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PubMedDate not supplied

Preliminary report on endothelial functional injury in brain arterioles of diabetic rats: in vivo observation of macromolecular transit across the vascular wall.

The coloring of longitudinal nuclei, resembling a convoy, was observed in vivo in the terminal arterioles of diabetic rat brain by means of a microcirculatory experimental model and Evans blue/albumin tracer. This emergency transit could confirm other well known passages across the vessel wall, or be considered as 'functional injury' of the diabetic endothelium, especially in case of the so-called brain-blood barrier.

Animals↗
PubMed2006

Disturbed endothelial function of the internal thoracic artery in patients with coronary artery disease.

OBJECTIVES AND BACKGROUND: The internal thoracic artery is an established arterial graft for myocardial revascularization. It never had been investigated, whether there are functional differences in this vessel between patients with or without coronary artery disease. METHODS: We investigated the left internal thoracic artery of 28 patients (15 with and 13 without coronary artery disease) with a duplex-system at rest and with a handgrip exercise. RESULTS: Concerning the measured flow velocities at rest there was only a significant difference between the diastolic mean and peak velocity between the two groups, the other investigated parameters demonstrate no significant difference. The peak diastolic and the mean diastolic velocity was less in patients with coronary artery disease during the handgrip-test. The flow reserve was decreased in patients with coronary artery disease (12.6+/-24.0% vs. 32.3+/-30.9%, P < 0.05). CONCLUSIONS: We demonstrated, that patients with coronary artery disease have a higher peripheral resistance and a lower diastolic velocity of the internal thoracic artery during stress testing. This corresponds to a disturbed vasomotion and may be an early marker of arteriosclerosis.

Adult↗
PubMed1992

Nitrates in different vascular beds, nitrate tolerance, and interactions with endothelial function.

The favorable anti-ischemic effect of nitrates is based on the unique distribution pattern of vascular relaxation that they evoke in different vascular sections. Nitrovasodilators reduce cardiac preload and wall tension, and thus myocardial oxygen consumption. They increase precollateral coronary perfusion pressure, thereby augmenting oxygen delivery to ischemic sections, especially to the subendocardial layers. These vasodilator actions are caused by the nitric oxide (NO)-induced activation of soluble guanylyl cyclase, which augments vascular cyclic guanosine monophosphate (cGMP) levels to suppress intracellular Ca2+ concentrations. After some metabolic steps NO is finally cleaved from all nitrovasodilators and is probably identical with, or very closely related to, endothelium-derived relaxing factor (EDRF). A dinitrosyl-iron complex may serve under biologic conditions to stabilize the NO- radical, which has an extremely short half-life. NO derived from nitrovasodilators is used therapeutically to substitute for a deficient endothelium-mediated vascular control and autacoid production.

Animals↗
PubMed1992

Endothelial function in chronic congestive heart failure.

There is evidence that the endothelium plays an important role in the control of human vascular tone by releasing endothelium-derived nitric oxide. The hypothesis that an impairment of this mechanism is involved in the increased peripheral vasoconstriction of patients with chronic congestive heart failure (CHF) was tested. Acetylcholine and N-monomethyl-L-arginine (L-NMMA), a specific inhibitor of nitric oxide synthesis from L-arginine, were infused in the brachial artery of healthy volunteer subjects (controls) and patients with severe CHF. The radial artery diameter was determined by a high-precision A-mode ultrasound device, using a 10 MHz probe. Forearm blood flow was calculated from vessel diameter and blood flow velocity measured simultaneously by Doppler. The blood flow response to acetylcholine was blunted in patients with CHF compared with that in control subjects. In contrast, the decrease in blood flow induced by L-NMMA was exaggerated in CHF, and the blood flow response to nitroglycerin was preserved. The changes in radial artery diameter induced by acetylcholine and L-NMMA were not significant in control subjects and CHF patients, but dilation of the radial artery by nitroglycerin was significantly reduced in CHF. The results demonstrate an impaired endothelium-dependent dilation of forearm resistance vessels in CHF, suggesting a reduced release of nitric oxide on stimulation. In contrast, the basal release of nitric oxide from endothelium of forearm resistance vessels is preserved or may even be enhanced, and may play an important compensatory role in chronic CHF by antagonizing neurohumoral vasoconstrictor forces in CHF.

Acetylcholine↗
PubMed1994

Endothelial function and vasodilator profile of the inferior epigastric artery.

In the inferior epigastric artery, endothelium-dependent relaxations in response to substance P, histamine, and acetylcholine were present. These were greater than reported values in saphenous veins but less than the documented responses in internal mammary and gastroepiploic arteries. Endothelium-independent stimulation with nifedipine, papaverine, sodium nitroprusside, and glyceryl trinitrate induced relaxations that also were reduced compared with established arterial conduits. These findings appear to justify the clinical use of the inferior epigastric artery as a coronary bypass graft with monitoring of its long-term results and possibly perioperative pharmacologic manipulations.

Abdominal Muscles↗
PubMed2004

Peripheral vascular endothelial function testing for the diagnosis of coronary artery disease.

BACKGROUND: Abnormalities in endothelium-dependent vasodilation may be detected in arteries before the development of overt atherosclerosis, and their presence may predict stress-induced ischemia as assessed by ST-segment depression and/or perfusion defects. Brachial artery ultrasound during reactive hyperemia is a noninvasive method of assessing peripheral vasomotion, measured by flow-mediated vasodilation (FMD). The purpose of the current study was to assess whether endothelium-dependent FMD of the brachial artery, by ultrasound imaging, predicts the presence of angiographically assessed coronary artery disease (CAD). METHODS: One hundred ninety-eight in-hospital patients (age, 59 +/- 9 years; 78 women) with chest pain syndrome and without previous myocardial infarction or revascularization procedures were enrolled in the present study. All of the patients, at testing time, were not receiving nitrate therapy and underwent, on different days, coronary angiography and endothelium-dependent FMD testing of the brachial artery by high-resolution ultrasound. The result of the flow-mediated dilation (%FMD) is defined as the percent change in the internal diameter of the brachial artery during reactive hyperemia related to baseline. A coronary vessel was considered to have a significant obstruction if its diameter was narrowed by 50% or more on quantitative computer-assisted analysis. A prognostically validated angiographic Duke score (from 0 = normal to 100 = severe left main disease) was calculated. RESULTS: The %FMD was lower in patients with (n = 69) compared with those without (n = 129) CAD (4.64% +/- 4.36% vs 7.39% +/- 5.68%; P =.01). By multivariate analysis, the %FMD (P =.01; odds ratio [OR], 1.13; 95% confidence interval [CI], 1.05 to 1.23), male sex (P =.01; OR, 3.47; 95% CI, 1.64 to 7.36), and cigarette smoking habit (P <.01; OR, 4.00; 95% CI, 2.50 to 6.35) were independent predictors of CAD. %FMD was poorly albeit significantly correlated with the severity of CAD (%FMD Duke score, P <.01, r = -0.25). The receiver operator characteristic curve showed the %FMD optimal cutoff value as < or =8.84, with sensitivity of 90%, specificity of 37%, negative predictive value of 90%, and positive predictive value of 43%. CONCLUSIONS: In patients with chest pain, a depressed FMD of the brachial artery was a sensitive indicator of CAD, but it showed poor specificity, and it appeared to be unable to predict both the extent and the severity of angiographically assessed CAD.

Aged↗
PubMed2004

Effects of rosiglitazone on endothelial function, C-reactive protein, and components of the metabolic syndrome in nondiabetic patients with the metabolic syndrome.

Fifty nondiabetic patients who met a modified National Cholesterol Education Program definition for the metabolic syndrome were randomized to receive either rosiglitazone (4 mg/day; n = 25) or placebo (n = 25) for 8 weeks. Compared with those receiving placebo, patients in the rosiglitazone group achieved significant reductions in fasting plasma insulin levels (-40%), homeostasis model assessment indexes (-45%), systolic and diastolic blood pressures, and high-sensitivity C-reactive protein levels (-31%). There were no changes in fasting plasma glucose with either treatment. Although rosiglitazone treatment greatly increased plasma levels of low-density lipoprotein cholesterol (18%) and apolipoprotein B (16%), it significantly improved both endothelium-dependent flow-mediated vasodilation (p <0.001) and endothelium-independent nitroglycerin-induced vasodilation (p = 0.01) of the right brachial artery.

Adult↗
PubMed2004

Skeletal muscle hemodynamics and endothelial function in patients after Fontan operation.

To elucidate the relation between exercise capacity and peripheral hemodynamics in patients after the Fontan operation, near-infrared spectroscopy was performed on the vastus lateralis muscle, and flow-mediated vasodilation of the brachial and posterior tibial arteries was done with high-resolution ultrasonography. In Fontan patients, diminished exercise capacity was related to a reduced blood flow supply and an attenuated post-exercise oxygen resaturation of the working skeletal muscle, which also was related to impaired endothelium-dependent vasodilation.

Adolescent↗
PubMed2004

Effect of oral L-arginine on blood pressure and symptoms and endothelial function in patients with systemic hypertension, positive exercise tests, and normal coronary arteries.

Thirteen hypertensive patients with microvascular angina were studied before and after receiving oral L-arginine (4 weeks, 2 g, 3 times daily). L-arginine significantly improved angina class, systolic blood pressure at rest, and quality of life. Maximal forearm blood flow, plasma L-arginine, L-arginine:asymmetric dimethyl arginine ratio, and cyclic guanylate monophosphate increased significantly after treatment. In medically treated hypertensive patients with micro-vascular angina, oral L-arginine may represent a useful therapeutic option.

Administration, Oral↗