SEARCH · PubMed Health

Results for “endothelial dysfunction”

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 865 records · Page 48Linked to original sources

PubMed2002

Systemic inflammation, endothelial dysfunction, dietary fatty acids and micronutrients as risk factors for stroke: a selective review.

As medicine moves into the 21st century, with added pressures of increasing costs and limited resources, successful reduction of the impact of stroke on the population will require shifting our emphasis away from treating end stages of generalized atherosclerosis and other underlying diseases to prevention of these diseases. However, before any potential interventions can be promoted with confidence, more needs to be known about the specific causes of stroke subtypes in various populations, especially potentially modifiable risk factors. In this selective review, we appraise current evidence on some markers of systemic inflammation (C-reactive protein), endothelial dysfunction (homocysteine, von Willebrand factor), dietary fatty acids and micronutrients as risk factors for stroke. Although a great deal of research into the role of these risk factors in cardiovascular diseases has been undertaken, little reliable information is available on their role in stroke, especially in the elderly. Evaluation of plasma fatty acids and specific antioxidants and micronutrients as well as markers of systemic inflammation, endothelial dysfunction (including C-reactive protein, homocysteine levels, von Willebrand factor, and paraoxonase activity) may prove to be valuable in the future determination of the risk of stroke.

Biomarkers↗

PubMed2003

[Investigation of von Willebrand-factor as a marker of endothelial dysfunction in atherosclerotic patients].

OBJECTIVE: To determine von Willebrand-factor activity as the marker of endothelium dysfunction in vascular diseases and to compare it to healthy controls. METHODS: von Willebrand-factor activity was determined by enzyme-linked immunosorbant assay (ELISA) in patients with acute coronary syndromes (29 patients, 67 +/- 13 years), acute stroke (15 pts, 67 +/- 12 years) on admission, 2nd and 6th day; and chronic vascular diseases (56 pts, 67 +/- 10 years) and was compared to the values of healthy controls (23 persons, 36 +/- 12 years). RESULTS: von Willebrand-factor activity was significantly (p < 0.001) higher in all the measured vascular patients than in the control group. The values of acute patients were significantly (p < 0.05-0.001) higher than those of patients with chronic vascular diseases. In the hospital phase von Willebrand-factor activity in acute patients increased continuously and on day 6 was significantly (p < 0.05-0.01) higher than on admission. von Willebrand-factor activity was significantly (p < 0.05) higher in troponin positive patients with acute coronary syndromes compared to the troponin negative subjects. CONCLUSIONS: von Willebrand-factor was found to be a suitable marker of endothelial dysfunction. The higher von Willebrand-factor activity in patients with vascular diseases compared to the control group can be caused by the endothelial dysfunction and extensive atherosclerosis. The significantly higher von Willebrand-factor activity in acute disorders suggests the more severe endothelium dysfunction and could be related to the development of acute event through increased platelet adhesion and aggregation.

Aged↗

PubMed1999

[Endothelial dysfunction--assessment of current status and approaches to therapy].

The vascular endothelium is the inner lining of all blood vessels and serves as an important autocrine and paracrine organ, that regulates vascular wall functions. Because of its strategic location between the circulating blood and the vascular wall, the endothelium interacts with cellular and neurohumoral mediators, thus controlling vascular contractile state and cellular composition. The vascular endothelium maintains vascular homeostasis by modulating blood vessel tone, by regulating local cellular growth and extracellular matrix deposition and by controlling hemostatic as well as inflammatory responses. One of the best characterized and most important substances released from the endothelium is nitric oxide (NO). NO is a soluble gas which is continuously synthesized from the amino acid L-arginine in endothelial cells by the constitutively expressed nitric oxide synthase. The most important stimuli represent physical factors such as shear stress and pulsatile stretching of the vessel wall as well as circulating and locally released vasoactive substances. The endothelium can be seen as a biosensor, reacting to a large variety of stimuli and therefore maintaining adequate NO release. A large number of risk factors for atherosclerosis including hypercholesterolemia, systemic hypertension, smoking and diabetes have been associated with impaired endothelial NO-mediated vasodilation. "Endothelial dysfunction" is an early marker of atherosclerosis and may be closely related to the disease process. In acute coronary syndromes dysfunctional endothelium may trigger the devastating event of plaque rupture by promoting adhesion of leukocytes, vasoconstriction, activation of platelets and thrombos formation. Atherosclerotic blood vessels are further characterized by activation through zytokines and expression of cellular adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and endothelial-leukocyte adhesion molecule-1 (E-Selectin). After adhesion to the endothelium mononuclear cells migrate to the subendothelial space to take up oxidized LDL, thus transforming into foam cells, a hall mark of early atherosclerotic lesions. A number of conditions including infection with Chlamydia pneumoniae may cause continuous activation of the endothelium and inflammation of the vessel wall. Continuous endothelial dysfunction and activation, caused by risk factors and infection, represent the basis for atherogenesis and acute coronary syndromes.

Coronary Artery Disease↗

PubMed2002

Association between plasma lipoprotein(a) and endothelial dysfunction in normocholesterolemic and non-diabetic patients with angiographically normal coronary arteries.

The present study was designed to examine whether elevated levels of lipoprotein(a) (Lp(a)) are related to the impairment of the endothelium-dependent vasoresponse to acetylcholine (ACh) in normocholesterolemic and non-diabetic human normal coronary arteries. ACh (30 microg) was injected into the left main coronary artery of 31 patients (serum low-density cholesterol <160mg/dl and fasting plasma glucose <126mg/dl) with angiographically normal coronary arteries, and the relation between diameter change and lipid levels was analyzed. The mean diameter change of all coronary segments examined (segments 6, 8, 11 and 13) was reduced by 14.6+/-26.5% in response to ACh, but increased by 23.3+/-6.0% in response to nitroglycerin, suggesting endothelial dysfunction in those arteries. The mean diameter change of the left anterior descending artery or left circumflex artery in each patient was negatively correlated only with the level of Lp(a). Stepwise multiple regression analysis also revealed that only Lp(a) among the lipids showed significant correlation with impaired vasodilation (p=0.033). These findings suggest that elevated levels of plasma Lp(a) might be a strong predictor of endothelial dysfunction in normocholesterolemic and non-diabetic subjects.

Acetylcholine↗

PubMed2003

[Urinary albumin excretion and noninvasive assessment of peripheral endothelial dysfunction with high-resolution ultrasound in type 2 diabetic subjects and nondiabetic controls].

BACKGROUND: Recent theory in pathogenesis of atherosclerosis has focused on the pathobiology of the artery wall including the emerging influence of the nitric oxide (NO) system on thrombogenicity and trigger mechanisms leading to morphologic changes culminating in the stenotic plaque. Therefore, diagnostic evaluation of disturbances in NO bioavailability might be of prognostic relevance regarding primary prevention of cardiovascular disease. Disturbances in NO production can be measured noninvasively with conventional high-resolution ultrasound. On the other hand, particularly in individuals with diabetes, microalbuminuria is thought to be associated with an increased risk of cardiovascular events. Thereby it is still unknown, whether an increase in renal albumin excretion can be regarded as an indicator of global endothelial dysfunction, or whether other partial functions such as the nitric oxide system might be disturbed earlier. PROBANDS AND METHODS: Therefore, the NO system and renal albumin excretion were examined in 129 subjects (56 with type 2 diabetes and 73 nondiabetics). Nitric oxide production was assessed by measuring flow-mediated vasodilatation (FMD) of the brachial artery using a 13-MHz linear array. Comparison was done between subjects with disturbed endothelial NO production (FMD < 5%) and subjects with normal regulation of the vascular tone (FMD > 5%). RESULTS: In normoalbuminuric individuals (< 20 microg/min, and < 20 mg/l, respectively), neither for the group of subjects with type 2 diabetes nor in the group of nondiabetics, relevant differences could be found in renal albumin excretion (RAE) rate between subjects with disturbed and normal FMD (RAE in diabetics 4.8 +/- 5.5 vs. 4.6 +/- 5.1 mg/l and in nondiabetics 5.1 +/- 2.6 vs. 4.9 +/- 2.7 microg/min). Both groups were well balanced regarding other risk factors of the metabolic syndrome (systolic/diastolic blood pressure, glucose and lipid metabolism). Furthermore, comparison of FMD in subjects with microalbuminuria (20-200 microg/min and 20-200 mg/l, respectively, n = 18) versus normoalbuminuric individuals (n = 111) again did not reveal a significant difference for the diabetic group (FMD median 4.3% [range 1.8-7.6%] vs. 5.0% [range 1.1-9.1%]) nor for the nondiabetic group (FMD median 4.7% [range 3.1-13.3%] vs. 5.2% [range -1.2-31.6%]). However, this analysis underlined the considerable influence of the classic cardiovascular risk factors. Particularly in the nondiabetic group, individuals with microalbuminuria showed higher blood pressure (p = 0.05) and a higher body mass index (p < 0.01). CONCLUSION: From these results, it is concluded that both procedures (renal albumin excretion rate and the measurement of endothelium-dependent vasodilatation) investigate two independent disturbances of the vascular wall. Furthermore, these results lead to the hypothesis that disturbances in endothelial NO production occur early and may already be operative before renal albumin excretion increases. Thus, for the purpose of actually identifying cardiovascular high-risk subjects early, peripheral endothelial dysfunction should be measured in addition to renal albumin excretion rate.

Adolescent↗

PubMed2004

Endothelial dysfunction and altered bradykinin response due to oxidative stress induced by serum deprivation in the bovine cerebral artery.

Oxidative stress plays a critical role in the pathogenesis of vasospasm after a subarachnoid hemorrhage. We demonstrate that 24-h incubation of the isolated bovine middle cerebral arteries in the serum-free media at 37 degrees C converted the response to bradykinin from relaxation to contraction, in a manner sensitive to free radical scavengers. In the freshly prepared strips, bradykinin induced an endothelium-dependent relaxation, while having no direct effect on the smooth muscle. However, in the strips treated in serum-free media, bradykinin failed to induce endothelium-dependent relaxation, but did demonstrate a direct contractile effect on smooth muscle. The addition of superoxide dismutase and ascorbic acid or 5% serum during the 24-h incubation in the serum-free media prevented the loss of endothelium-dependent relaxation and the development of a contractile response to bradykinin. SB203580 (4-(4-Fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole), a p38 mitogen-activated protein kinase inhibitor, and genistein (4',5,7-Trihydroxyisoflavone), a tyrosine kinase inhibitor, also demonstrated a similar preventive effect. In conclusion, serum-deprivation induced endothelial dysfunction and the responsiveness of smooth muscle to bradykinin due to failure of eliminating oxidative stress. p38 mitogen-activated protein kinase and tyrosine kinase were suggested to play a critical role in this endothelial dysfunction.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2000

Endothelial dysfunction and peroxynitrite formation are early events in angiotensin-induced cardiovascular disorders.

Angiotensin II (ANG II) is a well-established participant in many cardiovascular disorders, but the mechanisms involved are not clear. Vascular cell experiments suggest that ANG II is a potent stimulator of free radicals such as superoxide anion, an agent known to inactivate nitric oxide and promote the formation of peroxynitrite. Here we hypothesized that ANG II reduces the efficacy of NO-mediated vascular relaxation and promotes vascular peroxynitrite formation in vivo. ANG II was infused in rats at sub-pressor doses for 3 days. Systolic blood pressure and heart rate were unchanged on day 3 despite significant reductions in plasma renin activity. Thoracic aorta was isolated for functional and immunohistochemical evaluations. No difference in isolated vascular contractile responses to KCI (125 mM), phenylephrine, or ANG II was observed between groups. In contrast, relaxant response to acetylcholine (ACh) was decreased sixfold without a change in relaxant response to sodium nitroprusside. Extensive prevalence of 3-nitrotyrosine (3-NT, a stable biomarker of tissue peroxynitrite formation) immunoreactivity was observed in ANG II-treated vascular tissues and was specifically confined to the endothelium. Digital image analysis demonstrated a significant inverse correlation between ACh relaxant response and 3-NT immunoreactivity. These data demonstrate that ANG II selectively modifies vascular NO control at sub-pressor exposures in vivo. Thus, endothelial dysfunction apparently precedes other established ANG II-induced vascular pathologies, and this may be mediated by peroxynitrite formation in vivo. Wattanapitayakul, S., Weinstein, D. M., Holycross, B. J., Bauer, J. A. Endothelial dysfunction and peroxynitrite formation are early events in angiotensin-induced cardiovascular disorders.

Acetylcholine↗

PubMed2006

Gonadectomy prevents endothelial dysfunction in fructose-fed male rats, a factor contributing to the development of hypertension.

Insulin resistance has been shown to be associated with increased blood pressure (BP). The sex hormones estrogen and testosterone have opposing effects in the development of increased BP. Since testosterone has been implicated in increased BP following insulin resistance, we have tried to dissect out the effects of insulin resistance on endothelium-dependent vasorelaxation in the presence and absence of testosterone. Both gonadectomized and sham-operated male Wistar rats fed with a high-fructose diet developed insulin resistance, but BP increased only in the sham-operated rats. Reintroduction of testosterone in vivo restored the increase in BP, thereby abolishing the protective effects of gonadectomy. Fructose feeding did not affect plasma testosterone levels. Insulin resistance induced endothelial dysfunction in the mesenteric arteries of sham-operated rats, which was prevented by gonadectomy, thus suggesting a key role for testosterone in the pathogenesis of secondary vascular complications. Subsequent to blocking the actions of endothelium-dependent hyperpolarizing factor (EDHF), relaxation to acetylcholine (ACh) was lower in sham-operated fructose-fed rats compared with other groups, suggesting the involvement of nitric oxide (NO) in vasorelaxation. Inhibition of NO synthesis nearly abolished the ACh-evoked relaxation in both fructose-fed groups, thus suggesting a testosterone-independent impairment of EDHF-mediated relaxation. The improvement in endothelial function following gonadectomy could be ascribed to a NO component, although plasma nitrite and nitrate levels were unchanged. In summary, testosterone is essential in vivo for the development of endothelial dysfunction and hypertension secondary to insulin resistance, suggesting a facilitatory role for testosterone in increasing BP in fructose-fed male rats.

Acetylcholine↗

PubMed2003

Dietary L-arginine restores aspirin-induced endothelial dysfunction in rat aorta.

L-Arginine induced elevation of the vascular prostanoid led us to think that the risk of coronary spasm may increase in L-arginine consumers when they are subjected to cyclooxygenase inhibitors and this limits the therapeutic value of aspirin. So the aim was to investigate the interaction of aspirin and dietary L-arginine in male rats. Animals were divided into four groups and fed with normal food. The first group received tap water while the second, third and fourth groups were subjected daily to aspirin (8.6 mg/kg), L-arginine (143 mg/kg) and aspirin + L-arginine combination in their drinking water respectively for 7 days. Vasomotor responses were recorded in the aortic rings suspended for isometric-force recordings. Aspirin treatment significantly reduced the dilation to acetylcholine and sodium nitroprusside. Attenuated phenylephrine contractility was associated with normal acetylcholine response in L-arginine group. Addition of L-arginine to aspirin treatment completely prevented aspirin-induced endothelial dysfunction but defective response to sodium nitroprusside persisted. Dietary L-arginine without affecting maximal dilation to acetylcholine significantly increased the share of dilator prostanoid which appears to resist aspirin. These results demonstrated that dietary L-arginine increases dilator prostaoid in rat aortic rings. Contrary to our expectation, co-administered L-arginine protected aspirin induced endothelial dysfunction and ruled out the limitation of aspirin use in L-arginine consumers.

Acetylcholine↗

PubMed2004

Inhibition of diet-induced atherosclerosis and endothelial dysfunction in apolipoprotein E/angiotensin II type 1A receptor double-knockout mice.

BACKGROUND: Angiotensin II type 1 (AT1) receptor activation is potentially involved in the multifactorial pathogenesis of atherosclerosis. METHODS AND RESULTS: Apolipoprotein E-deficient (ApoE-/-) mice were crossed with AT1A receptor-deficient (AT1-/-) mice to obtain homozygous double-knockout animals (ApoE-/--AT1-/- mice). Wild-type (C57BL/6J), ApoE-/-, AT1-/-, and ApoE-/--AT1-/- mice were fed a high-cholesterol diet for 7 weeks. In contrast to wild-type and AT1-/- mice, this treatment led to severe atherosclerotic lesion formation in the aortic sinus and the aorta (oil red O staining) and to an impaired endothelium-dependent vasodilation (organ chamber experiments with isolated aortic segments) in ApoE-/- mice. In the age-matched ApoE-/--AT1-/- littermates, development of diet-induced endothelial dysfunction and atherosclerotic lesion formation was profoundly inhibited. Concomitantly, aortic release of superoxide radicals was increased 2-fold in ApoE-/- mice compared with wild-type animals, whereas aortic superoxide production was normalized in ApoE-/--AT1-/- mice (L-012 chemiluminescence). There were no significant differences in plasma cholesterol levels between ApoE-/- and ApoE-/--AT1-/- animals. Systolic blood pressure was significantly lower in ApoE-/--AT1-/- animals than in ApoE-/- mice (tail-cuff measurements). Oral treatment of ApoE-/- mice with either hydralazine or irbesartan reduced systolic blood pressure to the same level; however, only AT1 receptor antagonist treatment reduced atherosclerotic lesion formation and improved endothelial function. CONCLUSIONS: Genetic disruption of the AT1A receptor leads to inhibition of vascular oxidative stress, endothelial dysfunction, and atherosclerotic lesion formation in ApoE-/- mice irrespective of blood pressure and plasma cholesterol levels. These results indicate a fundamental role of AT1 receptor activation in atherogenesis.

Angiotensin II Type 1 Receptor Blockers↗

PubMed1992

Cardioprotection and attenuation of endothelial dysfunction by organic nitric oxide donors in myocardial ischemia-reperfusion.

The effects of two nitric oxide (NO) donors were evaluated in a 6-h model of feline myocardial ischemia-reperfusion. After 80 min of a 90-min ischemic period, SIN-1 or C87-3754 or their respective controls (i.e., 0.9% NaCl or C88-3934, a control compound which does not release NO) were given i.v. as a bolus (0.1 mg/kg) and infused at 1 mg/kg/h for the entire 4.5-h reperfusion period. Administration of the active NO donors significantly decreased the necrotic area/area-at-risk ratio from 29 +/- 3% in the vehicle group to 9 +/- 2 and 11 +/- 5% in the SIN-1 and C87-3754 groups, respectively (P less than .001). The inactive NO donor C88-3934 failed to reduce infarct size (31 +/- 3%). Neither NO donor reduced the accumulation of neutrophils in the necrotic area when compared to their respective control groups, but both agents significantly attenuated coronary endothelial dysfunction as shown by a vasorelaxation to acetylcholine of 62 +/- 2 and 64 +/- 3% in the SIN-1- and C87-3754-treated arteries, as compared to only a 27 +/- 3 and 34 +/- 4% vasorelaxation in the vehicle and inactive NO donor groups, respectively (P less than .001). Our studies show that SIN-1 and C87-3754 exert beneficial effects in a 6-h model of myocardial ischemia-reperfusion. Both NO donors decreased myocardial necrosis and decreased the reperfusion-induced endothelial dysfunction without significantly altering the pressure-rate index (i.e., an index of myocardial oxygen demand).

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2005

Attenuation of endothelial dysfunction by exercise training in STZ-induced diabetic rats.

The protective effects of exercise training on the diabetic-induced endothelial cell (EC) dysfunction were determined using intravital fluorescent microscopy. Male Sprague-Dawley rats were divided into three groups of control (Con), diabetes (DM), and diabetes with exercise--training (DM+Ex). Diabetes was induced by single intravenous injection of streptozotocin (STZ; 50 mg/kg BW). The exercise training protocol consisted of treadmill running, 5 times/week with the velocity of 13-15 m/min, 30 min/day periods for 12 and 24 weeks (wks). 24 wks after the STZ injection, blood glucose (BG), glycosylated hemoglobin (HbA1C), mean arterial blood pressure (MAP) and heart weight (HW) were significantly higher in DM rats (p < 0.001). However, DM+Ex rats had reduced the abnormalities of MAP (p < 0.01) and HW (p < 0.05) compared with DM rats. Furthermore, there was a significant decrease in heart rate (HR) of DM+Ex rats (p < 0.05) relative to Con rats. To examine the influence of exercise training on EC dysfunction, leukocyte-EC interactions in mesenteric venules and vascular reactivity responses to vasodilators in mesenteric arterioles were monitored by using intravital fluorescence microscopy. The diabetic state enhanced leukocyte adhesion in mesenteric postcapillary venules (p < 0.001). Moreover, an impaired vasodilatory response to the EC-dependent vasodilator, acetylcholine (Ach), not to sodium nitroprusside (SNP), was found in 12- and 24-wk diabetic rats (p < 0.01). The leukocyte adhesion and the impairment of EC-dependent vasodilation to Ach were attenuated by exercise training (p < 0.05). In addition, exercise training was also shown to have favorable preventive effects on hyperglycemia induced oxidative stress, as lower malondialdehyde (MDA) levels were observed from both groups of 12 and 24 weeks DM+Ex compared with DM (p < 0.01). In conclusion, our findings indicate that the endothelial dysfunction of diabetic rats could be characterized by increased leukocyte adhesion and impaired endothelium-dependent relaxation. Regular low intensity exercise training could improve both indices of endothelial dysfunction through amelioration of diabetic-induced oxidant/antioxidant levels. These findings support the notion that regular exercise training could be a fundamental form of therapy in preventing diabetic cardiovascular complications potentiated by endothelial dysfunction.

Acetylcholine↗

PubMed2005

Reduced vascular remodeling, endothelial dysfunction, and oxidative stress in resistance arteries of angiotensin II-infused macrophage colony-stimulating factor-deficient mice: evidence for a role in inflammation in angiotensin-induced vascular injury.

OBJECTIVE: Angiotensin (Ang) II-induced vascular damage may be partially mediated by reactive oxygen species generation and inflammation. Homozygous osteopetrotic mice (Op/Op), deficient in macrophage colony-stimulating factor (m-CSF), exhibit reduced inflammation. We therefore investigated Ang II effects on vascular structure, function, and oxidant stress generation in this model. METHODS AND RESULTS: Adult Op/Op, heterozygous (Op/+), and wild type (+/+) mice underwent 14-day Ang II (1000 ng/kg per minute) or saline infusion. Blood pressure (BP) was assessed by radiotelemetry, mesenteric resistance artery vascular reactivity was studied on a pressurized myograph, and vascular superoxide and NAD(P)H oxidase activity by lucigenin chemiluminescence. Ang II increased BP in Op/+ and +/+ mice but not in Op/Op. Ang II-treated Op/+ and +/+ mice showed reduced acetylcholine-mediated relaxation (maximal relaxation, respectively, 64% and 67% versus 84% and 93% in respective controls; P<0.05), which was unaffected by L-NAME. Ang II-infused Op/Op mice arteries showed significantly less endothelial dysfunction than vehicle-infused counterparts (maximal relaxation 87% versus 96% in shams). Resistance arteries from Ang II-infused +/+ and Op/+ mice had significantly increased media-to-lumen ratio and media thickness, neither of which was altered in Op/Op mice compared with untreated littermates. Vascular media cross-sectional area, NAD(P)H oxidase activity and expression, and vascular cell adhesion molecule (VCAM)-1 expression were significantly increased by Ang II only in +/+ mice (P<0.05). CONCLUSIONS: m-CSF-deficient mice (Op/Op) developed less endothelial dysfunction, vascular remodeling, and oxidative stress induced by Ang II than +/+ littermates, suggesting a critical role of m-CSF and proinflammatory mediators in Ang II-induced vascular injury.

Angiotensin II↗

PubMed2003

A video lesson series is effective in changing the dietary intakes and food-related behaviors of low-income homemakers.

OBJECTIVE: To examine the relative cost-effectiveness of a self-administered video series in delivering nutrition education to low-income homemakers. DESIGN: A quasi-experimental design was used, with subjects randomly assigned to traditional lessons (Traditional Group) or video lessons (Video Group). SUBJECTS/SETTING: 108 subjects were recruited, with 93 nonpregnant, low-income, female homemakers completing the study (response rate = 86%). Subjects had recently enrolled in the Expanded Food and Nutrition Education Program, or the Food Stamp Nutrition Education Program, and had a videocassette recorder and telephone. INTERVENTION: Both groups received 12 lessons from the Eating Right Is Basic Series, 3rd edition, with the Traditional Group being taught in face-to-face sessions and the Video Group receiving self-administered, video-lesson packets. OUTCOME MEASURES: Dietary intake and food behaviors were assessed at pre and post intervention with 24-hour recalls and a 14-item checklist. STATISTICAL ANALYSES: Chi(2) and t tests were used to compare the groups on demographics and pre-intervention dietary factors. Multiple analysis of variance was used for comparisons of change from pre to post intervention. RESULTS: Significant improvements were observed in both groups for fruits, calcium, and vitamins A and C. The Video Group improved on fiber intake (P<or=.005). The groups did not differ on dietary or behavior change (P=.2357). Duplication and implementation costs of the video series totaled 4,820 dollars, or 36% of the traditional lesson cost of 13,463 dollars. APPLICATIONS: Both methods achieved similar improvements in diet and behaviors, but the video method was less expensive. The video series seems to be a cost-effective method for delivering nutrition education to low-income homemakers.

Adolescent↗

PubMed2006

[Effects of simvastatin on homocysteine-induced endothelial dysfunction and inflammatory response].

OBJECTIVE: To investigate the effects of simvastatin (SIM) on homocysteine (HCY)-induced endothelial dysfunction and inflammatory response. METHODS: Human umbilical vein endothelial cells (HUVECs) were isolated from the umbilical cords from healthy lying-in women and cultured and added with HCY of the concentrations of 0.1, 0.25, 0.5, and 1 mmol/L respectively, or HCY 0.25 mmol/L + SIM of the concentrations of 1, 10 and 20 micromol/L respectively for 1 hour. ELISA was used to detect the cell viability with MTT method. Western blotting was used to examine the protein expression of the cell inflammatory factors, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, macrophage chemoattractant protein (MCP)-1, and intercellular adhesion molecule (ICAM)-1, ELISA was used to detect the contents of the cell inflammatory factors. RESULTS: HCY of different doses inhibited the viability of HUVECs dose-dependently (all P < 0. 01). The survival rates of the HCY-induced HUVECs pretreatment by SIM of the concentrations of 1, 10 and 20 micromol/L for 1 hour were 1.72 +/- 0.03 times, 2.54 +/- 0.09 times, and 3.14 +/- 0.11 times respectively that of the control group (all P < 0. 01). HCY of different concentration of 0.25 mmol/L increased the protein expression of TNF-alpha, IL-6, MCP-1, and ICAM-1 significantly; however, the expression levels of TNF-alpha, IL-6, MCP-1, and ICAM-1 of the 0.25 mmol/L HCY-treated HUVECs that were pretreated by SIM of the concentration of 10 micromol/L for 1 hour were, 0.23 +/- 0.05, 0.14 +/- 0.03, 0.13 +/- 0.04, and 0.21 +/- 0.07 respectively, not significantly different from those at the time of 0 hour (all P > 0.05). CONCLUSION: Simvastatin inhibits the homocysteine-induced endothelial impairment and inflammatory response.

Cells, Cultured↗

PubMed2001

[Influence of experience on intra- and interindividual variability in assessing peripheral endothelial dysfunction with high resolution ultrasound].

UNLABELLED: The non-invasive evaluation of endothelial dysfunction with high-resolution ultrasound has become a widely accepted tool in determination of high-risk subjects for early atherosclerosis. Furthermore it is often used as intermediate outcome in intervention studies. AIM: We examined the influence of examiner experience on intra- and inter-individual variability in the measurement of flow-associated vasodilation (FAD) independent of automated analysis systems. METHOD: FAD was measured on two occasions in 7 and 8 subjects respectively (mean age 32 +/- 3 years) by two investigators after different prior training procedures with a 13 MHz linear transducer (LA14A, ESAOTE Biomedica). RESULTS: The intra-individual variability expressed as median absolute difference in the measurements of FAD was 1.1 % (range from 0.03 % to 3.2 %) for examiner one with an experience of more than 50 FAD measurements through former studies and 2.9 % (range from 1.6 % to 9.2 %) for examiner two with only 10 training examinations under supervision. By a further training period of two months, with an increase of examinations of additional 20 measurements by both examiners, the intra-observer variability could be dropped to 0.9 % (range from 0.03 % to 1.3 %) for examiner two (p = 0.0025) with no significant change for examiner one (median 0.6 % with a range from 0.14 % to 3.7 %). As expected, the inter-individual variability was not influenced by this further training (median 1.0 % with a range of 0.5 % to 3.6 % versus a median of 1.6 % with a range from 0.15 % to 7.5 %). CONCLUSION: 30 training measurements of FAD under supervision should be regarded as minimum requirement for valid determination of endothelial function. The reachable result for the intra-observer variability is thereby within the range of computed analysis systems.

Adult↗

PubMed1997

Coronary endothelial dysfunction precedes heart failure and reduction of coronary reserve in awake dogs.

Endothelial dysfunction in coronary circulation is well documented in heart failure (HF). However, whether this dysfunction is a consequence of heart failure or precedes the development of HF remains unknown. To determine endothelium-dependent regulation in the remote coronary vasculature in a canine coronary microembolization-induced HF model, seven dogs were chronically instrumented for measurement of systemic hemodynamics, for selective coronary microembolization via an implanted coronary catheter and for measurement of coronary blood flow in the non-embolized coronary artery. Microembolizations were performed daily until hemodynamic and echocardiographic measurements showed HF. The responses of coronary blood flow to acetylcholine (0.25, 0.5, 5, 10 microg/kg), nitroglycerin (0.2, 0.8, 5, 25 microg/kg), adenosine (0.25, 0.5, 2, 5 micromol/kg) and brief coronary occlusions (5, 10, 15, 20, 30 s) were examined. Although no signs of HF developed and the responses of coronary blood flow to nitroglycerin, adenosine and occlusions were not altered, the response to acetylcholine was selectively reduced after 1 week of embolization (275,000+/-55,000 microspheres). Resting coronary flow increased from 21.3+/-1.4 ml/min in control state to 27.7+3.5 ml/min (P<0.001). As HF developed, characterized by an elevated left ventricular end-diastolic pressure (6.4+/-1.6 v 16+/-1.6 mmHg, P<0.001), a decreased area ejection fraction (54+/-5 v 36+/-5%, P<0.05) and a reduced beta-adrenergic response to isoproterenol, the responses of coronary blood flow to acetylcholine, nitroglycerine, adenosine and occlusions were consistently depressed. Resting coronary blood flow was decreased to 15.4+/-2.7 ml/min (P<0.01). Our results indicate, that there is a selectively impaired endothelium-mediated dilator capacity of the resistance coronary vasculature before the development of HF and a reduction of the coronary flow reserve.

Acetylcholine↗

PubMed2005

Exercise as an alternative to oral estrogen for amelioration of endothelial dysfunction in postmenopausal women.

BACKGROUND: Both exercise and postmenopausal estrogen therapy augment endothelial function. We hypothesized that their interaction would be additive. The study objectives were to determine in postmenopausal women (1) the effects of an acute bout of exercise on brachial artery endothelium-dependent flow-mediated vasodilation (FMD), (2) whether these responses to exercise are augmented by concurrent estrogen treatment, and (3) whether these 2 interventions, independently or together, achieve FMD values observed in premenopausal women. METHODS: In postmenopausal women (n = 13; age 54 +/- 2 [mean +/- SE] years), FMD was quantified during supine rest and again 60 minutes after treadmill exercise for 45 minutes at 60% V* O2max. Subjects were studied twice: before and after 4 weeks of oral estradiol. To obtain reference normal values, FMD was determined concurrently in 14 premenopausal (28 +/- 1 years) women under identical basal conditions. RESULTS: Flow-mediated vasodilation in postmenopausal women, markedly impaired when compared with premenopausal women (5.3% +/- 0.5% vs 12.1% +/- 1.5%, P < .01), was significantly increased by exercise (to 9.9% +/- 0.6%, P < .01). In contrast, after estrogen, FMD was augmented at rest (P < .01) but was not further enhanced after exercise (11.5% +/- 0.6% vs 9.9% +/- 0.5%, P = .3). Both interventions increased, independently, FMD to values in premenopausal women (P > .05). CONCLUSIONS: In postmenopausal women, both acute exercise and estrogen therapy normalize FMD. However, their effects are not additive, possibly because of redundancy of nitric oxide signaling pathways activated by these 2 interventions. When considered in the context of recent trials with adverse cardiovascular outcomes, these results reinforce the therapeutic potential of exercise as an alternative nonpharmacological intervention to estrogen in postmenopausal women with endothelial dysfunction.

Administration, Oral↗