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PubMed2000

Plasma soluble adhesion molecules and endothelium-dependent vasodilation in early human atherosclerosis.

Levels of soluble cellular adhesion molecules are increased in patients with atherosclerosis, and have been found to predict coronary heart disease. Therefore these molecules have been suggested to represent laboratory markers for inflammation and activation of endothelial cells. Impaired endothelium-dependent vasodilation has been demonstrated to be an early marker of atherosclerosis. We hypothesized that soluble adhesion molecules are related to impaired endothelium-dependent vasodilation and may serve as an early marker of atherosclerosis. Patients (n=52) with moderate and uncomplicated hypercholesterolaemia [low-density lipoprotein (LDL)-cholesterol 4.89+/-1.26 mmol/l] were compared with healthy controls (n=43; LDL-cholesterol 2.44+/-0.79 mmol/l). Endothelium-dependent vasodilation of the forearm vasculature was assessed by intra-arterial infusion of acetylcholine (12 and 48 microg/min). Forearm blood flow was measured by venous occlusion plethysmography. Plasma concentrations of the soluble forms of ICAM-1 (intercellular cell adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1) and E-selectin were measured by ELISA. Hypercholesterolaemic patients had impaired endothelium-dependent vasodilation in comparison with healthy controls (forearm blood flow after 48 microg/min acetylcholine: 21.3+/-10.6 and 30.4+/-16.3 ml. min(-1).100 ml(-1) respectively; P=0.002). Plasma concentrations of soluble adhesion molecules were not different between hypercholesterolaemic patients and controls (ICAM-1, 196+/-56 and 180+/-38 ng/ml respectively; VCAM-1, 431+/-137 and 405+/-65 ng/ml respectively; E-selectin, 39+/-17 and 37+/-12 ng/ml respectively). Moreover, levels of soluble adhesion molecules were not correlated with endothelium-dependent vasodilation. Thus, in hypercholesterolaemic patients without clinical atherosclerosis, levels of soluble adhesion molecules were not elevated in comparison with healthy controls. In addition, these markers of endothelial inflammation were not related to impaired endothelium-dependent vasodilation. Our data indicate that measurement of levels of soluble adhesion molecules cannot replace assessment of endothelium-dependent vasodilation in detection of early hypercholesterolaemic atherosclerosis.

Adolescent↗
PubMed2000

Vasodilator therapy for chronic aortic and mitral regurgitation.

The use of vasodilator therapy in chronic AR and MR may be beneficial in selected patients and harmful in others. The hemodynamics of the two conditions are different and must be taken into account. In AR, vasodilators reduce afterload mismatch and can preserve LV function and delay the need for surgery. However, if the patient has severely reduced diastolic blood pressure, vasodilators could potentially impair coronary perfusion. In MR, vasodilators may reduce regurgitant volume and LV preload depending on the mechanism of MR. In patients with MR caused by dilated cardiomyopathy, vasodilators reduce symptoms, and improve functional class. However, in mitral valve prolapse or hypertrophic cardiomyopathy, vasodilators may worsen the MR and should be avoided. In other primary causes of MR, vasodilators could potentially mask the development of LV dysfunction and lead to unnecessary and harmful delays in surgery.

Aortic Valve Insufficiency↗
PubMed1992

[Effect of hypoxia on vasodilation induced by substance P (SP) and calcitonin gene-related peptide (CGRP)].

In this paper, isolated rabbit arteries (renal artery, RA; femoral artery, FA; basilar artery, BA) were used to study the effect of hypoxia on vasodilation induced by substance P (SP) and calcitonin gene-related peptide (CGRP). The results showed that hypoxia caused a marked decrease of the arteries, response to SP (10(-7) mol/L) and CGRP (2.8 x 10(-9) mol/L). Repeated hypoxia even resulted in a complete disappearance of response. On the second hypoxia, CGRP (2.8 x 10(-9) mol/L) induced vasodilation on BA was vanished. On the third hypoxia, vasodilation induced by CGRP (2.8 x 10(-9) mol/L) on FA and that induced by SP (2 x 10(-7) mol/L) on BA were vanished, and CGRP (2.8 x 10(-9) mol/L) induced a lesser extent of vasodilation on RA. At the fourth time, SP (10(-7) mol/L) -induced vasodilation of FA disappeared, and that on RA was small. At the fifth time, the effect of SP (10(-7) mol/L) on RA was nearly vanished. It is concluded that the effect of hypoxia on CGRP-induced vasodilation is stronger than that on SP-induced vasodilation, and the effect is most pronounced on the BA.

Animals↗
PubMed1989

Adenosine does not mediate the pulmonary vasodilator response of adenosine 5'-triphosphate in the feline pulmonary vascular bed.

Adenosine and ATP produce dose- and tone-dependent responses in the feline pulmonary vascular bed. That is, at baseline (low) pulmonary vascular tone adenosine and ATP produce vasoconstrictor responses and at elevated pulmonary vascular tone adenosine and ATP produce vasodilator responses. The mechanism mediating the vasodilator responses to adenosine and ATP was investigated in the intact-chest cat under conditions of controlled pulmonary blood flow and left atrial pressure. When lobar vascular resistance was raised with U46619, intralobar injections of adenosine and ATP caused dose-related decreases in lobar arterial pressure. The pulmonary vasodilator responses to ATP and adenosine were not altered by atropine, propranolol, meclofenamate or cimetidine indicating that these responses were not mediated by the release of vasodilator prostaglandins or to activation of beta adrenergic, muscarinic or histamine (H2) receptors. The decreases in lobar arterial pressure in response to adenosine were reduced significantly by BWA1433U, an adenosine (P1) receptor antagonist. BWA1433U induced a parallel shift of the adenosine dose-response curve to the right; however, it had no significant inhibitory effect on the decrease in lobar arterial pressure in response to ATP. The P1 receptor antagonist in doses of 10 and 30 mg/kg i.v. had no significant effect on the vasodilator response to nitroglycerin. The present data suggest that vasodilator responses to adenosine in the feline pulmonary vascular bed are mediated by adenosine (P1) receptors, whereas responses to ATP are mediated by a different mechanism that does not involve release of a vasodilator prostaglandin.

Adenosine↗
PubMed1989

[Vasodilator agents and the vascular endothelium].

The recent discovery of endothelium-derived relaxation factor (EDRF) has altered the traditional classification of vasodilators used in angina pectoris and heart failure. If a vasodilator induces release of EDRF from the epithelium it is classified as endothelium-dependent, if not it is independent. Sodium nitroprusside and SIN-1 (active metabolite of molsidomine) are the main independent vasodilators since the endothelium relaxation factor appears to be principally a nitric oxide radical in these synthetic vasodilators. In contrast, calcium-channel blockers and a good number of endogenous chemical mediators (acetylcholine, bradykinin, serotonin, etc.) are endothelium-dependent. Furthermore, simple increase in blood flow through the large vessels can result in endothelium-dependent vasodilation (flow rate-dependence) the extent of which depends on the drug examined. The fact that the pharmacologic response of a vasodilator can be altered under certain pathologic conditions (atherosclerosis, hypertension, diabetes, etc.) further increases the importance of the role of the vascular endothelium in the action of vasodilators since endothelial modulation may then be completely diverted to secretion of endothelium-derived contracting factors (EDCFS).

Endothelium, Vascular↗
PubMed1988

[Therapy of heart failure with vasodilator agents].

Vasodilation in congestive heart failure is an established therapeutic principal. The ventricular unloading improves contractile geometry and thereby improves working conditions for the contractile element: myocardial oxygen consumption falls and myocardial efficiency improves. This effect is independent from the vasodilating substance employed; it is, however, dependent on the simultaneous induction of pre- and afterload reduction. Vasodilation improves regional perfusion. Differential improvement in organ bloodflow is related to the type of vasodilator employed. It seems essential for a therapeutic benefit that renal and coronary perfusion are improved and that shunt flow, especially with steal phenomena, is avoided. Skeletal muscle bloodflow improves only slowly under ACE-inhibitor therapy. It could be shown that the immediate vasodilation due to ACE inhibition is followed by a second phase of vasodilation, which may be related to the influence of ACE inhibition of intraarterial wall angiotensin converting enzyme. Another factor possibly responsible for the delayed response to vasodilation in congestive heart failure, may be functional and structural changes in skeletal muscle. Reversal of these changes requires time. Both factors - the vessel wall related mechanism, as well as changes in parenchymal structure and function - require prolonged periods of treatment until therapeutic benefit can be seen.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1986

[Long-term vasodilator therapy of chronic refractory heart failure in patients with dilated cardiomyopathy].

The effect of long-term vasodilator therapy (hydralazine, ecarazine or budralazine + isosorbide dinitrate) were evaluated for 20 patients with chronic congestive heart failure due to dilated cardiomyopathy (DCM) resistant to conventional therapy. There were 16 men and four women whose ages ranged from 30 to 74 years (mean 52 years). Fifteen patients were in NYHA class III, and five in class IV. All patients continued their previous therapeutic regimens during this study. Hemodynamic measurements were performed with a triple lumen flow-directed balloon-tipped catheter for 15 patients to evaluate the effects of vasodilator therapy. In the other five patients, heart rate, blood pressure, chest radiography for heart size (CTR) and M-mode echocardiography were monitored. The hemodynamic responses to the combined vasodilator therapy for 15 patients showed significant decreases in afterload and preload concomitant with an increase in cardiac output. The noninvasive evaluations of combined vasodilator therapy in five patients resulted in significant improvement in heart size and ejection fraction. In all 20 patients, symptoms were significantly improved. Side effects and drug toxicity were uncommon during vasodilator therapy. It is concluded that combined vasodilator treatment is the most ajunctive therapy for the management of severe refractory heart failure due to DCM. In addition, long-term nonparenteral vasodilators can be administered even in an outpatient clinic without hemodynamic monitoring.

Adult↗
PubMed1985

Vasodilative effect of nicorandil on coronary artery.

Vasodilative effects of nicorandil (2-nicotinamidoethylnitrate) and verapamil were compared using isolated canine coronary arterial strips contracted with either high potassium or prostaglandin F2 alpha (PGF2 alpha). When the vasodilative effects of these drugs were determined at 15 min after the application, nicorandil induced a dose-dependent relaxation of the strips contracted with high K. Vasodilative effect of nicorandil was inversely proportional to the concentration of K used to contract the arteries, showing 82 +/- 3.0% (mean +/- SE) and 21 +/- 3.6 of relaxation at the highest concentration of this drug (10(-5) mol/l) when the strips were contracted with 20 and 100 mmol/l K, respectively. Vasodilative effect of nicorandil on PGF2 alpha-induced contraction was found to be almost the same as that on 30 K-induced contraction. In contrast to nicorandil, verapamil induced a potent vasodilation of the coronary strips contracted with high K by a dose-dependent manner. Verapamil at the concentration of 10(-5) mol/l was found to induce a potent relaxation (87 +/- 0.8%) of the strips contracted with 100 K. However, verapamil showed a weak vasodilative effect on the strips contracted with PGF2 alpha (10(-5) mol/l), i.e., 10(-5) mol/l verapamil induced 22 +/- 1.1% relaxation of PGF2 alpha-induced coronary strips. These results suggest that nicorandil can exert its vasodilative effect against the coronary arterial contraction induced not only by high K, which is induced by a voltage dependent Ca influx, but also by PGF2 alpha, which is considered to be through the specific receptor of the membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Pharmacological characterization of presynaptic calcitonin gene-related peptide (CGRP) receptors on CGRP-containing vasodilator nerves in rat mesenteric resistance vessels.

Rat mesenteric arteries are innervated by calcitonin gene-related peptide (CGRP)-containing vasodilator nerves (CGRP nerves). This study investigated the presence of presynaptic CGRP receptors on CGRP nerves and the receptors' role in the regulation of CGRP release from these nerves. The rat mesenteric vascular bed was perfused with Krebs' solution containing 7 microM methoxamine plus 5 microM guanethidine to produce active tone and block adrenergic neurotransmission. In this preparation, periarterial nerve stimulation (PNS;2 Hz) and bolus infusion of CGRP (50 pmol) caused a decrease in perfusion pressure caused by vasodilation. Vasodilator response to PNS was abolished by 0.3 microM tetrodotoxin and by 1 microM human CGRP[8-37] (CGRP[8-37]), a CGRP receptor antagonist, which also abolished the response to bolus infusion of CGRP. Perfusion of CGRP (0.03-0.5 nM) dose-dependently inhibited vasodilator response to PNS, whereas it did not affect the response to bolus infusion of CGRP. The inhibitory effect of CGRP (0.3 nM) was antagonized by CGRP[8-37] (3 and 10 nM). Lower concentrations of CGRP[8-37] (1-10 nM) potentiated the vasodilator response to PNS, but higher concentrations (100 nM-1 microM) inhibited the response. The vasodilator response to bolus infusion of CGRP was dose-dependently inhibited by CGRP[8-37]. Eel calcitonin (5 and 50 microM), forskolin (0.01 and 0.1 microM), 3-isobutyl-1-methylxanthine (0.3 and 1 microM) and cyclic 8-bromo-adenosine 3':5'-monophosphate (10 and 100 microM) had no effect on the PNS-induced vasodilation. These results suggest that CGRP nerves are endowed with presynaptic CGRP receptors, which regulate CGRP release from the nerves via a negative feedback mechanism.

1-Methyl-3-isobutylxanthine↗
PubMed1998

NO-independent vasodilation to acetylcholine in the rat isolated kidney utilizes a charybdotoxin-sensitive, intermediate-conductance Ca(++)-activated K+ channel.

The role of K+ channels in the nitric oxide-independent renal vasodilator effect of acetylcholine (Ach) was examined to address the hypothesis that the mechanism underlying this response was different from that of bradykinin, because an earlier study indicated the possibility of different mediators. We used the rat isolated, perfused kidney that was constricted with phenylephrine and treated with nitroarginine and indomethacin to inhibit nitric oxide synthase and cyclooxygenase, respectively. The nonspecific K+ channel inhibitors, procaine and tetraethylammonium (TEA), reduced vasodilator responses to Ach and cromakalim, but not those to nitroprusside. Glibenclamide, an inhibitor of ATP-sensitive K+ channels, reduced vasodilator responses to cromakalim but did not affect those to Ach or nitroprusside. Charybdotoxin, an inhibitor of Ca(++)-activated K+ channels, reduced vasodilator responses to Ach without affecting those to cromakalim or nitroprusside. Iberiotoxin and apamin, inhibitors of large- and small-conductance Ca(++)-activated K+ channels, respectively, did not reduce vasodilation induced by Ach, cromakalim or nitroprusside. The inhibitor of cytochrome P450, clotrimazole, reduced the renal vasodilator effects of Ach and bradykinin but not those of nitroprusside or SCA 40, an agonist for Ca(++)-activated K+ channels. These results suggest that in the rat kidney, Ach, like bradykinin, utilizes a charybdotoxin-sensitive Ca(++)-activated K+ channel of intermediate conductance to elicit vasodilation and that this effect may be dependent on cytochrome P450 activity.

Acetylcholine↗
PubMed2003

Endothelium-dependent and -independent relaxation and VASP serines 157/239 phosphorylation by cyclic nucleotide-elevating vasodilators in rat aorta.

Endothelium-dependent vasodilation is thought to be mediated primarily by the NO/cGMP signaling pathway whereas cAMP-elevating vasodilators are considered to act independent of the endothelial cell layer. However, recent functional data suggest that cAMP-elevating vasodilators such as beta-receptor agonists, adenosine or forskolin may also be endothelium-dependent. Here we used functional and biochemical assays to analyze endothelium-dependent, cGMP- and cAMP-mediated signaling in rat aorta. Acetylcholine and sodium nitroprusside (SNP) induced a concentration-dependent relaxation of phenylephrine-precontracted aorta. This response was reflected by the phosphorylation of the vasodilator-stimulated phosphoprotein (VASP), a validated substrate of cGMP- and cAMP-dependent protein kinases (cGK, cAK), on Ser(157) and Ser(239). As expected, the effects of acetylcholine were endothelium-dependent. However, relaxation induced by the beta-receptor agonist isoproterenol was also almost completely impaired after endothelial denudation. At the biochemical level, acetylcholine- and isoproterenol-evoked cGK and cAK activation, respectively, as measured by VASP Ser(239) and Ser(157) phosphorylation, was strongly diminished. Furthermore, the effects of isoproterenol were repressed by eNOS inhibition when endothelium was present. We also observed that the relaxing and biochemical effects of forskolin were at least partially endothelium-dependent. We conclude that cAMP-elevating vasodilators, i.e. isoproterenol and to a lesser extent also forskolin, induce vasodilation and concomitant cyclic nucleotide protein kinase activation in the vessel wall in an endothelium-dependent way.

Acetylcholine↗
PubMed2005

K(+)-induced vasodilation in the rat kidney is dependent on the endothelium and activation of K+ channels.

Increased extracellular K+ is reported to cause endothelium-independent vasodilation and K+ has been proposed as an endothelium-derived hyperpolarizing factor. However, the endothelium is endowed with K+ channels that may also be responsive to increased K+. We examined the vasodilator effect of bolus administration of 20, 40 and 60 micromol KCl in the rat isolated kidney in which perfusion pressure was elevated with phenylephrine. KCl produced dose-dependent vasodilator responses that were virtually abolished by removal of the endothelium which also abolished the vasodilator effect of bradykinin without affecting that to nitroprusside. The vasodilator effect of KCl was unaffected by inhibition of cyclooxygenase, nitric oxide synthase or cytochrome P450 but reduced by inhibition of K+ channels with tetraethylammonium (TEA). Barium chloride reduced the vasodilator effects of KCl but charybdotoxin/apamin was without effect. These results indicate that KCl results in endothelium-dependent vasodilation that is independent of nitric oxide (NO), prostaglandins and cytochrome P450 but dependent on activation of endothelial K+ channels.

Animals↗
PubMed2005

Mechanism of the endothelium-dependent vasodilator effect of an alcohol-free extract obtained from a vinifera grape skin.

An alcohol-free grape-skin extract (GSE) obtained from skins of Vitis labrusca has significant anti-hypertensive, antioxidant and vasodilator effects. According to our previous results, the vasodilator effect of GSE in the isolated mesenteric vascular bed (MVB) of the rat is dependent on endothelium and partially dependent on nitric oxide (NO). In the MVB of the rat pre-contracted with norepinephrine (NE), bolus injections of GSE induced a long-lasting dose-dependent vasodilation that is significantly reduced after the treatment with 1H-[1,2,3] oxadiazolo [4,4-a] quinoxalin-1-one (ODQ). Additionally, in vessels pre-contracted with norepinephrine and depolarized with KCl (25 mM) or treated with Ca(2+)-dependent K(+)-channel blockers charybdotoxin (ChTx) plus apamin, the vasodilator effect of GSE was significantly reduced and almost abolished by ChTx plus apamin plus L-NAME. However, the vasodilator effect of GSE was unaffected by D-Arg[Hyp(3),Thi(5),D-Tic(7),Oic(8)]bradykinin (HOE-140), atropine, yohimbine, pyrilamine and 4-aminopyridine (4-AP). The vasoconstriction response elicited by bolus injection of KCl was not affected by GSE, whereas the vasoconstrictor response induced by NE was dose-dependently and completed inhibited by GSE in the presence but not in the absence of endothelium. However, NE-induced vasoconstriction in calcium-free condition or without endothelium was not reduced by GSE. The present results demonstrate that GSE induces a vasodilator effect in the rat MVB, which is dependent on NO in combination with endothelium-derived hyperpolarizing factor (EDHF). Additionally, our results indicated that extracellular Ca(2+) has an important role on the endothelium-dependent vasodilator effect induced by GSE.

Alcohols↗
PubMed1977

Thrombin-induced vasodilation in the hindlimb (dog).

The objective of this study is to test the hypothesis that the vasodilation produced by intra-arterial injection of thrombin to the hindlimb of a dog may be caused by the secondary release or production of some vasodilating substance. The vasodilator response to thrombin was compared with the vasodilator response to acetylcholine, isoproterenol, histamine and serotonin before and after blockade with atropine, propranolol, phenergan or methyl-D-lysergic acid butanolamide (UML-491), respectively. Though the appropriate blocking agent blocked the vasodilator response to the respective drug, the thrombin-induced vasodilation was not blocked. These data support the hypothesis that thrombin-induced vasodilation is a response to the thrombin moiety.

Acetylcholine↗
PubMed1984

Ambulatory long-term vasodilator therapy for chronic refractory heart failure: hemodynamic evaluation and clinical response.

We evaluated long-term combined vasodilator therapy (hydralazine or ecarazine + isosorbide dinitrate) in 29 patients with chronic congestive heart failure resistant to the optimal conventional therapy. There were 24 men and 5 women, aged 28 to 76 years (mean 52 y/o). The etiology of heart failure was congestive cardiomyopathy in 24 patients, ischemic cardiomyopathy in 4 patients and advanced mitral regurgitation due to calcified mitral annulus in 1 patient. There were 21 patients in NYHA class III and 8 patients in NYHA class IV. All patients continued their previous therapeutic regimen during the period of this study. Hemodynamic measurements were performed with a triple lumen flow-directed balloon-tipped catheter in 20 patients to evaluate the effects of vasodilator therapy. In the rest of 9 patients, heart rate, blood pressure, chest X-ray examination for heart size (CTR) and M-mode echocardiograms for ejection fraction (EF) were monitored. The hemodynamic responses to the combined vasodilator therapy in 20 patients showed significant decreases in afterload and preload concomitant with an increase in cardiac output. The noninvasive evaluation of combined vasodilator therapy in 9 patients resulted in significant improvement in CTR and EF. We also noted a significant improvement in their symptoms of 29 patients. Side effects and drug toxicity were uncommon during vasodilator therapy. It is concluded that the combined vasodilator therapy is most useful adjunctive therapy in the management of severe refractory heart failure. Moreover, long-term nonparenteral vasodilators can be administered even at outpatient clinic without hemodynamic monitoring.

Adult↗
PubMed1995

Treatment of pulmonary hypertension in patients with chronic obstructive pulmonary disease: position of vasodilators with special focus on urapidil.

Pulmonary hypertension, generally defined by a resting pulmonary artery mean pressure higher than 20 mmHg, is a common complication of advanced chronic obstructive pulmonary disease (COPD). Pulmonary hypertension in COPD is of the "precapillary type" and is almost exclusively accounted for by the increased pulmonary vascular resistance (PVR). Among the factors leading to an increased PVR, acute as well as chronic alveolar hypoxia is by far the most important. Pulmonary hypertension is usually mild (between 20 and 35 mmHg) in COPD patients, but pulmonary artery pressure (PAP) may increase markedly and suddenly during exercise, sleep and episodes of acute respiratory failure. These acute increases of afterload can favour the development of right heart failure. Furthermore, even if the progression of pulmonary hypertension is rather slow (PAP increases by + 0.5 mmHg/year as a mean), the level of PAP is a good indicator of prognosis in COPD patients. Consequently the treatment of pulmonary hypertension is justified in COPD. There are two treatments available so far, which are not mutually exclusive: vasodilators and long-term oxygen therapy (LTOT). LTOT may partly reverse hypoxic pulmonary vasoconstriction but is not always effective in reducing PAP in COPD. Patients with severe and persistent pulmonary hypertension despite oxygen and bronchodilator may be candidates for vasodilator therapy. Numerous vasodilators have been tested, but none has proved entirely satisfactory. Ideally the predominant vasodilator effect would occur in the pulmonary rather than in the systemic vascular bed, and systemic blood pressure should be maintained. The drug should not cause tachycardia and should be well tolerated. At the present time, inhaled nitric oxide (NO) is the only selective pulmonary vasodilator currently available, but NO inhalation is limited by toxicological consideration. Urapidil is known to be an alpha 1-adrenoceptor antagonist and an agonist of central 5HT1A-receptors, and should be considered as a vasodilator. Several studies have already demonstrated that this antihypertensive agent exerts favourable effects on pulmonary and cardiac haemodynamics when administered intravenously or orally to COPD patients with secondary pulmonary hypertension or cor pulmonale. Furthermore in patients with COPD or bronchial hyperreactivity no adverse effect is observed on ventilatory function, bronchial reactivity and gas exchange. Nevertheless, the potential benefit of this vasodilator needs to be confirmed in combination with LTOT by a pragmatic evaluation of its clinical efficacy and safety in COPD patients with secondary pulmonary hypertension.

Antihypertensive Agents↗
PubMed1996

Flow-mediated vasodilation during pacing of the free epigastric artery bypass graft early and late postoperatively.

OBJECTIVES: The free epigastric artery bypass graft is proposed as an alternative conduit to the saphenous vein graft, known for its high rate of attrition. The aim of our study was to assess its endothelial function in vivo. BACKGROUND: The endothelium of arterial bypass grafts plays a role in both the performance and the patency of such grafts. METHODS: We studied 73 epigastric grafts early (mean +/- SD 10 +/- 3 days) and 36 late (12 +/- 5 months) after coronary bypass surgery with quantitative angiography at rest, after 2 min of atrial pacing (130 beats/min) and after injection of isosorbide dinitrate (1 to 2 mg) into the graft. RESULTS: At rest, mean epigastric graft diameter was lower in the late than in the early postoperative period (2.26 +/- 0.39 vs. 2.61 +/- 0.49 mm, p < 0.001). Early after operation, epigastric grafts with a small or an intermediate runoff, but not those with a large runoff, were capable of vasodilation with nitrates (+0.09 +/- 0.10 mm). Late after operation, vasodilation after administration of isosorbide dinitrate was similar in epigastric grafts with a large runoff and in those with a small or intermediate runoff (+ 0.23 +/- 0.09 vs. +0.23 +/- 0.18 mm). Significant vasodilation during pacing was observed late (+4 +/- 9%, p < 0.01) but not early postoperatively, except in a subset of patients with grafts capable of vasodilation after nitrates. A correlation between the response to nitrates and the response during pacing was observed early (r = 0.579, p < 0.001) and late postoperatively (r = 0.530, p = 0.02). CONCLUSIONS: Flow-mediated vasodilation during pacing was observed in most epigastric grafts late, but not early, after operation. This endothelium-dependent dilation was correlated with the importance of the vasodilation observed with nitrates (endothelium-independent), which was related to the importance of the runoff only in the early postoperative period. The ability of epigastric grafts late postoperatively to dynamically adapt their dimensions to an acute increase in demand could contribute to the good functional results of this new alternative arterial graft.

Cardiac Catheterization↗
PubMed1996

Flow-mediated vasodilation of human epicardial coronary arteries: effect of inhibition of nitric oxide synthesis.

OBJECTIVES: This study sought to investigate the role of nitric oxide, an endothelium-derived relaxing factor, in flow-mediated vasodilation in human epicardial coronary arteries. BACKGROUND: Endothelium-derived relaxing factors may be released from the coronary artery endothelium in response to increases in blood flow. METHODS: We studied the effect of the nitric oxide synthesis inhibitor NG-monomethyl-L-arginine (L-NMMA) on the flow-mediated vasodilation of epicardial coronary arteries in 12 patients, using quantitative angiographic and Doppler flow velocity measurements. Adenosine at 100 micrograms/min was infused into the left anterior descending coronary artery to test the dilator response of the proximal artery to increases in blood flow. Acetylcholine at 3 and 30 micrograms/min was infused into the left coronary ostium to determine endothelium-dependent vasodilation of the proximal left anterior descending artery. Adenosine and acetylcholine were infused before and after the intracoronary infusion of L-NMMA (25 mumol/min for 5 min). RESULTS: Infusion of L-NMMA caused a significant decrease in the baseline diameter of the proximal left anterior descending artery (from 2.90 +/- 0.14 to 2.74 +/- 0.13 mm [mean +/- SEM], p < 0.01). Adenosine increased coronary blood flow before and after L-NMMA (+399.5 +/- 27.5% and +511.9 +/- 33.3%, respectively). Flow-mediated vasodilation was observed in the proximal left anterior descending artery before and after L-NMMA (+9.2 +/- 1.5%, p < 0.01 and +8.6 +/- 2.1%, p < 0.01, respectively). A dose of 3 micrograms/min of acetylcholine significantly dilated the proximal left anterior descending artery before L-NMMA (+7.6 +/- 1.0%, p < 0.01), but acetylcholine-induced vasodilation was attenuated after L-NMMA (-1.8 +/- 1.0%). CONCLUSIONS: Our data suggest that nitric oxide modulates basal coronary artery tone but that mediators other than nitric oxide may be responsible for the flow-mediated vasodilation of human epicardial coronary arteries.

Acetylcholine↗