SEARCH · Search PubMed

Results for “vasodilation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 775 records · Page 43Linked to original sources

PubMed1993

Calcium-induced vasodilation due to increase in nitric oxide formation in the vascular bed of rabbit ear preparation.

Participation of calcium-induced vasodilation (due to an increase in synthesized nitric oxide (NO) content in endothelial cells) in the arterio-venous circulation, including the vascular bed was investigated by the vessel perfusion method in the isolated rabbit ear preparation. The perfusion medium used was a tris-buffered solution. When CaCl2 (6.25, 12.5 and 25 mg) was injected in the perfused vessel of the rabbit ear preparation, dose-dependent vasocontraction was observed when vascular tone was kept at a normal level. However, CaCl2 dose-dependently induced vasodilation of the vessel when it was continuously contracted by norepinephrine (1.2 x 10(-7) M). This calcium-induced vasodilation was inhibited in the presence of NG-nitro-L-arginine (5 x 10(-5) M), a selective inhibitor of NO synthesis, and methylene blue, a guanylate cyclase inhibitor, although it was rarely affected by indomethacin (10(-5) M), a cyclooxygenase inhibitor. Calcium-induced vasodilation was also obtained in the in situ circulation containing vascular bed, and this suggests that the vasodilation was due to a Ca(2+)-induced increase in the synthesis of NO derived from endothelial cells.

Animals↗

PubMed1999

Long-term treatment with angiotensin converting enzyme inhibitor restores reduced calcitonin gene-related peptide-containing vasodilator nerve function in mesenteric artery of spontaneously hypertensive rats.

Effects of long-term treatment with angiotensin converting enzyme (ACE) inhibitor on decreased function of calcitonin gene-related peptide (CGRP)-containing vasodilator nerves (CGRP nerves) in mesenteric resistance artery were investigated in spontaneously hypertensive rats (SHR). Eight-week-old SHR were treated for 7 weeks with 0.1% captopril, 0.01% temocapril, 0.05% pindolol or 0.005% hydralazine in drinking water. Long-term treatment with each drug significantly lowered mean blood pressure of SHR. In isolated and perfused mesenteric vascular beds with active tone, periarterial nerve stimulation (PNS) (0.5 to 8 Hz) produced frequency-dependent vasodilations, which were abolished by CGRP(8-37) (CGRP-receptor antagonist) and significantly smaller in SHR than in normotensive Wistar Kyoto rats. Treatment of SHR with captopril and temocapril but not with pindolol and hydralazine resulted in significantly greater PNS-induced vasodilation than in non-treated SHR, but ACE-inhibitor treatment did not affect vasodilation induced by exogenous CGRP. In captopril-treated SHR preparations, PNS evoked significantly larger CGRP-like immunoreactive release than in non-treated SHR. In non-treated 15-week-old SHR preparations, direct perfusion of captopril or temocapril (0.1 microM and 1 microM) did not modify frequency-dependent vasodilation in response to PNS. These results suggest that long-term ACE inhibitor treatment prevents or restores CGRP nerve function reduction in SHR.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2006

Cardiac re-synchronization therapy: effects on myocardial perfusion at rest, after vasodilation and oxygen consumption.

AIM: Cardiac resynchronization therapy (CRT) has been shown to improve haemodynamics and clinical symptoms in heart failure patients. The present study evaluated the effects of a 4-month CRT on myocardial blood flow (MBF) at rest, after vasodilation and on myocardial oxygen consumption (MVO(2)). PATIENTS, METHODS: We studied 16 patients with idiopathic dilated cardiomyopathy prior to and during CRT performed as biventricular pacing. Resting MBF and MVO(2) were determined from an (11)C-acetate PET study and vasodilator MBF from a (13)N-ammonia study. RESULTS: MBF at rest (0.55 +/- 0.10 ml/min/g), after vasodilation (1.20 +/- 0.45 ml/min/g), and MVO2 (0.082 +/- 0.014/min) did not change by mid-term CRT at a global level (0.57 +/- 0.11 ml/min/g; 1.32 +/- 0.49 ml/min/g; 0.085 +/- 0.018/min), whereas the rate pressure product (RPP) normalised MVO(2) decreased from 0.104 +/- 0.024 to 0.086 +/- 0.018/min (p = 0.02). At baseline, the regional analysis revealed significantly higher values for all parameters in the lateral wall than for those in the other walls. Under CRT the regional differences between the resting parameters equalized and all parameters showed significant lower coefficients of variation. CONCLUSION: Effects of mid-term CRT on resting MBF, vasodilator MBF and MVO(2) occur at a regional level. The resynchronization is associated with a more homogenous distribution pattern of these parameters among the myocardial walls. Substantial alterations to global MBF at rest, after vasodilation or to MVO(2) are not detectable. Regarding the RPP normalised MVO(2), there is evidence of improved ventricular efficiency through CRT.

Aged↗

PubMed1986

Changes in caloric nystagmus induced by vasodilating drugs.

Systemic blood flow, blood flow to the peripheral skin, middle ear, and temporal bone, and that to the inner ear of normal volunteers was manipulated selectively through the use of vasodilator drugs. The effect of selective vasodilation was monitored via changes in the temporal course of the slow-phase velocity of nystagmus evoked by bithermal caloric irrigation. Drug influenced eye velocities were compared with control values measured before drug administration. Eye velocities measured after niacin (a peripheral vasodilator) administration generally were greater than control values, whereas eye velocities measured after papaverine (a central vasodilator) and histamine (a systemic vasodilator) administration typically were less than control values. These findings, with the exception of the cool caloric/niacin condition, are consistent with a model of vestibular dynamics and measurements of cochlear blood flow in animal models.

Adult↗

PubMed1982

The effect of vasodilator therapy on systolic and diastolic time intervals in congestive heart failure.

To determine the effects of vasodilator drugs on systolic and diastolic time intervals in patients with congestive heart failure, these noninvasive measurements were made in 50 patients with moderately severe disease before and after vasodilator therapy. These data were compared with direct hemodynamic measurements obtained simultaneously from a flow-directed triple-lumen pulmonary artery catheter placed in each patient. Oral vasodilators included isosorbide dinitrate 20 mg (n-8), hydralazine 75 mg (n-8), and 100 mg (n-8), and first-dose prazosin 2 mg (n-8) and 5 mg (n-8). Ten additional patients received intravenous dose-response infusions of isosorbide dinitrate, nitroglycerin, and nitroprusside. Increases in cardiac output and stroke volume effected a decrease (improvement) in the systolic time interval parameter of ventricular performance, PEP/LVET. The correlation coefficient for vasodilator-induced changes in cardiac output vs changes in PEP/LVET was -0.82 (P less than 0.05) and for changes in stroke volume and PEP/LVET was -0.75 (P less than 0.05). In general, the diastolic time period was not significantly affected by these drugs. The systolic time intervals are a simple and useful method for evaluation of vasodilator therapy in patients with congestive heart failure.

Administration, Oral↗

PubMed1998

Role of non-nitric oxide non-prostaglandin endothelium-derived relaxing factor(s) in bradykinin vasodilation.

The most conspicuous effect of bradykinin following its administration into the systemic circulation is a transient hypotension due to vasodilation. In the present study most of the available evidence regarding the mechanisms involved in bradykinin-induced arterial vasodilation is reviewed. It has become firmly established that in most species vasodilation in response to bradykinin is mediated by the release of endothelial relaxing factors following the activation of B2-receptors. Although in some cases the action of bradykinin is entirely mediated by the endothelial release of nitric oxide (NO) and/or prostacyclin (PGI2), a large amount of evidence has been accumulated during the last 10 years indicating that a non-NO/PGI2 factor accounts for bradykinin-induced vasodilation in a wide variety of perfused vascular beds and isolated small arteries from several species including humans. Since the effect of the non-NO/PGI2 endothelium-derived relaxing factor is practically abolished by disrupting the K+ electrochemical gradient together with the fact that bradykinin causes endothelium-dependent hyperpolarization of vascular smooth muscle cells, the action of such factor has been attributed to the opening of K+ channels in these cells. The pharmacological characteristics of these channels are not uniform among the different blood vessels in which they have been examined. Although there is some evidence indicating a role for KCa or KV channels, our findings in the mesenteric bed together with other reports indicate that the K+ channels involved do not correspond exactly to any of those already described. In addition, the chemical identity of such hyperpolarizing factor is still a matter of controversy. The postulated main contenders are epoxyeicosatrienoic acids or endocannabinoid agonists for the CB1-receptors. Based on the available reports and on data from our laboratory in the rat mesenteric bed, we conclude that the NO/PGI2-independent endothelium-dependent vasodilation induced by BK is unlikely to involve a cytochrome P450 arachidonic acid metabolite or an endocannabinoid agonist.

Animals↗

PubMed2001

Sex hormone modulation of serotonin-induced coronary vasodilation in isolated heart.

The present study was designed to evaluate the differences in the coronary vasodilator actions of serotonin (5-HT) in isolated heart obtained from naive or castrated male and female rats that were treated with either estrogen or testosterone. Hearts from 12 groups of rats were used: male and female naive animals, castrated, castrated and treated with 17beta-estradiol (0.5 microg kg(-1) day(-1)) for 7 or 30 days, and castrated and treated with testosterone (0.5 mg kg(-1) day(-1)) for 7 or 30 days. After treatment, the vascular reactivity of the coronary bed was evaluated. Baseline coronary perfusion pressure (CPP) was determined and dose-response curves to 5-HT were generated. Baseline CPP differed between male (70 +/- 6 mmHg, N = 10) and female (115 +/- 6 mmHg, N = 12) naive rats. Maximal 5-HT-induced coronary vasodilation was higher (P<0.05) in naive female than in naive male rats. In both sexes, 5-HT produced endothelium-dependent coronary vasodilation. After castration, there was no significant difference in baseline CPP between hearts obtained from male and female rats (75 +/- 7 mmHg, N = 8, and 83 +/- 5 mmHg, N = 8, respectively). Castration reduced the 5-HT-induced maximal vasodilation in female and male rats (P<0.05). Estrogen treatment of castrated female rats restored (P<0.05) the vascular reactivity. In castrated male rats, 30 days of estrogen treatment increased (P<0.05) the responsiveness to 5-HT. The endothelium-dependent coronary vasodilator actions of 5-HT are greater in female rats and are modulated by estrogen. A knowledge of the mechanism of action of estrogen on coronary arteries could aid in the development of new therapeutic strategies and potentially decrease the incidence of cardiovascular disease in both sexes.

Animals↗

PubMed2005

Asymmetrical dimethylarginine plasma concentrations are related to basal nitric oxide release but not endothelium-dependent vasodilation of resistance arteries in peritoneal dialysis patients.

Vascular dysfunction in chronic renal failure may be linked to reduced nitric oxide (NO) bioactivity and increased circulating concentrations of the endogenous NO synthase inhibitor asymmetrical dimethyl L-arginine (ADMA). The association between ADMA and basal endothelial NO release and endothelium-dependent vasodilation in resistance arteries of chronic renal failure patients is unknown. Forearm blood flow responses to the endothelium-dependent vasodilator acetylcholine, the endothelium-independent vasodilator nitroglycerine, and the endothelium-dependent vasoconstrictor N(G)-monomethyl-L-arginine (L-NMMA) were assessed in 37 peritoneal dialysis patients. L-arginine and ADMA plasma concentrations were measured by HPLC. ADMA (mean +/- SEM: 0.68 +/- 0.02 micromol/L) was associated with basal forearm blood flow (r = -0.33; P < 0.05) and L-NMMA induced vasoconstriction (r = -0.55; P < 0.0005), but not with dilator effects of acetylcholine or nitroglycerine. L-arginine (68 +/- 3 micromol/L) tended to correlate with acetylcholine-induced vasodilation (r = 0.32; P = 0.05) but was not associated with other parameters. ADMA is related to basal but not to acetylcholine-stimulated NO bioactivity in patients on peritoneal dialysis. Impaired endothelium-dependent vasodilation found in chronic renal failure is not explained by elevated circulating NO synthase inhibitors in renal failure.

Arginine↗

PubMed1982

Selection of vasodilator drugs for patients with severe chronic heart failure: an approach based on a new classification.

Although vasodilator drugs are of proven worth in the management of patients with severe heart failure, a useful system of classification of vasodilator drugs has not yet been devised. The traditional system of classification based on the dominant arterial and/or venous sites of action as determined by limb plethysmography has major conceptual and practical limitations. This article discusses the merits of a new classification format based on pharmacological mechanisms of action. According to this new system, vasodilator drugs can be divided into two groups: (1) direct-acting agonists (hydralazine, minoxidil, nitrates and nitroprusside) which demonstrate dose-dependent responses and generalised vasodilator effects, and thus require invasive monitoring for dose titration; and (2) neurohumoral antagonists (prazosin, trimazosin, phentolamine, captopril and teprotide), whose effects are qualitatively and quantitatively independent of the dose administered, show marked regional heterogeneity and have characteristic temporal patterns of response. This new classification system permits the rational formulation of clinical recommendations concerning the choice of a vasodilator drug for patients with severe chronic heart failure. However, widespread application of this new classification system awaits the development of reliable means of identifying patients with neurohumoral-dependent vasoconstriction without the necessity of a therapeutic trial.

Heart Failure↗

PubMed1983

Vasodilator therapy in chronic congestive heart failure.

Vasodilator agents are relatively new additions to the armamentarium for the management of patients with congestive heart failure. Myocardial failure, irrespective of the aetiology, tends to create a vicious cycle characterised by reduced cardiac output and elevated systemic vascular resistance, which further decrease cardiac output by increasing left ventricular ejection impedance. The rationale for the use of vasodilators is to interrupt the vicious cycle by decreasing the left ventricular ejection impedance by peripheral vasodilatation. Although most vasodilator agents produce qualitatively similar haemodynamic responses, quantitatively their haemodynamic effects differ considerably. Knowledge of the haemodynamic effects of the various vasodilators helps in the selection of a particular drug for the management of such patients. This article reviews the mechanisms of action, haemodynamic effects, pharmacokinetics, clinical usage and adverse effects of non-parenteral vasodilator agents currently available for the management of patients with chronic heart failure.

Captopril↗

PubMed1985

Preservation of myocardial oxygen balance and functional reserve by coronary vasodilators.

Reduced myocardial function at very high heart rates may be due to limited coronary blood supply. The effects of the vasodilators nitroglycerin (10 micrograms kg-1 min-1) and elevated CO2 upon regional function during tachycardia were studied. In open-chest anaesthetized dogs, regional contractile force, epicardial tissue blood flow and local NADH redox level were recorded during graded ventricular pacing. It was found that the vasodilating action of nitroglycerin in the unpaced heart was much lower than produced by CO2 (23.6 +/- 5.8% vs. 137.6 +/- 33.5%). Maximal pacing at 275 bpm caused only a moderate flow elevation in control (20 +/- 6.8%) and CO2 conditions (20.3 +/- 4.03%), but marked vasodilation during nitroglycerin infusion (85.2 +/- 14.6%). Regional function during tachycardia was improved similarly by both vasodilators. NADH levels increased with heart rates under all experimental conditions, but the absolute NADH levels were consistently lower following vasodilator treatments. The lowest NADH levels were observed during nitroglycerin treatment at all heart rates. It is suggested that nitroglycerin augments myocardial functional reserve by preserving oxygen balance more than predicted by its vasodilatory effect alone.

Animals↗

PubMed1995

A comparison of the relaxation responses of isolated cavernosal smooth muscles by endothelium-independent and endothelium-dependent vasodilators in diabetic men with impotence.

This study was intended to explore the effects of endothelium-independent, direct smooth muscle relaxants(papaverine, verapamil) and endothelium-dependent vasodilators(acetylcholine, bradykinin, adenosine) on the isolated cavernosal smooth muscle strips taken from diabetic men with impotence. When smooth muscle contraction was evoked with norepinephrine for the study of relaxation to these vasodilators, the tension induced was similar in diabetic and non-diabetic men with importance. Papaverine showed the strongest relaxation response followed by verapamil, acetylcholine, bradykinin and adenosine both in non-diabetic and in diabetic men. Relaxation of the cavernosal tissues to endothelium-independent vasodilators was similar in non-diabetic and diabetic men. However, the relaxation response of the tissues to endothelium-dependent vasodilators was significantly reduced in the diabetic group compared with that in the non-diabetic group (p < 0.05). In conclusion, the impairment of endothelium-mediated relaxation of cavernosal smooth muscle seems to play a more important role in the pathogenesis of diabetogenic impotence rather than the problem of smooth muscle itself. This finding forms a rational basis for the use of intracavernosal injections of vasodilators to induce endothelium-independent relaxation of the cavernosal smooth muscle in the patients with diabetogenic impotence.

Adult↗

PubMed1992

Interactions between vasodilator drugs and human hemoglobin.

1. The in vitro effect of the vasodilators papaverine, dipyridamole, nifedipine, prenylamine and glyceryl di-, tri- and tetranitrate on the oxygen saturation curve of human hemoglobin (Hb) was evaluated. The Hb dissociation curve was measured spectrophotometrically both for freshly obtained heparinized blood and for purified Hb A after incubation with the drugs. 2. For both purified Hb and whole blood samples, incubation with papaverine, dipyridamole and nifedipine modified P50 (PO2 for half saturation of the Hb/oxygen sites) at pH 7.4: 30.9 mmHg for 0.72 mM papaverine vs 23.9 mmHg for control; 23.9 mmHg for 1.43 mM dipyridamole vs 20.8 mmHg for control; 1.09 mmHg for 2.73 mM nifedipine vs 1.14 mmHg for control stripped Hb. The effects of the three vasodilators on Hb were correlated with pH, methemoglobin formation, temperature and incubation time. 3. P50 values were determined for Hb of the blood of angina patients treated with one of the vasodilators, and blood 2,3-diphosphoglycerate (2,3-DPG) levels were also measured. In contrast to the in vitro data, neither P50 nor 2,3-DPG levels were significantly modified in the blood of patients treated with one of the vasodilators. 4. These in vitro studies demonstrated that the vasodilators papaverine and dipyridamole decrease, and nifedipine increases the oxygen affinity of Hb in red blood cells or as a purified hemoglobin.

2,3-Diphosphoglycerate↗

PubMed1992

Use of ultrasonic and microsphere techniques to evaluate regional aspects of vasodilator therapy in myocardial ischaemia, arterial hypertension and heart failure.

PURPOSE: To review regional aspects of vasodilator therapy in myocardial ischemia, arterial hypertension and heart failure. DATA IDENTIFICATION: Results were obtained from experiments (1) performed either in experimental animals or in human volunteers or patients; (2) using either ultrasonic or microsphere techniques; (3) on the effects of different drug classes, including angiotensin converting enzyme inhibitors, calcium antagonists, potassium channel openers and nitrates; and (4) on the arterial and arteriolar vasodilating effects of different drug classes. CONCLUSIONS: The regional vasodilator effects, both arteriolar and arterial, of the major classes of drugs used in the treatment of coronary insufficiency, arterial hypertension and cardiac failure appear to be heterogenous. This heterogeneity is seen with a given drug in different vascular beds; within a class of drugs in a single vascular region; and between the regional vasodilator profiles of different classes of drugs. From the clinical point of view, the consequences of this heterogeneous vasodilation may be either positive (increase in flow, favourable redistribution of flow) or negative (steal phenomenon, opening of shunts).

Animals↗

PubMed1992

Inhibition of human internal mammary artery contractions. An in vitro study of vasodilators.

The internal mammary artery is currently the preferred conduit for myocardial revascularization; however, perioperative vasospasm of the internal mammary artery may limit its use as a bypass graft. The ability of various vasodilators to inhibit internal mammary artery contraction was investigated with the use of discarded segments of human internal mammary artery not used in coronary artery bypass grafting. Ring segments of human internal mammary arteries were suspended on strain gauges in muscle baths containing 37 degrees C Krebs solution for measurement of isometric tension in vitro. Arterial contraction was stimulated by elevating the extracellular potassium concentration to 70 mmol/L or by exposure to a 10 mumol/L concentration of norepinephrine, and inhibition of contraction by vasodilators was measured. The order of potency to inhibit potassium-induced contraction was as follows: nifedipine > verapamil > nitroprusside > papaverine. At maximal effective doses, nifedipine, verapamil, and papaverine almost completely inhibited potassium-induced contraction, whereas nitroprusside inhibited contraction by only 55%. When norepinephrine was used to contract the arteries, a biphasic relaxation curve was seen with nifedipine, but not with other vasodilator drugs. The order of potency to inhibit norepinephrine-induced contraction was as follows: nifedipine > nitroprusside > verapamil > papaverine. Maximal inhibition of norepinephrine contraction by these vasodilators ranged from 68% to 95%. Nitroglycerin, isoproterenol, and adenosine produced little or no inhibition of internal mammary artery contraction caused by potassium or norepinephrine. Although nifedipine was the most potent vasodilator, papaverine produced the greatest maximal inhibition of both potassium- and norepinephrine-induced contraction of human internal mammary artery.

Adenosine↗

PubMed2004

[Establishment of a clinical method for evaluating flow-mediated vasodilation(FMD) in brachial artery].

We have established a clinical routine method for evaluating the endothelial function in forearm circulation in humans. Flow-mediated vasodilation(FMD) was used as the endothelium-dependent and the response to nitroglycerin(NTG) as the endothelium-independent vasodilation. Diameter of the brachial artery was measured by high-frequency ultrasonographic imaging before and after hyperemia following artery occlusion. Because vasodilation reached the maximal level when the artery was occluded for 5 min, this time was selected as the occlusion time. FMD was greater (12 vs 9%) after upper-arm occlusion than after forearm occlusion. The peak time to maximal vasodilation was 50 sec after forearm occlusion and 70 sec after upper-arm occlusion. During NO synthesis inhibitor infusion, vasodilation after forearm occlusion was abolished, whereas that after upper-arm occlusion was attenuated by half. Therefore, the mechanisms for FMD may differ by occlusion position. The response to NTG was attenuated by aging. FMD was significantly decreased by coronary artery disease and coronary risk factors such as hypertension, hyperlipidemia and diabetes, but the response to NTG was not changed by these diseases. These measurements may offer useful tools for assessment of endothelial function.

Arteriosclerosis↗

PubMed1979

[Hemodynamic guidelines in the treatment of acute myocardial infarction by means of vasodilators].

Two types of vasodilators are used for treatment of acute myocardial infarction: Nitrates on the one hand with predominant venodilation and agents like Phentolamie and Nitroprusside on the other hand with venodilation as well as arteriolar vasodilation. Different opinions exist with respect to indication of these vasodilators. They are used for reduction of arterial blood pressure, for reduction of left ventricular filling pressure and for increase of cardiac output. A marked decrease in ejection fraction is the hemodynamic basis of application of vasodilators in the latter indication. By reduction of peripheral vascular resistance emptying of the left ventricle in these patients is enhanced.) As a working hypothesis in clinical situation elevated filling pressure indicates a decreased ejection fraction. The first part of this investigation deals with relation of left ventricular and diastolic pressure to ejection fraction. A good correlation between these two parameters was found in 717 patients with coronary artery disease. However variability was so wide that regression from enddiastolic pressure to ejection fraction in the individual seemed impossible. In 26.6% of patients with ejection fraction over 0.6%, filling pressure was 20 mm Hg or more. On the other hand, in 34.7% of patients with ejection fraction below 0.3% filling pressure was 20 mm Hg or less. As a consequence of practical value, reduced ejection fraction has to be assumed, if a patient presents elevated filling pressure and reduced cardiac output. In the second part, the hemodynamic effects of Phentolamine in 12 patients with acute myocardial infarction and elevated filling pressure (PCV resp. PADP greater than 18 mm Hg) are described. Maximal effects on hemodynamic variables were: reduction of peripheral vascular resistance by 31.4%, of left ventricular filling pressure by 16.2%, and of mean arterial pressure by 17.0%. Cardiac output increased by 25.8% and heart rate rose by 14.8%. At optimal efficacy, stroke volume increased by 23.7%. Further increase of infusion rate with concomitant fall of peripheral vascular resistance resulted in decrease of stroke volume and tachycardia. Most serious side effects consisted in sudden fall of blood pressure. Therefore intraarterial monitoring of blood pressure is demanded. The third part deals with hemodynamic effects of nitrates (Isosorbiddinitrate 10 mg p.o.) in patients with acute myocardial infarction and elevated filling pressure. One hour after application peripheral vascular resistance decrease by 16.5%, filling pressure by 20.8%, and mean arterial pressure by 9.0%. Cardiac output stroke volume and heart rate did not change significantly. No side effects were observed with Isosorbiddinitrate although two cases of nitrate syncope occurred with Nitroglycerin, resulting in bradycardia and hypotension. Indications for vasodilator therapy therefore has to be handled as follows: Nitrates should be given to patients with elevated filling pressure and normal cardiac output...

Arrhythmias, Cardiac↗

PubMed2006

Correlation analysis between different parameters of conduit artery and microvascular vasodilation.

Impaired endothelial responsiveness to specific vasodilator stimuli has been used as a surrogate marker of cardiovascular risk. Multiple methods allow testing endothelial responses in both microvessels and conduit arteries, but it is still unclear whether there is a relationship in endothelial function between these two different vascular beds. Twenty-five healthy young non smoking male volunteers (age range 24-45) were enrolled. Radial (conduit) artery (endothelium-dependent) flow-mediated dilation (FMD), microvascular cutaneous reactive hyperemia (using laser Doppler) and acetylcholine-induced microvascular vasodilation (laser Doppler iontophoresis) were measured. Data were analyzed in a randomized fashion in order to test the existence of a correlation among these measures of endothelium (in)dependent vasodilation. Conduit artery FMD showed a negative correlation with resting radial artery diameter (R=0.44, P<0.05). There was a correlation between peak responsiveness to acetylcholine and peak reactive hyperemia (R=0.41, P<0.05). Conversely, absolutely no correlation was shown between FMD and measures of microvascular vasomotion, including reactive hyperemia (P=ns) and acetylcholine-induced vasodilation (P=ns). Using three different human in vivo models, we test conduit artery and microvascular endothelial vasodilation. While microvascular flow reserve measurements induced by endothelium-dependent and independent stimuli appear to be linearly correlated, we show no correlation in endothelium-dependent vasomotion between the micro- and macrocirculation.

Adult↗