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Results for “Endothelial function”

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PubMed2000

Effects of red ginseng upon vascular endothelial function in patients with essential hypertension.

This study is to estimate the effect of Korean red ginseng on vascular endothelial cell dysfunction in patients with hypertension. Seventeen patients with hypertension who were divided into ginseng-treated (7) and non-treated (10) groups and 10 normotensive subjects were included. To assess the function of the vascular endothelial cell, changes of forearm blood flow to infusion of acetylcholine, sodium nitroprusside and bradykinin in incremental doses were measured by venous occlusion plethysmography. In the ginseng-treated hypertensive group, forearm blood flows at the highest dose of acetylcholine and bradykinin were significantly higher than those of the non-treated hypertensive group and were not different from those of the control group. In the case of sodium nitroprusside infusion, no significant differences were observed between the control, non-treated and treated groups. In conclusion, Korean red ginseng can improve the vascular endothelial dysfunction in patients with hypertension possibly through increasing synthesis of nitric oxide.

Acetylcholine↗

PubMed2004

Traction injury during minimally invasive harvesting of the saphenous vein is associated with impaired endothelial function.

OBJECTIVE: Many methods of minimally invasive surgical harvesting of the great saphenous vein have been developed because of the morbidity related to the long skin incision after traditional (open) great saphenous vein harvesting. One such method involves the use of multiple small incisions separated by 10- to 15-cm skin bridges through which the saphenous vein is harvested. We hypothesized that this method of saphenous vein harvesting might subject the saphenous vein to considerable traction forces, resulting in impaired endothelial cell function. METHODS: Four-millimeter great saphenous vein segments were obtained from patients undergoing elective coronary artery bypass graft surgery. Group A (minimally invasive surgery) consisted of 23 rings from 20 patients (age, 65.8 +/- 11.1 years, mean +/- SD). Group B (open harvesting) consisted of 33 rings from 8 patients (age, 69.8 +/- 8.6 years). All great saphenous vein segments were undistended and were used within 24 hours of harvesting. Isometric tension experiments were performed on each ring of the great saphenous vein by using a force-displacement transducer to measure the force of contraction in grams. Measurements included developed force after exposure to high-potassium depolarizing solution and 50 micromol/L phenylephrine and decrease in force of contraction (relaxation) after exposure to 1 and 10 micromol/L acetylcholine. RESULTS: There were no differences between the minimally invasive surgery and open harvesting groups in their responses to high-potassium depolarizing solution or phenylephrine: high-potassium depolarizing solution, contractions of 4.26 +/- 0.72 g (mean +/- SEM) and 3.95 +/- 0.38 g, respectively (P =.70); phenylephrine, contractions of 3.49 +/- 0.63 g and 2.73 +/- 0.39 g, respectively (P =.41). There was no net relaxation in segments from the minimally invasive surgery group after exposure to 1.0 or 10 micromol/L acetylcholine. In contrast, rings from the open harvesting group demonstrated relaxation of -0.41 +/- 0.07 g and -0.32 +/- 0.09 g after exposure to 1.0 and 10 micromol/L acetylcholine, respectively. CONCLUSIONS: In undistended saphenous vein segments isolated from patients undergoing minimally invasive surgical and open techniques of harvesting, there was no acetylcholine-mediated endothelium-dependent relaxation in the minimally invasive surgery group. Therefore harvesting of the great saphenous vein through multiple small incisions might result in endothelial dysfunction, possibly caused by traction injury.

Aged↗

PubMed1994

Chronic inhibition of nitric oxide production accelerates neointima formation and impairs endothelial function in hypercholesterolemic rabbits.

To determine if endogenous local levels of nitric oxide (NO) modulate atherogenesis, we studied the effect of inhibiting NO with NG-nitro-L-arginine methyl ester (L-NAME) on early neointima formation in cholesterol-fed rabbits. Male rabbits were fed for 5 weeks with a 0.5% cholesterol diet alone or treated in addition during the last 4 weeks with L-NAME (12 mg/kg per day SC) via osmotic minipump. Endothelial cell function was assessed in isolated aortic rings by vascular reactivity and levels of cyclic GMP. In L-NAME-treated rabbits there was inhibition of endothelium-dependent relaxations to acetylcholine and the calcium ionophore A23187 as well as impaired cyclic GMP accumulation in response to acetylcholine. Neointima formation in the ascending thoracic aorta was assessed by determining media and intima cross-sectional areas with computerized image analysis. Compared with rabbits that consumed the cholesterol diet alone, L-NAME-treated rabbits had significant increases in lesion area (0.29 +/- 0.04 versus 0.15 +/- 0.03 mm2) and in lesion/media ratio (0.06 +/- 0.01 versus 0.03 +/- 0.01). Plasma levels of cholesterol and fluorescent lipid peroxide products were unchanged, suggesting no difference in cholesterol metabolism or oxidation. Because arterial blood pressure was not altered by L-NAME treatment, the increased atherogenesis could not be attributed to an increase in blood pressure. These results indicated that local inhibition of NO accelerates early neointima formation possibly because of modulating monocyte recruitment or foam cell lipid accumulation.

Amino Acid Oxidoreductases↗

PubMed1989

Normal endothelial function and decreased vasoreactivity of experimental arterial grafts.

During autogenous vascular grafting endothelial cell damage inevitably occurs. In this study we examined the functional and morphologic integrity of experimental arterial grafts. The right external iliac artery was grafted into the right carotid artery of 12 male New Zealand white rabbits. The left external iliac artery was used as the control artery. Four weeks after surgery, isometric tension studies were performed on rings of control artery and arterial graft. Control arteries and arterial grafts precontracted with norepinephrine demonstrated endothelium-dependent relaxation of 28.3% +/- 5.6% and 16.1% +/- 1.7%, respectively, in response to acetylcholine (5 x 10(-6) mol/L). Both control arteries and arterial grafts contracted in response to norepinephrine, histamine, and serotonin. The median effective dose (ED50) of norepinephrine was 4.1 +/- 1.3 x 10(-7) mol/L for control arteries and 62.1 +/- 17.9 x 10(-7) mol/L for arterial grafts (p less than 0.005). Similarly, arterial grafts were less sensitive to histamine; the ED50 of histamine for control arteries was 4.6 +/- 1.3 x 10(-7) mol/L and 51.4 +/- 13.0 x -7 mol/L for arterial grafts (p less than 0.005). In contrast, reactivity to serotonin was unaltered. The ED50 was 4.1 +/- 1.3 x 10(-7) mol/L for control arteries and 4.5 +/- 1.3 x 10(-7) mol/L for arterial grafts. Scanning and transmission electron microscopy revealed a largely intact endothelial surface. These data are markedly different from our previous findings with vein grafts in which serotonin supersensitivity was associated with an absence of endothelium-mediated relaxation to acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed2003

Abnormal coronary microvascular endothelial function in humans with asymptomatic left ventricular dysfunction.

BACKGROUND: Coronary endothelial dysfunction may potentially lead to myocardial ischemia and to the progression of heart failure. Though endothelial dysfunction is associated with advanced heart failure in humans, relatively little is known regarding their temporal relationship. Thus, the current study was designed to test the hypothesis that coronary endothelial dysfunction is present in patients with asymptomatic left ventricular dysfunction. METHODS AND RESULTS: Three hundred patients without symptoms of heart failure, with normal or mildly diseased coronary arteries at angiography underwent coronary vascular reactivity evaluation using intracoronary adenosine, acetylcholine (ACH) and nitroglycerin. Patients were divided into 2 groups based on the left ventricular ejection fraction (EF): patients with asymptomatic left ventricular dysfunction (ALVD), EF <45% (n = 11); and patients with EF > or =45% (n = 289, controls). Except for a lower high-density lipoprotein level in patients with ALVD, there were no significant differences between the groups in regards to conventional cardiovascular risk factors. There was no difference in the change (mean +/- SE) in epicardial diameter in response to ACH (-21.7% +/- 7.2% vs -13.8% +/- 1.5%, P =.3). The change in coronary blood flow in response to ACH was significantly attenuated in the patients with ALVD when compared to the controls (-18.5% +/- 14.9% vs 74.0% +/- 7.2%, P <.013). By multivariate analysis, EF was an independent predictor of coronary microvascular dilation with ACH (P <.001). CONCLUSION: The current study demonstrates that coronary microvascular endothelial dysfunction is present in ALVD. Thus, coronary endothelial dysfunction may be an early event in the pathophysiology of heart failure.

Adult↗

PubMed2000

Abnormalities of endothelial function in the pathogenesis of stroke: the importance of endothelin.

Endothelial cells play a key role in the local regulation of the vascular smooth muscle tone by producing and releasing relaxing and contracting factors. Endothelin (ET)-1, one of the most potent endogenous vasoconstrictor substances known, is produced by endothelial cells. In the cerebral vasculature ET-1 is thought to be involved in several pathological conditions, including vasospasm following subarachnoid hemorrhage and stroke. This review contains evidence suggesting that endothelial dysfunction may contribute to the development of ischemic stroke and discusses the current knowledge concerning the role of ET-1 in the pathogenesis of stroke in animal models and in humans.

Animals↗

PubMed2002

Noninvasive study of endothelial function in white coat hypertension.

Several studies have demonstrated that endothelial dysfunction is present in patients with essential hypertension. However, the presence of endothelial dysfunction in patients with white coat hypertension has not been studied. We evaluated the variation in the diameter of the brachial artery produced by flow-mediated dilation after a mechanical stimulus in patients with recently diagnosed mild to moderate sustained essential hypertension compared with patients with white coat hypertension. A total of 29 patients fulfilled inclusion criteria; 15 healthy volunteers were also included. After 24-hour ambulatory blood pressure monitoring, 15 patients were classified with sustained essential hypertension; 14 patients with white coat hypertension. Vascular ultrasound scans were performed according to the method described by Celermajer et al, with modification for noninvasive determination of endothelial dysfunction. Basal brachial artery diameter did not differ significantly among the 3 groups. Changes in arterial diameter 60 seconds after cuff deflation were higher in the control group compared with both hypertensive groups, but no significant differences were found between the sustained essential hypertension group and the white coat hypertension group. Flow-mediated dilation was similar in white coat hypertensives and sustained essential hypertensives. The presence of endothelial dysfunction in subjects with white coat hypertension suggests that it should not be considered a harmless trait and that white coat hypertension has common features with sustained essential hypertension.

Adult↗

PubMed1997

Endothelial function and the kidney. An emerging target for cardiovascular therapy.

Endothelial dysfunction is emerging as an important factor in the early development of acute and chronic renal disease. Drugs aimed specifically at rectifying this aberration are being developed, although other established agents such as calcium antagonists, angiotensin converting enzyme (ACE) inhibitors and HMG CoA reductase inhibitors also have beneficial effects in this setting. Calcium antagonists are particularly effective at ameliorating acute renal ischaemia associated with endothelial dysfunction. Combination therapy with a calcium antagonist and an ACE inhibitor might optimise the beneficial effects of calcium channel blockade on the sequelae of endothelial dysfunction in chronic renal failure.

Angiotensin-Converting Enzyme Inhibitors↗

PubMedDate not supplied

[Endothelial function and the microcirculation in diabetes mellitus].

The role of endothelial dysfunction in the pathogenesis of diabetic microangiopathy is reviewed. Reversible alterations in microcirculation, consisting of increased capillary pressure, blood flow and endothelial permeability, can be detected at an early stage in diabetes mellitus. Irreversible structural modifications of the vascular wall, such as thickening of the basal membrane due to the extracellular accumulation of proteins, take place at later stages. Atherosclerosis further affects microcirculation in diabetes mellitus by decreasing autoregulatory capacity and blood flow reserve. Endothelial dysfunction has been observed to precede the onset of microvascular lesions, as demonstrated by reduction in the vasodilatory response to vasoactive agents and by alterations in the antithrombotic properties of the endothelium. Experimental data available so far suggest that endothelial dysfunction may be directly related to hyperglycemia. Abnormalities in lipoprotein metabolism, generation of glycation end products, and increased oxidative stress may also be responsible for the endothelial dysfunction in diabetes mellitus. Insulin resistance appears to be related to endothelial dysfunction in non-insulin-dependent diabetes mellitus through a reduction in the biological activity of endothelial-derived nitric oxide.

Animals↗

PubMed2001

Soluble adhesion molecules, endothelial function and vitamin E in type 1 diabetes.

BACKGROUND: Elevated levels of soluble adhesion molecules are found in subjects with vascular disease and inconsistently in subjects with conditions predisposing them to atherosclerosis, such as hypercholesterolaemia and diabetes. Oxidized low-density lipoprotein (LDL), protein kinase C and lower than normal levels of NO appear to be important for expression of adhesion molecules, raising the possibility that vitamin E is useful for downregulating levels. We have recently shown that administration of 1000 IU vitamin E for 3 months will improve endothelial vasodilator function (EVF) in uncomplicated type-1 diabetes. OBJECTIVE: To determine whether levels of soluble adhesion molecules in young subjects with uncomplicated diabetes are elevated, whether there is a relationship between levels of soluble adhesion molecule and EVF as well as parameters of diabetes and lipid levels and whether an improvement in EVF related to vitamin E therapy is also associated with a decrease in levels of soluble adhesion molecules. DESIGN: A randomized, placebo-controlled, study. RESULTS: There was no difference between levels of soluble vascular cell adhesion molecule-1 (VCAM-1; 621 +/- 17 versus 635 +/- 37 ng/ml) and P-selectin (59 +/- 2 versus 57 +/- 6 ng/ml) for the diabetic and control groups. For the diabetic cohort, levels of soluble VCAM-1 were inversely related to flow-mediated vasodilatation of the brachial artery (r = -0.41, P < 0.005) and directly related to levels of total cholesterol (r = 0.44, P < 0.005) and LDL cholesterol (r = 0.42, P < 0.01) and duration of diabetes (r = 0.55, P < 0.0005) but there was no relationship with susceptibility of LDL to oxidation or vitamin-E content of LDL. Levels of soluble P-selectin were directly related to duration of diabetes (r = 0.43, P < 0.05) and inversely related to size of LDL particles (r = 0.32, P < 0.05) but were not related to EVF. Vitamin E produced no change in levels of soluble P-selectin and VCAM-1. CONCLUSIONS: Levels of soluble VCAM-1 and P-selectin in young subjects with type-1 diabetes and no evidence of overt vascular disease do not appear to be elevated and are not influenced by vitamin-E supplementation.

Adolescent↗

PubMed2001

Interaction of hypertension and diabetes on impairment of endothelial function.

OBJECTIVE: To investigate whether the interaction of hypertension and diabetes aggravates endothelial dysfunction and leads to smooth muscle dysfunction. METHODS: Noninvasive methods were used to the investigated patients with type 2 diabetes mellitus (2-DM) (Group 1), patients with hypertension (Group 2) and patients with both 2-DM and hypertension (Group 3), as well as a normal control group (Group 4) by studying a brachial artery without evidence of atherosclerotic plaque formation. RESULTS: Results showed that endothelium-dependent vasodilation decreased significantly in Group 1 (5.74% +/- 3.32%, P < 0.05), Group 2 (4.14% +/- 2.93%, P < 0.01), and Group 3 (2.78% +/- 2.08%, P < 0.001) as compared to the control (9.45% +/- 3.88%). The nitroglycerin-induced vasodilation (smooth muscle function) in Group 3 was significantly decreased as compared to the control group (14.11% +/- 4.63% vs 23.53% +/- 6.77%, P < 0.001), but there were no differences in nitroglycerin-induced vasodilation between Group 1, Group 2 and Group 4. On univariate analysis, a reduced vasodilator response to nitroglycerin was associated with endothelium-dependent vasodilation (r = 0.54, P < 0.001). CONCLUSION: Our results indicate that the interaction of 2-DM and hypertension aggravates endothelial dysfunction and further impairs the smooth muscle function.

Aged↗

PubMed1994

Recovery after dietary vitamin E supplementation of impaired endothelial function in vitamin E-deficient rats.

1. Thoracic aortae, isolated from rats supplemented with dietary vitamin E after vitamin E deficiency, were analysed for changes in vascular reactivity. 2. Following 4 or 12 months of dietary vitamin E deficiency, endothelium-dependent vasodilator responses to acetylcholine were significantly impaired. However, when animals were fed after the first 4 months of vitamin E deprivation with a vitamin E-supplemented diet for 8 months, endothelium-mediated responses were completely restored. 3. In contrast, the endothelium-independent vasodilator or vasoconstrictor responses to sodium nitroprusside and noradrenaline, respectively were not altered either by vitamin E deficiency or supplementation. 4. These data indicate that vitamin E supplementation reversed the impairment of endothelial cell function which occurs during vitamin E deficiency.

Acetylcholine↗

PubMed1987

[Endothelial function and spasm of the coronary artery].

The tone of isolated segments of human coronary arteries with manifestations of atherosclerotic lesions was increased by serotonin (10(-6) M) or prostaglandin F2 alpha (10(-6) M). Insignificant endothelium-dependent relaxation induced by bradikinin, calcium ionofore A-23187 or substance P was observed in several segments with marked (plaque) as well as macroscopically invisible sclerotic lesion. Segments of human coronary arteries without sclerotic damage demonstrated endothelium-dependent relaxation in response to activators of endothelial relaxation factor. Functional disturbance of coronary artery endothelium in endothelial relaxation factor production may be one of the causes of increased smooth muscle tonic contractions, responsible for coronary artery spasm underlying angina pectoris and myocardial infarction.

Animals↗

PubMed2005

Effects of recombinant adenovirus-mediated uncoupling protein 2 overexpression on endothelial function and apoptosis.

Increased oxidative stress in vascular cells plays a key role in the development of endothelial dysfunction and atherosclerosis. Uncoupling protein 2 (UCP2) is an important regulator of intracellular reactive oxygen species (ROS) production. This study was undertaken to test the hypothesis that, UCP2 functions as an inhibitor of the atherosclerotic process in endothelial cells. Adenovirus-mediated UCP2 (Ad-UCP2) overexpression led to a significant increase in endothelial nitric oxide synthase (eNOS) and decrease in endothelin-1 mRNA expression in human aortic endothelial cells (HAECs). Moreover, UCP2 inhibited the increase in ROS production and NF-kappaB activation, and apoptosis of HAECs induced by lysophophatidylcholine (LPC) and linoleic acid. LPC and linoleic acid caused mitochondrial calcium accumulation and transient mitochondrial membrane hyperpolarization, which was followed by depolarization. UCP2 overexpression prevented these processes. In isolated rat aorta, Ad-UCP2 infection markedly improved impaired vascular relaxation induced by LPC. The data collectively suggest that UCP2, functions as a physiologic regulator of ROS generation in endothelial cells. Thus, measures to increase UCP2 expression in vascular endothelial cells may aid in preventing the development and progression of atherosclerosis in patients with metabolic syndrome.

Adenoviridae↗

PubMed2004

Restoration of the endothelial function in the aortic rings of apolipoprotein E deficient mice by pharmacological inhibition of the nuclear enzyme poly(ADP-ribose) polymerase.

Oxidant-mediated activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) plays a role in the development of endothelial dysfunction and the pathogenesis of various cardiovascular diseases. The aim of the current study was to investigate whether activation of PARP contributes to the development of endothelial dysfunction in the apolipoprotein E (ApoE) deficient mice. We tested whether PARP inhibition prevents the development of endothelial dysfunction and whether it restores function in vessels with established endothelial dysfunction. ApoE deficient mice were kept on high-fat diet for 12 weeks with and without INO-1001 treatment. Chronic treatment with the PARP inhibitor INO-100 reduced the degree of the endothelial dysfunction (the ability of the vessel to relax to acetylcholine) in the thoracic aortae of ApoE deficient mice. In addition, in vitro incubation of vessels from ApoE deficient mice with established endothelial dysfunction with the PARP inhibitor acutely improved the ability of the rings to relax to acetylcholine. We conclude that the early atherosclerotic functional alterations that develop in the endothelium of the ApoE deficient mice are, at least in part, reversible, and are dependent on the activation of the nuclear enzyme PARP in the endothelial cells.

Acetylcholine↗

PubMed1999

High flaxseed (linseed) diet restores endothelial function in the mesenteric arterial bed of spontaneously hypertensive rats.

The effect of high flaxseed diet (HFD) on blood pressure (BP) and mesenteric arterial bed (MAB) reactivity was studied in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. HFD did not affect BP in either SHR (control, 157 +/- 3; HFD, 153 +/- 3 mmHg) or WKY (control, 114 +/- 2; HFD, 117 +/- 2 mmHg) rats. Increases in perfusion pressure of the endothelium-intact MAB to phenylephrine and norepinephrine were higher (p < 0.05) in SHR than in WKY rats and the HFD failed to alter these responses. Vasorelaxant responses to acetylcholine (ACh) and bradykinin (BK) were greater (p < 0.05) in SHR maintained on HFD compared to SHR on control diet. While HFD also enhanced ACh responses in WKY, the effect was less than in SHR. Responses to sodium nitroprusside (SNP), were similar in all groups. Since ACh and BK-induced responses of the MAB were augmented in SHR on HFD, with no changes in BP, it is suggested that HFD improves endothelial vasorelaxant function through a pressure-independent mechanism.

Acetylcholine↗

PubMed1997

Endothelial function in subcutaneous resistance arteries from elderly hypertensive and normotensive subjects.

1. Previous studies have indicated that younger hypertensive subjects may have abnormal endothelium-dependent relaxation, which could contribute to the elevated peripheral resistance seen in established hypertension. This study was designed to examine the functional behaviour of the endothelium of small arteries from elderly hypertensive and normotensive subjects. 2. Resistance arteries were obtained from gluteal biopsies taken under local anaesthesia in 28 subjects of mean age 70 (range 60-76) years, and studied in an isometric myograph. Eighteen subjects had untreated essential hypertension, and 10 were normotensive. 3. After measurement of the contractile response to noradrenaline, relaxation responses to a variety of endothelium-dependent (acetylcholine and bradykinin) and endothelium-independent (iloprost and sodium nitroprusside) mechanisms were assessed in vessels precontracted with noradrenaline. Endothelium-dependent responses were also studied after incubation with NG-nitro-L-arginine to inhibit nitric oxide synthase. 4. There were no significant differences in the contraction or relaxation responses between elderly subjects with or without high blood pressure. Inhibition of nitric oxide synthase prevented any relaxation with acetylcholine and significantly attenuated the relaxation with bradykinin. Near-complete relaxation was however achieved with the endothelium-independent vasodilator sodium nitroprusside. 5. Hypertension in elderly subjects is not associated with a reduction in endothelial vasodilating function in the subcutaneous vessels of the gluteal region compared with age-matched normotensive controls. The results of this study do not support the hypothesis of a defect of resistance artery endothelium-dependent relaxation in the pathophysiology of hypertension in the elderly.

Acetylcholine↗

PubMed1994

Vascular endothelial growth factor. A cytokine modulating endothelial function in rheumatoid arthritis.

Angiogenesis is important in the proliferation of inflammatory synovial tissue. Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen that is also angiogenic in vivo. We examined the potential role of VEGF in mediating chemotaxis and proliferation of endothelial cells in rheumatoid arthritis (RA) using samples of synovial tissue and synovial fluid from 55 arthritic patients. Synovial fluid VEGF by ELISA was higher in RA synovial fluids (386 +/- 122 ng/ml) (SE) compared with osteoarthritis (OA) synovial fluids (< 0.8 ng/ml) (p < 0.05) or synovial fluids from patients with other arthritides (6.6 +/- 2 ng/ml). In addition to its known mitogenic properties, we found that human rVEGF was chemotactic for HUVECs at concentrations above 0.02 nM. Incubation of RA synovial fluids with neutralizing anti-VEGF resulted in 23 to 66% (mean 53 +/- 4%) inhibition of HUVEC chemotaxis. Conditioned medium from four of five RA synovial tissue explants was mitogenic for bovine adrenal capillary endothelial cells. Anti-VEGF neutralized from 19 to 42% (mean 28 +/- 4%) of this mitogenic activity. To determine the cellular source of VEGF in synovial tissue, we employed immunohistochemistry. VEGF+ cells were rarely (< 1%+) found in normal synovial tissues. In contrast, RA and OA synovial tissues exhibited VEGF+ lining cells (8% and 13%, respectively). A few synovial tissue macrophages were VEGF+ in both RA and OA (5% and 2%, respectively). These results elucidate a newly described function for VEGF as a potent chemotaxin for endothelial cells as well as a role for VEGF in RA-associated endothelial migration and proliferation.

Arthritis, Rheumatoid↗