3) a corresponding low fat meal (fat 18.4 g) without added fat. RESULTS: Endothelium-dependent dilation decreased between fasting and postprandial studies after the used fat meal (5.9 +/- 2.3% vs. 0.8 +/- 2.2%, p = 0.0003), but there was no significant change after the unused fat meal (5.3 +/- 2.1% vs. 6.0 +/- 2.5%) or low fat meal (5.3 +/- 2.3% vs. 5.4 +/- 3.3%). There was no significant difference in endothelium-independent dilation after any of the meals. Plasma free fatty acid concentration did not change significantly during any of the meals. The level of postprandial hypertriglyceridemia was not associated with change in endothelial function. CONCLUSIONS: Ingestion of a meal rich in fat previously used for deep frying in a commercial fast food restaurant resulted in impaired arterial endothelial function. These findings suggest that intake of degradation products of heated fat contribute to endothelial dysfunction.

Adult↗

PubMed2000

[Effect of L-arginine on platelet aggregation, endothelial function adn exercise tolerance in patients with stable angina pectoris].

AIM: Examination of the action of donor NO (L-arginine) on platelet aggregation, endothelial function and exercise tolerance in patients with stable angina of effort (SAE). MATERIAL AND METHODS: 42 patients with SAE (functional class I-II) and 10 healthy volunteers (control group) were assigned to two groups. 22 patients of group 1 were randomized to cross-over. They received cardiket (60 mg/day for 10 days or cardiket (60 mg/day) in combination with L-arginine (15 g/day for 10 days). 20 SAE patients of group 2 and control group received L-arginine (15 g/day for 10 days). In each group blood lipids were examined, and bicycle exercise test (BET) was performed. In addition, platelet aggregation and endothelial function were studied in group 2 and control group before and after the course of L-arginine. RESULTS: Compared to control group, endothelial function significantly improved in group 2 (from 5.0 +/- 2.9 to 7.8 +/- 4.1% vs 7.1 +/- 1.9 to 6.6 +/- 4.8%) (M +/- SD). BET duration increased in all the patients. After ADP addition in concentrations 1.5, 2.0, and 5.0 micromol/l platelet aggregation declined in 17 patients except 3 in whom the aggregation remained unchanged. CONCLUSION: Positive effect of L-arginine on endothelial function, exercise tolerance and platelet aggregation was observed in patients with stable angina of effort (functional class I-II). Therefore, arginine can be recommended as an adjuvant in the treatment of patients with ischemic heart disease.

Angina Pectoris↗

PubMed2001

The effects of oral methionine and homocysteine on endothelial function.

BACKGROUND: Raised homocysteine is a risk factor for vascular disease. Homocysteine is formed from methionine, and dietary manipulation of homocysteine in primates and humans with oral methionine is associated with endothelial dysfunction. A cause-effect relation has not been clearly established. AIM: To study the effect of oral methionine and then oral homocysteine on endothelial function. METHODS: 22 healthy adults were recruited for two randomised crossover studies, each containing 11 subjects. Endothelial function was determined by measuring forearm blood flow in response to intra-arterial infusion of acetylcholine (endothelium dependent) and sodium nitroprusside (endothelium independent). Subjects received methionine or placebo (study 1), or homocysteine or placebo (study 2). Methionine and homocysteine were determined at baseline and t = 4 hours. Endothelial function was determined at four hours. The responses to the vasoactive substances are expressed as the area under the curve of change in forearm blood flow from baseline. RESULTS: Study 1: plasma methionine and homocysteine concentrations increased significantly versus placebo. The increases were associated with a reduction of endothelium dependent responses (mean (95% confidence interval), arbitrary units), from 48.8 (95% CI 36.4 to 61.2) to 29.9 (95% CI 18.0 to 41.1), p < 0.04; endothelium independent responses were unchanged. Study 2: homocysteine concentration increased significantly while methionine remained unchanged. Endothelium dependent responses were reduced from 34.6 (95% CI 20.6 to 48.6) to 22.8 (95% CI 12.0 to 33.6), p < 0.03. CONCLUSIONS: Homocysteine and not methionine is responsible for the changes in endothelial function. This supports the hypothesis that homocysteine promotes atherosclerosis by inducing endothelial dysfunction.

Administration, Oral↗

PubMed2006

Effect of a single high-fat meal on endothelial function in patients with the metabolic syndrome: role of tumor necrosis factor-alpha.

BACKGROUND AND AIMS: A single high-fat meal may induce endothelial activation and dysfunction in both normal subjects and in patients with type 2 diabetes. The aim of this study was to assess the effect of a high-fat meal on endothelial function in patients with the metabolic syndrome. METHODS AND RESULTS: Twenty-five patients with the metabolic syndrome (ATP III criteria) were matched for sex, age and body mass index with 25 subjects without the metabolic syndrome. All subjects ate under supervision a high fat meal (760 calories) with 59% energy from fat, 12% energy from protein and 29% energy from carbohydrates. Compared with the control group, subjects with the metabolic syndrome had reduced endothelial function, as assessed with the l-arginine test, and higher circulating levels of TNF-alpha. Following the high-fat meal, both triglyceride and TNF-alpha levels increased more in subjects with the metabolic syndrome than in subjects without, while endothelial function decreased more in subjects with the metabolic syndrome. There was a significant relation between increases in TNF-alpha levels and decreases in endothelial function score in subjects with the metabolic syndrome (r=-0.39, P=0.03). CONCLUSION: TNF-alpha levels are increased in subjects with the metabolic syndrome; moreover, a high-fat meal produces further increase in its levels associated with endothelial dysfunction.

Adult↗

PubMed2004

Constituents of red wine other than alcohol improve endothelial function in patients with coronary artery disease.

BACKGROUND: Several studies suggest that red wine is beneficial in coronary artery disease (CAD). Although the long-term effect of moderate red wine consumption on endothelial function is currently under investigation, there is little knowledge about its effect on postprandial endothelial function and haemostatic factors. The aim of the present study was to investigate the postprandial effects of alcohol content and the antioxidants of red wine on endothelial function and fibrinogen levels in CAD patients. METHODS: Fifteen males with angiographically documented CAD were recruited for the study. All volunteers ingested 250 ml of either red wine or de-alcoholized red wine on two different days. Blood samples (for analysis of fibrinogen and blood lipids) were collected and flow-mediated dilatation (FMD) was determined before and 30, 60 and 90 min following consumption of each beverage RESULTS: FMD was higher following the consumption of de-alcoholized red wine [type of wine effect, P=0.05 repeated measures analysis of variance (ANOVA)]. Furthermore, the pattern of the response was different between the two beverages, as FMD increased following the ingestion of de-alcoholized red wine, but it decreased after consumption of regular red wine (type of wine by time interaction effect, P=0.006 repeated measures ANOVA). Fibrinogen concentrations were unaltered CONCLUSIONS: Acute ingestion of red wine without alcohol led to higher FMD than ingestion of regular red wine in CAD patients. The acute effect of red wine on endothelial function may be different than its long-term effect and it could be attributed to its constituents other than alcohol.

Antioxidants↗

PubMed1997

Coronary risk factors, endothelial function, and atherosclerosis: a review.

The traditional risk factors for coronary heart disease, which include hypercholesterolemia, hypertension, cigarette smoking, diabetes mellitus, and high-fat diet, have all been associated with impairments in endothelial function. Impaired endothelium function may promote the development of atherosclerosis through its effects on vasoregulation, platelet and monocyte adhesion, vascular smooth muscle cell growth, and coagulation. Increased oxidative stress may be another mechanism by which endothelial dysfunction contributes to atherosclerosis, although controversy exists on this issue. Risk factor modification, particularly lowering elevated concentrations of low-density lipoprotein cholesterol, improves endothelial function. At least seven clinical studies have demonstrated improved endothelial function with cholesterol reductions in patients with markedly elevated or even borderline elevations in cholesterol concentrations, whether or not coronary heart disease is present. Other interventions that improve endothelial function include blood pressure reduction, smoking cessation, and administration of estrogen to postmenopausal women.

Animals↗

PubMed2003

Enhanced external counterpulsation improves endothelial function in patients with symptomatic coronary artery disease.

OBJECTIVES: The goal of this study was to examine the effect of enhanced external counterpulsation (EECP) on endothelial function. BACKGROUND: Enhanced external counterpulsation improves symptoms and exercise tolerance in patients with symptomatic coronary artery disease (CAD). However, the exact mechanisms by which this technique exerts its clinical benefit are unclear. METHODS: Reactive hyperemia-peripheral arterial tonometry (RH-PAT), a noninvasive method to assess peripheral endothelial function by measuring reactive hyperemic response in the finger, was performed in 23 patients with refractory angina undergoing a 35-h course of EECP. In each patient RH-PAT measurements were performed before and after the first, at midcourse, and the last EECP session. In addition, RH-PAT response was assessed one month after completion of EECP therapy; RH-PAT index, a measure of reactive hyperemia, was calculated as the ratio of the digital pulse volume during reactive hyperemia divided by that at rest. RESULTS: Enhanced external counterpulsation led to symptomatic improvement (>/=1 Canadian Cardiovascular Society class) in 17 (74%) patients; EECP was associated with a significant immediate increase in average RH-PAT index after each treatment (p < 0.05). In addition, average RH-PAT index at one-month follow-up was significantly higher than that before EECP therapy (p < 0.05). When patients were divided by their clinical response, RH-PAT index at one-month follow-up increased only in those patients who experienced clinical benefit. CONCLUSIONS: Enhanced external counterpulsation enhances peripheral endothelial function with beneficial effects persisting at one-month follow-up in patients with a positive clinical response. This suggests that improvement in endothelial function may contribute to the clinical benefit of EECP in patients with symptomatic CAD.

Aged↗

PubMed1997

Is endothelial function of the radial artery altered in human essential hypertension?

There is controversy over whether endothelial function is impaired in human essential hypertension. All studies to date have used measurements of forearm blood flow by plethysmography to assess endothelium-dependent vasodilation and endothelial function. In contrast to these studies, which have focused on resistance vessels, we have determined what effects the endothelium has on underlying smooth muscle cells in conduit arteries by measuring arterial compliance of the radial arteries (change in diameter of radial artery over pressure for each arterial pulse). In 13 normotensive healthy subjects and 11 young patients with essential hypertension, arterial compliance of the radial artery was assessed directly with a new high-precision ultrasonic device (NIUS 02) after infusion of acetylcholine (endothelium-dependent response) or sodium nitroprusside (endothelium-independent response). Arterial compliance of the radial artery was similar at baseline and with increasing doses of acetylcholine and sodium nitroprusside in normotensive and in hypertensive subjects. The increase in arterial compliance from baseline at each individual concentration of acetylcholine and sodium nitroprusside was the same in both normotensive and hypertensive subjects. However, after a single oral dose of a combination of the angiotensin converting enzyme inhibitor spirapril and the calcium entry blocker isradipine, the increase in arterial compliance in response to the maximum dose of intraarterial acetylcholine was enhanced in normotensives (0.38 +/- 1.23 to 0.76 +/- 1.01 mm2/mm Hg x 10(-3), P < .05), but not in hypertensives (+0.41 +/- 1.26 to 0.36 +/- 1.31 mm2/mm Hg x 10(-3), not significant), and differed significantly between normotensive and hypertensive subjects (P < .05). Thus, pharmacologic stimulation disclosed a blunted response of endothelium-dependent action in the arterial compliance of the conduit arteries in hypertensive subjects. This suggests an impaired endothelial function reserve in persons with essential hypertension.

Acetylcholine↗

PubMed2004

Optimizing donor heart outcome after prolonged storage with endothelial function analysis and continuous perfusion.

BACKGROUND: By minimizing tissue ischemia, continuous perfusion (CP) during organ transport may increase the safety of "marginal donors." My colleagues and I investigated whether an analysis of donor heart viability predicts recovery of grafts challenged with a 24-hour preservation interval. METHODS: Dog hearts underwent cold static storage (CS) for 8 hours (n = 8) or 24 hours (n = 2) or CP for 24 hours with cold asanguinous, oxygenated solution (n = 8). Myocardial systolic and diastolic function and oxygen and lactate consumption were assessed at base line, during CP, and after Langendorff blood reperfusion. Base line endothelial function was evaluated by the percentage transcoronary change ([coronary sinus - aorta]/aorta) in myeloperoxidase and by platelet function and coronary flow reserve after 20 seconds of coronary artery occlusion. During CP, the endothelium was assessed by transcoronary protein release and coronary resistance. Edema was assessed by weight gain and histology. RESULTS: Base line systolic and metabolic functions showed no relation to post-Langendorff function. Compared with CS, CP resulted in a greater recovery in systolic function (87% +/- 35% vs 65% +/- 15% of baseline; p = 0.05) and a shorter interval required for lactate consumption to exceed production (7.0 +/- 6.8 minutes vs 15.0 +/- 8.9 minutes; p = 0.06). Endothelial function was heterogeneous: coronary flow reserve, 2.7 +/- 0.7; percentage change in myeloperoxidase, -8.4% +/- 6.8%; and change in platelet function, 4.3% +/- 3.5%, as determined by thromboelastography angle at base line. Protein release during CP for 24 hours was 8.3 +/- 7.1 g. Two factors predicted more than 75% systolic pressure generation recovery: use of CP and normal endothelial function (p = 0.05; Fisher's exact test). However, CP led to edema according to histology, weight gain (72 +/- 29 g), and impaired diastolic function versus CS (end-diastolic pressure-volume relationship, 1.4 +/- 0.4 mm Hg/mL vs 0.8 +/- 0.3 mm Hg/mL; p = 0.08). CONCLUSIONS: Better systolic function despite 16 hours' more preservation than cold storage corroborates the idea that CP supports aerobic metabolism at physiologically important levels. Viability analysis focused on endothelial function and identified organs that were able to tolerate this 24-hour preservation interval.

Aerobiosis↗

PubMed2000

Endothelial function and peripheral vasomotion in the brachial artery in neurally mediated syncope.

BACKGROUND: Paradoxical peripheral vasodilation is one of the suspected mechanisms of neurally mediated syncope. Parasympathetic stimulation following sympathetic activation during orthostatic stress mainly contributes to this vasodilation. HYPOTHESIS: Since endothelial function modulates peripheral vascular tone, this study aimed to determine whether endothelial function and inappropriate peripheral vasomotion has a significant role in the pathogenesis of neurally mediated syncope. METHODS: To investigate whether endothelial function is augmented or whether abnormal peripheral vasomotion exits, flow-mediated dilation (FMD, endothelium-dependent vasodilation) and sublingual glyceryl trinitrate-induced dilation (0.3 mg, GTN-D, endothelium-independent vasodilation) were measured in the brachial artery in 16 patients with neurally mediated syncope, aged 33 +/- 10 years, by using high-resolution ultrasound. All patients underwent positive head-up tilt testing. These measures were compared with those in 16 control subjects matched with the patients by age, gender, and coronary risk factors. For FMD, percent diameter changes were obtained from baseline to hyperemic conditions (1 min after 5 min occlusion of the forearm artery). There were five smokers in both the patient and the control groups, but there was no structural heart disease in either group. RESULTS: Baseline brachial artery diameters were comparable (3.8 +/- 0.6 vs. 3.8 +/- 0.7 mm, NS). Flow-mediated dilation in patients with neurally mediated syncope had a normal value of 9.8 +/- 5.0% despite the inclusion of five smokers. Flow-mediated dilation and GTN-D in patients with neurally mediated syncope were significantly greater than those in controls (9.0 +/- 5.0 vs. 3.0 +/- 3.5%, p<0.05; 18.4 +/- 5.5 vs. 14.1 +/- 4.4%, p<0.05). CONCLUSIONS: Augmented endothelial function and/or abnormal peripheral vasomotion in peripheral arteries are important in patients with neurally mediated syncope in selected populations.

Adult↗

PubMed2004

Exercise and endothelial function: role of endothelium-derived nitric oxide and oxidative stress in healthy subjects and hypertensive patients.

Recent epidemiologic studies have shown that aerobic exercise, one of lifestyle modifications, reduces cardiovascular morbidity and mortality in the general population. However, the mechanisms underlying the anti-atherogenic and anti-hypertensive effects of exercise remain unclear. Hypertension is associated with alteration in endothelial function mediated through reduced nitric oxide (NO) bioavailability. Endothelial dysfunction is an early feature of atherosclerosis and vascular diseases in humans. Exercise training has been shown to improve endothelial function in animal models of hypertension and in patients with essential hypertension. These findings suggest that endothelial dysfunction in hypertension is reversible. Lifestyle modifications including exercise are expected to prevent cardiovascular complications through an augmentation of endothelial function in hypertensive patients. It is thought that exercise increases NO production and decreases NO inactivation, leading to an increase in NO bioavailability. In this review, we will focus on recent findings and on possible mechanisms underlying the beneficial effects of exercise on endothelial function in patients with hypertension.

Endothelium, Vascular↗

PubMed2004

Folic acid and vitamin E supplementation effects on homocysteinemia, endothelial function and plasma antioxidant capacity in young myocardial-infarction patients.

We examined the effects of folate (either alone or co-supplemented with Vitamin E) on endothelial function in hyperhomocysteinimic patients and correlated results with serum antioxidant capacity. A randomized trial was carried out in 30 young patients with recent acute myocardial infarction (AMI) and high plasma homocysteine concentrations. Intervention consisted of high doses of folate, either alone (group A) or in combination with Vitamin E (group B), for three months. Main outcome measures were endothelial function, serum antioxidant capacity, and homocysteinemia. Folic acid treatment reduced plasma homocysteine concentrations in both groups by 41% and, as compared with baseline values, was associated with a significant (P<0.001) improvement of endothelial function (from 0.322 (0.03) to 0.450 (0.02)mm in group A and from 0.338 (0.03) to 0.584 (0.04)mm in group B). However, there was no difference in endothelial function improvement between folic acid and folic acid plus Vitamin E group. Plasma antioxidant capacity significantly (P<0.001) increased in both groups. In conclusion, beneficial effects of folic acid on vasomotion appear to be independent of antioxidant action but, rather, seem to be strongly associated with reduction of homocysteinemia. Confirming previous reports, the effects of Vitamin E are still equivocal.

Adult↗

PubMed2003

Variability in hypoxia-induced corneal swelling is associated with variability in corneal metabolism and endothelial function.

PURPOSE: To determine if the variability in contact lens-induced corneal swelling is associated with variability in corneal oxygen consumption (Q(C)) or corneal endothelial function. METHODS: Corneal swelling was induced in 30 non-contact lens wearers by 2 hours of closed-eye contact lens wear, using thick (oxygen transmission [Dk/t] = 4.0 x 10-9) and thin (Dk/t = 12 x 10-9) hydrogel lenses of identical design. Following the induction of swelling, corneal thickness was continually measured by pachymetry until open-eye steady-state (OESS) thickness was achieved. The percentage of recovery per hour was calculated as a measure of endothelial function. Tear oxygen tension (PO(2)) beneath the hydrogels was measured in the open eye and after 5 minutes of eye closure to obtain estimates of Q(C). A change in corneal pH during eye closure while wearing the hydrogels was used as a measure of hypoxic acidosis. Associations between corneal swelling and endothelial cell density or corneal epithelial thickness were also tested. RESULTS: There were modest but significant (P < 0.05) correlations between thick-lens corneal swelling and thick-lens closed-eye PO(2) (r = -0.36); thin lens corneal swelling and thin-lens closed-eye and open-eye PO(2) (r = -0.40 and -0.39, respectively). Corneal swelling also increases with increasing Q(C) (r = + 0.29 to + 0.33). Corneal swelling was associated with the decrease in pH during lens wear (r = + 0.30 and + 0.20 for thick and thin lenses, respectively). Thick- and thin-lens corneal swelling was significantly associated with percentage of recovery per hour (r = -0.40 and -0.34, respectively). Multiple regression analysis of corneal swelling with PO(2) and percentage of recovery per hour suggested an additive effect, however the effects were not significant. There was a modest inverse association between corneal swelling and OESS, however there were no associations between corneal swelling and endothelial cell density or epithelial thickness. CONCLUSIONS: The variability in contact lens-induced corneal swelling is associated with both corneal metabolic activity (Q(C) and pH) and endothelial function (percentage of recovery per hour). Our interpretation is that individuals with larger Q(C) produce more lactic acid (i.e., more swelling) whereas stronger endothelial function resists swelling. The modest correlations, however, suggest that other factors also are involved in explaining the phenomenon of corneal swelling.

Acidosis↗

PubMed2006

Effects of acquired obesity on endothelial function in monozygotic twins.

OBJECTIVE: To determine whether acquired obesity or accompanying metabolic changes such as adiponectin deficiency, insulin resistance, dyslipidemia, or visceral fat are associated, independent of genetic influences, with endothelial dysfunction by studying young adult monozygotic (MZ) twin pairs discordant for obesity. RESEARCH METHODS AND PROCEDURES: Nine obesity-discordant (intra-pair difference in BMI, 3.8 to 10.1 kg/m(2)) and nine concordant (0 to 2.3 kg/m(2)) 24- to 27-year-old MZ twin pairs were identified from a population-based FinnTwin16-sample. Endothelial function was measured by blood flow responses to intrabrachial infusions of an endothelium-dependent (acetylcholine) and an endothelium-independent (sodium nitroprusside) vasodilator. Whole body insulin sensitivity was measured using the euglycemic insulin clamp technique, and forearm and body composition were measured with magnetic resonance imaging and DXA. In addition, serum levels of adiponectin, high-sensitivity C-reactive protein, and lipids were determined. RESULTS: The heavier co-twins of the discordant pairs had significantly lower whole body insulin sensitivity than the leaner co-twins. Blood flows/muscle volume during infusions of acetylcholine and sodium nitroprusside were not altered by obesity. However, intra-pair differences in serum adiponectin, intra-abdominal fat, and C-reactive protein were significantly correlated with those in endothelial function. Only the relationship between intra-pair differences in adiponectin and endothelial function persisted in multiple linear regression analysis. Obesity-concordant co-twins had comparable insulin sensitivity and endothelial function. DISCUSSION: In young adult MZ twins discordant for obesity, acquired adiponectin deficiency rather than obesity per se is an independent correlate of endothelial dysfunction.

Acetylcholine↗