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At least 1,585 records · Page 88Linked to original sources
PubMed2000

Midterm endothelial function and remodeling of radial artery grafts anastomosed to the aorta.

BACKGROUND: The purpose of this study was to elucidate the midterm endothelium-dependent vasodilatory capacity of radial artery grafts anastomosed to the aorta, as well as their morphometric evolution with the time. METHODS: Five years after surgery we evaluated the response of aorta-anastomosed radial artery grafts to the endovascular infusion of acetylcholine in 11 of the first 61 patients operated on at our institution, and we compared it to the response with that of internal thoracic artery grafts. Moreover, the first 20 patients who had a perfect radial artery graft on angiography at 1 year were restudied at 5 years and subjected to a comparative analysis of the diameters of the radial artery graft and the grafted coronary arteries. RESULTS: At midterm angiography, dilation of the 2 types of grafts was similar in response to acetylcholine administration (radial artery, from 2.61 +/- 0.39 to 2. 90 +/- 0.34 mm; internal thoracic artery, from 2.68 +/- 0.21 to 2.93 +/- 0.27 mm; P =.01 for both). The diameters of aorta-anastomosed radial artery grafts and grafted coronary arteries increased between both 1 and 5 years according to angiographic studies (radial artery grafts, from 2.08 +/- 0.45 to 2.54 +/- 0.53 mm; grafted coronary arteries, from 1.92 +/- 0.47 to 2.18 +/- 0.41 mm; P <.001 for both), but the increase was greater for the radial artery grafts (P <.001). CONCLUSIONS: Aorta-anastomosed radial artery grafts maintain an appreciable capacity for endothelium-dependent vasodilatation 5 years after implantation and undergo a progressive increase in luminal diameter with time. These observations contradict the presumed tendency for progressive fibrous intimal hyperplasia to develop in radial artery grafts.

Acetylcholine↗
PubMed1996

Homocysteine, EDRF, and endothelial function.

Nitric oxide, a heterodiatomic molecule, serves as an endothelium-dependent vasodilator and an antithrombotic agent in the vasculature. Because of its reactivity under physiological conditions, accumulating data suggest that nitric oxide forms adducts with several classes of biologic compounds, one of which is the sulfhydryl functionality, to form thionitrites or S-nitrosothiols. In this overview, we will examine the effects of S-nitrosothiols in the vascular system as modulators of tone and inhibitors of platelet activation to understand better what role these compounds may play in physiological and pathological states. With this background, we will review the role nitric oxide (EDRF) plays in helping to ameliorate vascular injury by homocysteine.

Animals↗
PubMed1996

Endothelial function in myocardial protection.

Impairment of coronary flow, or low coronary reflow, is an important feature of ischemia-reperfusion injury. It is known to be associated with a significant diminution of basal and stimulated release of nitric oxide. The degree of recovery of low coronary reflow and of basal and stimulated release of nitric oxide diminishes with age and is influenced by the type of cardioplegic solution used. Underlying mechanisms include L-arginine (the physiologic substrate of nitric oxide) deficiency, G protein alteration, and nitric oxide inhibition by free radicals. Under normal conditions, basal release of nitric oxide is known to play a crucial role in the maintenance of basal coronary flow and appears to be essential for sustaining mechanical activity. Methods of preservation targeting reperfusion, ischemia, and preischemia have been evaluated. Pharmacologic modulation, crystalloid solution at 4 degrees C, and induction of heat-shock proteins (an intrinsic protective mechanism) reverse the postischemic dysfunction of nitric oxide release.

Animals↗
PubMed1999

How to assess endothelial function in human blood vessels.

This brief review discusses the ways, if and when available, to examine endothelium-dependent changes diameter in human blood vessels. It stresses the problems in ensuring proper matching between arteries (and veins) from different human sources. It briefly considers the evidence in vitro supporting the role of endothelium-derived nitric oxide, hyperpolarizing factor and contracting factors (including metabolites of arachidonic acid and endothelin). It emphasizes the difficulty in extrapolating observations obtained in isolated arteries (and veins) to the intact human circulation. The overall conclusion is that the interpretations derived from animal work apply to the human vasculature.

Biological Factors↗
PubMed2001

L-Arginine improves endothelial function in renal artery of hypertensive Dahl rats.

OBJECTIVES: To clarify whether endothelium-derived contracting factor (EDCF) is developed in renal artery of hypertensive Dahl rats and whether prolonged oral L-arginine treatments prevent development of EDCF and hypertension. DESIGN: The effect of prolonged salt treatment with or without L-arginine on the renal artery was examined. METHODS AND RESULTS: Dahl salt-sensitive and -resistant rats were fed a 0.4 or an 8% NaCl diet for 4 weeks. High sodium intake increased arterial pressure in Dahl salt-sensitive rats. The rings of renal arteries were suspended for isometric tension recording. Only in the hypertensive rats, more than 1 micromol/l acetylcholine induced an endothelium-dependent contraction response. The contraction was completely inhibited by indomethacin or ONO-3708 [prostaglandin H2 (PGH2)/thromboxane A2 (TXA2) receptor antagonist], and partially inhibited by OKY-046 (TXA2 synthetase inhibitor). Acetylcholine-induced relaxation was significantly depressed in hypertensive rats, which was partially improved by SQ29548 (PGH2/TXA2 receptor antagonist). Oral L-arginine, but not ONO-8809 (orally active PGH2/TXA2 receptor antagonist) treatment, inhibited the contraction and amended the relaxation. The endothelium-independent contraction to TXA2 receptor agonist U46619 and relaxation to nitroprusside were not altered by L-arginine treatment The L-Arginine treatment reduced blood pressure and sodium retention with increases in urinary NO2-/NO3- and cGMP excretion. Hydralazine treatment also inhibited development of EDCF. CONCLUSIONS: The present results suggest that impaired endothelium-dependent relaxation to acetylcholine is caused in part by induction of EDCF synthesis/release in renal arteries of hypertensive Dahl rats. L-arginine can attenuate sodium retention and development of hypertension, which lead to a decrease in EDCF synthesis in renal arteries.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2001

Treatment with irbesartan or atenolol improves endothelial function in essential hypertension.

OBJECTIVES: To investigate if antihypertensive treatment could improve endothelium-dependent vasodilatation in hypertensive patients, and whether the angiotensin II subtype-1 (AT1)-receptor antagonist irbesartan and the beta1-receptor antagonist atenolol would differ in this respect. SUBJECTS AND METHODS: Thirty-four patients (28 men and six women) with mild-to-moderate essential hypertension (diastolic blood pressure 90-120 mmHg) were randomized to once daily 150-300 mg irbesartan or 50-100 mg atenolol in a double-blind fashion, preceded by a placebo run-in period. Forearm blood flow (FBF) was assessed by venous occlusion plethysmography during local intra-arterial infusions of methacholine and sodium nitroprusside, to evaluate endothelium-dependent and endothelium-independent vasodilatation, respectively. Measurements of FBF were undertaken at the end of the run-in placebo period and repeated after 3 months of active antihypertensive treatment. RESULTS: Irbesartan and atenolol induced a similar decline in blood pressure (from 171/107 to 158/98 mmHg, P < 0.05), and improved endothelium-dependent vasodilatation (e.g. an increase in FBF response to 4 microg/min methacholine from 325 +/- 29% to 411 +/- 41%, P < 0.05), with no difference between the two study drugs. No significant changes in endothelium-independent vasodilatation were induced by irbesartan or by atenolol. CONCLUSIONS: The present study shows that 3 months of antihypertensive therapy with irbesartan or atenolol improves endothelium-dependent vasodilatation.

Adrenergic beta-Antagonists↗