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PubMed2003

Flavanol-rich cocoa induces nitric-oxide-dependent vasodilation in healthy humans.

BACKGROUND: Consumption of flavonoid-rich beverages, including tea and red wine, has been associated with a reduction in coronary events, but the physiological mechanism remains obscure. Cocoa can contain extraordinary concentrations of flavanols, a flavonoid subclass shown to activate nitric oxide synthase in vitro. OBJECTIVE: To test the hypothesis that flavanol-rich cocoa induces nitric-oxide-dependent vasodilation in humans. DESIGN: The study prospectively assessed the effects of Flavanol-rich cocoa, using both time and beverage controls. Participants were blinded to intervention; the endpoint was objective and blinded. METHODS: Pulse wave amplitude was measured on the finger in 27 healthy people with a volume-sensitive validated calibrated plethysmograph, before and after 5 days of consumption of Flavanol-rich cocoa [821 mg of flavanols/day, quantitated as (-)-epicatechin, (+)-catechin, and related procyanidin oligomers]. The specific nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) was infused intravenously on day 1, before cocoa, and on day 5, after an acute ingestion of cocoa. RESULTS: Four days of flavanol-rich cocoa induced consistent and striking peripheral vasodilation (P = 0.009). On day 5, pulse wave amplitude exhibited a large additional acute response to cocoa (P = 0.01). L-NAME completely reversed this vasodilation (P = 0.004). In addition, intake of flavanol-rich cocoa augmented the vasodilator response to ischemia. Flavanol-poor cocoa induced much smaller responses (P = 0.005), and none was induced in the time-control study. Flavanol-rich cocoa also amplified the systemic pressor effects of L-NAME (P = 0.005). CONCLUSION: In healthy humans, flavanol-rich cocoa induced vasodilation via activation of the nitric oxide system, providing a plausible mechanism for the protection that flavanol-rich foods induce against coronary events.

Adolescent↗
PubMedDate not supplied

Alpha-adrenoceptor blockade by phentolamine causes beta-adrenergic vasodilation by increased catecholamine release due to presynaptic alpha-blockade.

We tested whether the alpha 1- and alpha 2-blocking agent phentolamine can be used to assess the contribution of alpha-adrenergic constriction in circulatory control. In 15 conscious dogs at rest, phentolamine (2 mg/kg i.v.) caused hypotension (-17 mm Hg mean arterial pressure), vasodilation (-29% total peripheral resistance), tachycardia, and an increase in cardiac output, oxygen consumption, and plasma catecholamines. Following beta-adrenoceptor blockade (2 mg/kg i.v. nadolol), phentolamine still produced hypotension and increased plasma catecholamine levels, but neither vasodilation nor augmented oxygen consumption. During beta-blockade, phentolamine caused a 28-fold decrease in the vasoconstrictor response to norepinephrine infusions. An equihypotensive dosage of the alpha 1-adrenoceptor blocking agent prazosin (1.2 mg/kg i.v.) did not elevate heart rate, cardiac output, plasma catecholamines, or oxygen consumption. The prazosin-induced vasodilation was not attenuated by prior beta-blockade, in contrast to the phentolamine-induced vasodilation. It is concluded that phentolamine increased catecholamine release by presynaptic alpha 2-blockade, thereby suppressing the autoinhibition of transmitter release. This excess of catecholamines causes a rise of oxygen consumption and vasodilation by beta-adrenergic stimulation. Under beta-blockade, this excess competitively counteracts the postsynaptic vascular alpha-blockade. The combination of pre- and postsynaptic effects invalidates the use of phentolamine in the assessment of alpha-adrenoceptor-mediated vasoconstrictor tone.

Animals↗
PubMed1990

Vasodilator action of endothelin-1 in the perfused rat heart.

The effects of bolus injections of porcine endothelin (ET-1, 1-100 pmol) on the coronary microvasculature of isolated perfused rat heart were examined. Results show that ET-1 possesses dose-dependent vasodilator as well as vasoconstrictor properties. The vasodilator effect was transient and preceded its more pronounced and persistent vasoconstrictor action. ET-1-induced vasodilation in rat heart was not associated with release of prostacyclin (PGI2), as shown by radioimmunoassay (RIA) analysis of cardiac effluent and was not blocked by the cyclooxygenase inhibitors flurbiprofen (2 microM) or BW755c (7.5 microM). Neither was the dilatory response to ET-1 inhibited by haemoglobin (10 microM) or potentiated by superoxide dismutase (20 U/ml) but it was abolished by methylene blue (20 microM). However, methylene blue itself caused coronary dilation which could mask the vasodilator action of ET-1. These results show that in isolated perfused rat heart ET-1 possesses a vasodilator action that is not mediated by PGI2 and that may also be independent of release of endothelium-derived relaxing factor (EDRF).

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Endothelium-dependent forearm vasodilation is reduced in normotensive subjects with familial history of hypertension.

Endothelium-dependent vasodilation is reduced in essential hypertensive subjects. To evaluate whether this abnormality is a primary defect or is a consequence of blood pressure increment, in offspring of essential hypertensive and normotensive subjects (n = 13 subjects for each group) matched for age, sex, body weight, and blood pressure, we studied the response of forearm vasculature to acetylcholine (ACh) (an endothelium-dependent vasodilator), sodium nitroprusside (a direct vasodilator of vascular smooth muscle), and forearm ischemia (13 min plus 1 min of exercise) to induce maximal vasodilation. Drugs were infused into the brachial artery at cumulative doses (ACh: 0.15, 0.45, 1.5, 4.5, and 15 micrograms/100 ml of forearm tissue/min; sodium nitroprusside: 1, 3, and 10 micrograms/100 ml of forearm tissue/min) while forearm blood flow was measured by strain-gauge venous plethysmography. The intra-arterial blood pressure and heart rate were continuously monitored. Despite a comparable forearm vascular response to sodium nitroprusside and to forearm ischemia, the effect of ACh was significantly (p < 0.001) reduced in offspring of hypertensive subjects compared to the offspring of normotensive subjects. These data indicate that ACh-mediated forearm vasodilation is reduced in normotensive subjects with a familial history of essential hypertension, a finding that suggests that endothelium dysfunction can precede the appearance of hypertension and that this abnormality might play a role in the pathogenesis of essential hypertension.

Acetylcholine↗
PubMed1993

Muscarinic receptor subtypes mediating vasodilation and vasoconstriction in isolated, perfused simian coronary arteries.

Using the cannula insertion method, we investigated the vascular responses of isolated simian coronary artery to acetylcholine (ACh). When the preparation was partially precontracted by 20 mM KCl, ACh and carbachol induced vasodilation dose dependently in coronary artery with endothelium, but ACh and carbachol contracted the coronary artery after removal of the endothelium by 1 mg saponin. A selective M1 receptor agonist 4-[N-(3-chlorophenyl)carbamoyloxy]-2-butinyltrimethylammonium++ + chloride (McN-A-343) did not affect the perfusion pressure of the precontracted coronary arteries significantly. Both these responses to ACh were inhibited by the M3 receptor antagonist 4-dipheny-lacetoxy N-methylpiperidine methobromide (4-DAMP) in a dose-dependent manner, but not by a selective M2 receptor antagonist AF-DX 116 (11-[[2-[(diethylamino)methyl]-1-piperidinyl] acetyl]-5,11-dihydro-6H-pyrido[2,3-b][1,4]benzo-diazepine-6-one). A selective M1 receptor antagonist pirenzepine did not affect ACh-induced vasoconstriction significantly and inhibited the vasodilation partially only at the highest dose (100 nmol). The effects of three antagonists on the vasodilative responses to carbachol were also studied and almost the same results were observed. Removal of the endothelium did not affect sodium nitroprusside (SNP)-induced vasodilation significantly. Pirenzepine, AF-DX 116, and 4-DAMP did not affect the action of isoproterenol. These data suggest that the vasodilation elicited by ACh is mediated by release of endothelium-derived relaxing factors (EDRF) consequent to the activation of M3 receptors on endothelial cells, and the constriction is mediated by stimulation of M3 receptors on smooth muscle cells in isolated simian coronary arteries.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1999

Improvement of bradykinin endothelium-mediated vasodilation of forearm resistance circulation by quinaprilat in patients with coronary artery disease with or without left ventricular dysfunction.

Angiotensin-converting enzyme (ACE) inhibition potentiates bradykinin and acetylcholine endothelium-mediated vasodilation. Three groups were studied. Group I (n = 10) was the reference group; group II was composed of nine patients with coronary artery disease; and group III of seven patients with coronary artery disease and left ventricular dysfunction. Forearm blood flow was measured with plethysmography. Acetylcholine and bradykinin were administered in a random order in the brachial artery at infusion rates of 40 and 80 microg/min and 10, 30, 100 pmol/min, respectively. Then quinaprilat was infused alone at the rate of 50 microg/min and then coinfused with acetylcholine and bradykinin. Five of the reference subjects were pretreated with acetylsalicylate. Acetylcholine and bradykinin increased forearm blood flow in a dose-dependent manner in the three groups. However, the vasodilator responses to both agents were significantly lower in the two groups of patients than in the reference group. Quinaprilat significantly enhanced the vasodilator response to acetylcholine only in subjects of the reference group, whereas it enhanced the vasodilator response to each dose of bradykinin, both in subjects of the reference group and in patients. Pretreatment with aspirin did not change the vasodilator responses in any group. In healthy persons, quinaprilat had no effect on its own on forearm blood flow but enhanced the response to bradykinin and even acetylcholine. In patients with coronary disease, short-term administration of quinaprilat was able to improve the impaired response to bradykinin. The response to acetylcholine, however, could not be significantly enhanced in contrast to that in healthy subjects.

Acetylcholine↗
PubMed2001

Nebivolol: endothelium-mediated vasodilating effect.

Nebivolol, a racemic mixture of (S,R,R,R) and (R,S,S,S) enantiomers, is the most beta1-selective adrenoceptor antagonist currently available for clinical use. However, its haemodynamic effects differ from those of classical beta-adrenoceptor antagonists as a result of a vasodilating action. Nebivolol is devoid of alpha-adrenergic antagonist actions, and the detailed mechanism of its vasodilator action is unknown. Nebivolol relaxes precontracted strips of canine coronary and carotid artery only if the endothelium is intact, and such relaxation is antagonized by inhibition of nitric oxide (NO) synthase, implicating the endothelial L-arginine/NO mechanism. Nebivolol and atenolol have been compared in phenylephrine preconstricted dorsal hand veins of 11 healthy men. Nebivolol caused venodilation, which was antagonized by N(G)-monomethyl-L-arginine (LNMMA), whereas atenolol did not, suggesting that such a mechanism could also operate in human veins. Venodilation could be functionally important in reducing cardiac pre-load. Beta2-adrenoceptor stimulation increases forearm blood flow (FBF) by activating the L-arginine/NO pathway but nebivolol lacks direct beta2-adrenoceptor agonist activity. Resistance vessel function has been studied by measuring FBF by venous occlusion plethysmography in healthy men during brachial artery infusions of racemic nebivolol and its enantiomers, atenolol, carbachol (a stable analogue of acetylcholine that vasodilates this vascular bed, in part by activating the L-arginine/NO pathway), nitroprusside (a NO donor that causes non-endothelium-dependent vasodilation through the same effector mechanism as endothelium-dependent agonists) and LNMMA. Nebivolol (354 microg/min) increased FBF by 91 +/- 18% (mean +/- SE, n = 8; p < 0.01), whereas an equimolar dose of atenolol had no significant effect. LNMMA inhibited responses to nebivolol and carbachol to a significantly greater extent than it reduced responses to nitroprusside. Antagonism of nebivolol by LNMMA was abolished by L-arginine. The (S,R,R,R) and (R,S,S,S) enantiomers caused similar increases of FBF. To determine whether brachial artery infusion of nebivolol causes vasodilation in the forearm resistance vasculature of patients with essential hypertension and to investigate the possible involvement of the L-arginine/NO pathway, we studied otherwise healthy volunteers with uncomplicated essential hypertension. Nebivolol (88.5, 177 and 354 microg/min, each dose for 6 min) caused similar vasodilatation as in normotensive subjects, and these responses were sensitive to inhibition by LNMMA. If acute effects of nebivolol on the L-arginine/NO pathway persist during chronic treatment of patients with hypertension or heart failure, this could reduce cardiac after-load as well as pre-load, improve organ perfusion and reduce atherogenesis and thrombosis.

Adrenergic beta-1 Receptor Antagonists↗
PubMed2004

The relationship between flow-mediated brachial artery vasodilation and coronary vasomotor responses to bradykinin: comparison with those to acetylcholine.

Flow-mediated dilation (FMD) of brachial artery provides a noninvasive assessment of coronary endothelial dysfunction. Acetylcholine (ACh) has been used as an agent for estimating coronary endothelial function. In contrast to ACh, there is no evidence for a relationship between FMD and coronary vasodilation to bradykinin (BK). The aim of this study was to compare the flow-mediated vasodilation of brachial artery with coronary vasomotor responses to intracoronary ACh or BK in patients with an angiographically normal left anterior descending coronary artery. Ninety-one patients underwent the cardiac catheterization examination with coronary endothelial function testing and the brachial ultrasound study. BK (0.2, 0.6, 2.0 microg/min) and ACh (3, 10, 30 microg/min) were administered into the left coronary artery in a stepwise manner. Coronary blood flow was evaluated by the Doppler flow velocity measurement. Coronary diameters were measured by the quantitative coronary angiography. The assessment of endothelial function in the brachial artery was made in response to reactive hyperemia with high-resolution ultrasound. Bradykinin induced dose-dependent increases in epicardial coronary diameter and blood flow. There was a significant positive correlation between FMD- and BK-induced vasodilations of epicardial coronary arteries (0.2 microg/min: r = 0.30; 0.6 microg/min: r = 0.42; 2.0 microg/min: r = 0.44, P < 0.01, respectively) and resistance coronary arteries (0.2 microg/min: r = 0.40; 0.6 microg/min: r = 0.56; 2.0 microg/min: r = 0.59, P < 0.0001, respectively). FMD correlated with ACh-induced vasomotions of resistance but not epicardial coronary arteries. No correlation was seen between nitroglycerin-induced brachial artery vasodilation and BK-induced coronary vasodilation. The endothelial dysfunction of peripheral arteries correlated well with that of the coronary arteries especially vasomotor responses to BK.

Acetylcholine↗
PubMed2005

Role of vascular endothelial growth factor receptor 1 and vascular endothelial growth factor receptor 2 in the vasodilator response to vascular endothelial growth factor in the neonatal piglet lung.

OBJECTIVE: Vascular endothelial growth factor (VEGF) regulates vascular proliferation and causes vasodilation. In the pulmonary circulation, the vasorelaxing effect of VEGF has been attributed to nitric oxide, whereas in other vascular beds, prostacyclin and other mechanisms are also involved. This vascular effect follows binding to two receptors, VEGF receptor 1 (VEGFR1) and VEGF receptor 2 (VEGFR2), the latter of which is thought to be the main receptor responsible for the vasorelaxing effect of VEGF. The role of VEGFR1 in the neonatal pulmonary vasculature remains to be determined. DESIGN: Prospective randomized laboratory investigation. SETTING: Animal laboratory. SUBJECTS: Newborn Yorkshire-Landrace piglets. INTERVENTIONS: To determine the mechanisms of action of VEGF in the neonatal pulmonary vasculature, the effect of VEGF (10-10 M) was tested in isolated perfused piglet lungs, alone and in the presence of a VEGFR2 kinase inhibitor, N-nitro-l-arginine (L-NNA), indomethacin (Indo), L-NNA + Indo, and GF109203X, a protein kinase C inhibitor. The effect of a VEGFR1 agonist, placenta growth factor (PlGF), was also studied with or without L-NNA. Perfusate was collected, and cyclic guanosine monophosphate (cGMP), as well as 6-keto prostaglandin F1alpha and thromboxane B2, the stable metabolites of prostacyclin and thromboxane, respectively, was measured. MEASUREMENTS AND MAIN RESULTS: VEGF caused vasorelaxation with a concomitant increase in cGMP. PlGF also decreased vascular tone and increased cGMP. VEGFR2 kinase inhibitor did not prevent the reduction in perfusion pressure seen with VEGF but blocked the increase in cGMP. Pretreatment with L-NNA completely inhibited VEGF and PlGF vasodilation and prevented the increase in cGMP seen with both agonists. Pretreatment with Indo or GF109203X did not reduce the dilator response to VEGF. CONCLUSIONS: VEGF vasodilation may follow nitric oxide release in the piglet pulmonary circulation. VEGF vasorelaxation may not only occur through binding to VEGFR2, since PlGF, the specific VEGFR1 agonist, also causes vasodilation. Therefore, vasodilator response to VEGF may involve both types of receptor in the neonatal piglet pulmonary vasculature.

Animals↗
PubMed2005

The nicorandil-induced vasodilation in humans is inhibited by miconazole.

Nicorandil, N-(2-hydroxyethyl)-nicotinamide nitrate, exerts its vasodilatory effects by opening ATP-sensitive potassium (K-ATP) channels and by acting as the exogenous nitric oxide (NO). It is not clear, however, whether the actions of other endothelium-dependent vasodilators, such as NO, endothelium-derived hyperpolarizing factor (EDHF), and prostaglandins, contribute to nicorandil-induced vasodilation in the vasculature in humans. We evaluated forearm blood flow (FBF) response to intraarterial infusion of nicorandil alone and in the presence of glibenclamide, a K-ATP channel inhibitor, N(G)-monomethyl-L-arginine, an NO synthase inhibitor, indomethacin, a cyclooxygenase inhibitor, or miconazol, a cytochrome P-450 inhibitor, in 24 healthy male subjects. FBF was measured using strain-gauge plethysmography. Infusion of nicorandil significantly increased the FBF response in a dose-dependent manner. Intraarterial infusion of glibenclamide attenuated nicorandil-induced vasodilation (160.9 +/- 21.2% versus 90.2 +/- 19.4%, P < 0.01), and miconazole also attenuated the FBF response to nicorandil (160.9 +/- 21.2% versus 66.1 +/- 9.2%, P < 0.001). N-monomethyl-L-arginine or indomethacin did not alter the FBF response to nicorandil. These findings suggest that nicorandil causes vasodilation in forearm circulation in humans, at least in part through a pathway that is dependent on K-ATP channels and cytochrome P-450, but not on endogenous NO and prostaglandins. EDHF may contribute to nicorandil-induced vasodilation in humans.

Adult↗
PubMed2005

Dehydroepiandrosterone sulfate induces acute vasodilation of porcine coronary arteries in vitro and in vivo.

Although an inverse relationship between dehydroepiandrosterone sulfate (DHEAS) and coronary artery disease has been demonstrated in men, the vascular effects of DHEAS are not well defined. The vasoactive effects of intracoronary DHEAS and testosterone (0.1 nM to 1 microM) were examined in vivo in 24 pigs. Epicardial cross-sectional area was measured by intravascular ultrasound, and coronary flow velocity by intravascular Doppler velocimetry. We also examined the effects of antagonism of the androgen receptor, nitric oxide synthase, and potassium channels on DHEAS-induced vasodilation in vitro in coronary rings from male and female pig hearts. DHEAS and testosterone induced increases in cross-sectional area, average peak velocity, and coronary blood flow. The maximal increase in coronary blood flow in response to testosterone was 1.26-fold (P=0.02), and in average peak velocity 1.43-fold (P=0.05), greater than that to DHEAS, whereas increases in cross-sectional area were similar. Vasodilation to both hormones was rapid, with maximal responses occurring <10 minutes after administration. In vitro, DHEAS and testosterone induced vasodilation in coronary rings, greater with testosterone. At doses of 0.1 and 1 microM, the vasodilator effects of DHEAS and testosterone were inhibited by the androgen receptor antagonist flutamide but not the estrogen receptor antagonist ICI 182,780. At 10 microM, neither DHEAS- nor testosterone-induced vasorelaxation was inhibited by flutamide, ICI 182,780, L-NAME, or deendothelialization, but both were attenuated by pretreatment with glibenclamide. No gender differences were observed in any of the responses examined. In conclusion, DHEAS is an acute coronary artery vasodilator, but less potent than testosterone. Its effect might be mediated via androgen receptors and may involve ATP-sensitive potassium channels.

ATP-Binding Cassette Transporters↗
PubMed2006

Angiotensin II/AT2 receptor-induced vasodilation in stroke-prone spontaneously hypertensive rats involves nitric oxide and cGMP-dependent protein kinase.

BACKGROUND: Angiotensin II (Ang II) induces vasodilation, in part, through angiotensin type 2 receptor (AT2R)-induced actions in conditions associated with angiotensin type 1 receptor (AT1R) blockade and AT2R upregulation. Ang II/AT2R-induced vasodilation involves nitric oxide (NO)-cyclic guanosine monophosphate (cGMP)-dependent processes. We previously demonstrated that AT2R-mediated effects involve inhibition of the RhoA/Rho kinase pathway. However, molecular mechanisms underlying this phenomenon are unknown. AIMS: In the present in-vivo study we tested the hypothesis that AT2R-elicited vasodilation is associated with nitric oxide synthase (NOS) activation and NO production, and that a cGMP-dependent protein kinase (cGKI), which inactivates RhoA, is upregulated when stroke-prone spontaneously hypertensive rats (SHRSP) are treated with AT1R blockers. METHODS: SHRSP and Wistar-Kyoto (WKY) rats were treated with the AT1R blocker valsartan for 14 days. Dilatory responses to Ang II with or without the NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME) were performed in norepinephrine-precontracted vessels in the presence of valsartan. Expression of AT2R, endothelial NOS (eNOS) and cGKI was assessed by immunoblotting. NO bioavailability and NAD(P)H oxidase activity were evaluated by chemiluminescence. RESULTS: Ang II elicited vasodilation in valsartan-treated SHRSP. L-NAME inhibited this effect, indicating a role for NO. eNOS expression and NO concentration were increased twofold by valsartan, only in SHRSP. Expression of cGKI was reduced in SHRSP and restored after valsartan treatment. NAD(P)H oxidase activity was approximately threefold higher in SHRSP versus WKY (P < 0.05) and reduced by valsartan. CONCLUSIONS: Ang II, via AT2R, facilitates vasodilation through NOS/NO-mediated pathways and upregulation [corrected] of CGK1 [corrected] after chronic AT1R antagonism. These effects may contribute in part to beneficial actions of AT1R blockers in the treatment of hypertension.

Angiotensin Receptor Antagonists↗
PubMed2003

Comparison of the vasodilating effect of nitroglycerin, verapamil, and tolazoline in hand angiography.

PURPOSE: To compare the vasodilating effect and safety of intraarterial verapamil with the long-accepted standard vasodilators nitroglycerin and tolazoline in hand angiography. MATERIALS AND METHODS: The authors studied 25 patients who underwent brachial artery angiography. In 22 cases, there was poor or moderate visualization of the forearm and hand vasculature. To improve blood flow to the periphery, subsequent angiograms with intraarterial vasodilating agents were obtained. First, nitroglycerin was administered (n = 22). In cases of continuous poor or moderate visualization of the forearm and hand vasculature, another angiogram was obtained with verapamil (n = 21). If opacification remained poor or moderate, eventually tolazoline was injected (n = 20). To avoid pharmacologic interactions of the different vasodilating drugs, a minimum 15-minute interval between series was observed. The degree of opacification of the forearm and hand arteries was graded on a scale from 1 to 5: visualization of the forearm arteries only was defined as 1, of the forearm arteries and superficial/deep palmar arch as 2, of the forearm arteries, superficial/deep palmar arch, and digital arteries to the level of the metacarpophalangeal joints as 3, to the level of the proximal interphalangeal joints as 4, and to the distal interphalangeal joints as 5. RESULTS: All three vasodilating agents demonstrated highly significant improvement in blood flow; verapamil and tolazoline showed statistically greater effects than nitroglycerin. Verapamil caused the fewest and least severe adverse effects. CONCLUSION: Intraarterial verapamil and tolazoline are comparable in terms of vasodilatory efficacy in hand arteries. However, because of its favorable adverse effect profile, verapamil is recommended for optimizing visualization of the peripheral arterial vascular system.

Adult↗
PubMed2000

Ultrasound measurement of brachial flow-mediated vasodilator response.

Brachial artery flow-mediated vasodilation is increasingly used as a measure of endothelial function. High resolution ultrasound provides a noninvasive method to observe this flow-mediated vasodilation by monitoring the diameter of the artery over time following a transient flow stimulus. Since hundreds of ultrasound images are required to continuously monitor brachial diameter for the 2-3 min during which the vasodilator response occurs, an automated diameter estimation is desirable. However, vascular ultrasound images suffer from structural noise caused by the constructive and destructive interference of the backscattered signals, and the true boundaries of interest that define the diameter are frequently obscured by the multiple-layer structure of the vessel wall. These problems make automated diameter estimation strategies based on the detection of the vessel wall boundary difficult. We obtain a robust automated measurement of the vasodilator response by automatically locating the artery using a variable window method, which gives both the lumen center and width. The vessel wall boundary is detected by a global constraint deformable model, which is insensitive to the structural noise in the boundary area. The ambiguity between the desired boundary and other undesired boundaries is resolved by a spatiotemporal strategy. Our method provides excellent reproducibility both for interreader and intrareader analyzes of percent change in diameter, and has been successfully used in analyzing over 4000 brachial flow-mediated vasodilation scans from several medical centers in the United States.

Adult↗
PubMed1995

Response of digital arteries to endothelium dependent and independent vasodilators in patients with Raynaud's phenomenon.

The cause of the digital artery spasm seen in Raynaud's phenomenon (RP) is unclear. A dysfunction of endothelium-dependent vasodilation might contribute to the development of this spasm. We studied the digital artery responses to endothelium-dependent and independent vasodilators in eight Raynaud's phenomenon patients and eight sex-matched controls. A sequential series of infusions alternating with physiological saline were administered at a rate of 1 mL min-1 via the radial artery. The infusions contained acetylcholine chloride (ACh) 110 nm mL-1 and 550 nm mL-1, L-arginine 50 mumol mL-1, prostacyclin (PGI2) 2.5 ng mL-1 and glyceryl trinitrate (GTN) 4.5 nm mL-1. Digital artery diameter (DAD) and cutaneous temperature were measured. DAD was measured using a high frequency A-mode ultrasound scanner. There was no significant difference in mean brachial artery pressure, digital cutaneous temperature and DAD between the two groups at the start of the study. Comparing responses in the groups, there was a significantly greater increase in DAD and cutaneous temperature to Ach (endothelium-dependent vasodilator) at both concentrations in controls. A significantly greater increase in DAD was obtained in response to GTN (endothelium-independent vasodilator) in the RP subjects. There was no significant difference in response to L-arginine and PGI2 between the groups. These results suggest that a dysfunction of endothelium-dependent vasodilation is present in RP patients.

Acetylcholine↗
PubMed1989

Vasodilator responses to dopamine in rat perfused mesentery are age-dependent.

1. Dose-dependent vasodilator responses to dopamine, isoprenaline, noradrenaline, 3-isobutyl-1-methylxanthine (IBMX) and sodium nitroprusside were obtained in isolated perfused mesentery preparations, taken from reserpine-treated rats of different ages. The preparations were pretreated with phenoxybenzamine (1 microM) and perfused with physiological salt solution containing cocaine (10 microM), additional KCl (20 mM) and vasopressin (0.1 microM). 2. Vasodilator responses to dopamine were abolished by the dopamine1 (DA1)-selective antagonist SCH 23390 (10 nM) and those to isoprenaline by propranolol (1 microM), but the vasodilator responses to noradrenaline were abolished only when SCH 23390 and propranolol were used together. This indicated that dopamine was acting via DA1-receptors, isoprenaline via beta-adrenoceptors and that noradrenaline could act via DA1-receptors and beta-adrenoceptors in this preparation. 3. Responses to all the vasodilator drugs decreased in magnitude between the ages of 1 and 2 months. Responses to dopamine declined further in 4 month-old rats and were negligible at 6 or 22-24 months of age. Responses to isoprenaline were well maintained up to 6 months of age, but were negligible at 22-24 months. 4. It is concluded that, in the rat mesenteric vasculature, there is a non-specific decline in responses to vasodilator drugs during development (1 to 2 months). Subsequently there is a specific decline in DA1-receptor-mediated and beta-adrenoceptor-mediated responses; the former are lost at an earlier age than the latter. This different time course suggests that age influences receptor numbers, or their coupling to adenylate cyclase, rather than a post-receptor event in the adenylate cyclase/cyclic AMP pathway.

Aging↗
PubMed1983

Effects of antidromic trigeminal nerve stimulation in relation to parasympathetic vasodilation in cat nasal mucosa.

High threshold stimulation of the trigeminal nerve in sympathectomized cats caused an atropine and hexamethonium resistant vasodilation in the nasal mucosa. Stimulation of efferent parasympathetic neurons to the nose caused a partially atropine sensitive vasodilation which was abolished by hexamethonium. Combined trigeminal and parasympathetic nerve stimulation did not reveal any obvious functional interactions between these two systems. Local intra-arterial infusions of substance P, VIP and acetylcholine caused a dose dependent vasodilation in the nasal mucosa. The relative vasodilatory potencies were substance P greater than to VIP greater than acetylcholine. Local infusions of capsaicin, known to release substance P from nerve endings, caused a marked longlasting biphasic vasodilation which was atropine and hexamethonium resistant. In conclusion, the present findings illustrate the presence of two vasodilator mechanisms of different nervous origin in the nasal mucosa. The trigeminal response is probably mediated via release of substance P, while the parasympathetic effect seems to be caused by acetylcholine and VIP.

Acetylcholine↗
PubMed1994

Regional vasodilating properties of isoflurane in stunned swine myocardium.

Studies about the coronary vasodilating properties of isoflurane indicate that this drug induces coronary vasodilation. No work has examined isoflurane-induced vasodilation in known stunned myocardium. This study was conducted to determine isoflurane's coronary vasodilation potency in stunned myocardium and to compare the results obtained with normal myocardium. We determined the vasodilating properties of isoflurane in regionally perfused swine myocardium. Six domestic swine were anesthetized with pentobarbital and fentanyl. The left anterior descending artery (LAD) was cannulated and perfused with blood drawn from the carotid artery and passed thorough a membrane oxygenator. LAD arterial flow was controlled by a calibrated roller pump with continuous digital readout, and LAD arterial pressure was measured directly. The anterior interventricular vein was cannulated and dimension crystals placed in the LAD-perfused myocardium. Myocardial stunning was induced by reduction of coronary blood flow (CBF) to 30% of control flow for 20 minutes. One hour after reperfusion, the vasodilatory response to 0%, 1%, and 2% isoflurane administered via the membrane oxygenator was determined and compared to maximum vasodilatation produced by regional intracoronary administration of adenosine. Systemic blood pressure and heart rate remained constant throughout the experiment. At 2% isoflurane, systolic shortening and regional myocardial oxygen consumption decreased 53% and 17%, respectively. The same concentration increased CBF by 33% and reduced coronary vascular resistance (CVR) by 25%. One percent isoflurane affected neither CBF nor CVR. Regional coronary administration of adenosine produced much greater changes in CBF (+509) and CVR (-89.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗