Beneficial effect of vitamin E administration on nitric oxide function in subjects with hypercholesterolaemia

1998 ◽  
Vol 95 (3) ◽  
pp. 361-367 ◽  
Author(s):  
Daniel GREEN ◽  
Gerry O'DRISCOLL ◽  
James M. RANKIN ◽  
Andrew J. MAIORANA ◽  
Roger R. TAYLOR
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Vitamin E ◽  
Endothelial Function ◽  
Sodium Nitroprusside ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Elevated Serum ◽  
Tocopherol Concentration ◽  
Forearm Vascular Resistance

1.Vitamin E administration improves endothelial function in hypercholesterolaemic animals but, generally, has not been found to do so in man. The aim of this study was to determine whether vitamin E administration improves basal or stimulated function of the nitric oxide (·NO) dilator system in patients with hypercholesterolaemia. 2.Seven subjects aged 47±3 (±S.E.M.) years with moderately elevated serum cholesterol concentrations (6.0±0.1 ;mmol/l) were given 4 weeks of placebo therapy followed by 500 i.u. of vitamin E twice daily for 4 weeks. Endothelium-dependent and -independent vasodilatation were assessed by intrabrachial infusion of acetylcholine and sodium nitroprusside, and forearm blood flow was measured by strain-gauge plethysmography. Basal ·NO function was assessed by infusion of NG-monomethyl-l-arginine. 3.Plasma α-tocopherol concentration was enhanced after administration of vitamin E (34.6±1.8 to 86.9±9.6 ;μmol/l; P< 0.001). In addition, vitamin E administration significantly increased acetylcholine-mediated vasodilatation whether the results were expressed in terms of changes in absolute forearm blood flow (P< 0.01), forearm vascular resistance (P< 0.05) or forearm blood flow ratios (P< 0.001). Similarly, absolute forearm blood flow (P< 0.05), forearm vascular resistance (P< 0.01) and forearm blood flow ratio (P< 0.01) responses to NG-monomethyl-l-arginine were augmented by vitamin E therapy. Sodium nitroprusside responses were unaltered. 4.These results indicate that 4 weeks therapy with 1000 i.u. of vitamin E daily improves basal and stimulated ·NO-related endothelial function in subjects with hypercholesterolaemia.

Endothelium-derived nitric oxide mediates hypoxic vasodilation of resistance vessels in humans

1996 ◽  
Vol 271 (3) ◽  
pp. H1182-H1185 ◽  
Author(s):  
M. L. Blitzer ◽  
S. D. Lee ◽  
M. A. Creager
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Vasodilator Response ◽  
Healthy Humans ◽  
Resistance Vessels ◽  
Oxide Synthase ◽  
Forearm Vascular Resistance

Endothelium-derived nitric oxide (EDNO) contributes to basal systemic vascular resistance under normoxic conditions. The purpose of this investigation was to determine whether EDNO contributes to the regulation of limb vascular resistance during hypoxia in healthy humans. Forearm blood flow was assessed by venous occlusion plethysmography. Hypoxia was induced by delivering a mixture of N2 and O2 via a gas blender adjusted to reduce the PO2 to 50 mmHg. During hypoxia, forearm blood flow increased from 2.4 +/- 0.2 to 3.0 +/- 0.3 ml.100 ml-1.min-1 (P < 0.001), and forearm vascular resistance decreased from 38 +/- 3 to 29 +/- 3 units (P < 0.001). The nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA, 2,000 micrograms/min intra-arterially) was administered to eight subjects. The percent increase in forearm vascular resistance after administration of L-NMMA was greater during hypoxia than normoxia (67 +/- 14 vs. 39 +/- 15%, P < 0.05). L-NMMA reduced the forearm vasodilator response to hypoxia from 27 +/- 3 to 11 +/- 5% (P = 0.01). To exclude the possibility that this attenuated response to hypoxia was a consequence of vasoconstriction and not specific for nitric oxide synthase inhibition, six subjects received intra-arterial phenylephrine. Phenylephrine did not affect the vasodilator response to hypoxia (17 +/- 3 vs. 21 +/- 6%, P = NS). It is concluded that EDNO contributes to hypoxia-induced vasodilation in the forearm resistance vessels in healthy humans.

Effect of Chronic Smoking on Endothelium-Dependent Vascular Relaxation in Humans

1993 ◽  
Vol 85 (1) ◽  
pp. 51-55 ◽  
Author(s):  
Marie-Cécile Jacobs ◽  
Jacques W. M. Lenders ◽  
Jan A. Kapma ◽  
Paul Smits ◽  
Theo Thien
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cigarette Smoking ◽  
Sodium Nitroprusside ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Vascular Relaxation ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

1. Cigarette smoking is one of the major risk factors for the development of atherosclerosis. It is not clear, however, whether chronic cigarette smoking impairs the normal physiological function of the endothelium before the development of morphological vascular lesions. To test this, we investigated endothelium-dependent vascular relaxation in young habitual smoking subjects. 2. In 11 non-smokers and 10 habitual smokers we measured the changes in bilateral forearm blood flow, arterial blood pressure and forearm vascular resistance (ratio between mean arterial blood pressure and forearm blood flow) during three interventions: postocclusive forearm hyperaemia, intrabrachial infusion of methacholine which causes vasodilatation by stimulating the release of endothelium-dependent relaxing factor, and intrabrachial infusion of sodium nitroprusside which causes vasodilatation independently from the endothelium by a direct effect on the vascular smooth muscle wall. 3. During infusion of the highest dose of methacholine, forearm vascular resistance decreased by 91.7 ± 1.4% in the smokers and by 89.9 ± 1.8% in the non-smokers. During infusion of sodium nitroprusside, forearm vascular resistance decreased by 80.0 ± 3.8% in the smokers as compared with 80.7 ± 6.1% in the non-smokers. There was no difference in basal forearm vascular resistance or in post-ischaemic reactive hyperaemia between smokers and non-smokers. Thus, vasodilatation induced by both methacholine and sodium nitroprusside was not significantly different between smokers and non-smokers. 4. We conclude that in young habitual cigarette smokers the endothelium-dependent vasodilatation in the forearm seems to be preserved, suggesting that habitual smoking does not result in permanent endothelial dysfunction in the human forearm.

Age-independent forearm vasodilatation by acetylcholine and adenosine 5′-triphosphate in humans

1990 ◽  
Vol 78 (1) ◽  
pp. 89-93 ◽  
Author(s):  
Tsutomu Imaizumi ◽  
Akira Takeshita ◽  
Satoshi Suzuki ◽  
Megumu Yoshida ◽  
Shinichi Ando ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Vascular Resistance ◽  
Brachial Artery ◽  
Forearm Blood Flow ◽  
Resistance Arteries ◽  
Dose Dependent ◽  
Forearm Vascular Resistance ◽  
Age Independent

1. Forearm vasodilator responses to acetylcholine, ATP and sodium nitroprusside were examined in healthy young (20 ± 1 years, n = 9), middle-aged (46 ± 2 years, n = 6) and old (57 ± 1 years, n = 6) subjects. 2. A brachial artery was cannulated with a 20-gauge cannula through which drugs at graded doses were locally infused for 2 min at each dose. During drug infusions, forearm blood flow was continuously measured at 15 s intervals using a plethysmograph. Forearm vascular resistance was calculated from forearm blood flow and mean blood pressure obtained in the opposite arm. Basal forearm blood flow and forearm vascular resistance did not differ between the three groups. 3. Acetylcholine and ATP were used to examine endothelium-dependent vasodilatation, and sodium nitroprusside was used to examine endothelium-independent vasodilatation. All three drugs caused dose-dependent increases in forearm blood flow (P < 0.01) and decreases in forearm vascular resistance (P < 0.01). The increases in forearm blood flow or decreases in forearm vascular resistance in response to infusions of the three drugs did not differ between the three groups. 4. These results suggest that endothelium-dependent and endothelium-independent vasodilatation in forearm resistance arteries do not alter with ageing in humans.

Forearm and finger blood flow responses to passive body tilts

1979 ◽  
Vol 46 (2) ◽  
pp. 288-292 ◽  
Author(s):  
Y. A. Mengesha ◽  
G. H. Bell
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Pulse Rate ◽  
Forearm Blood Flow ◽  
Body Tilt ◽  
Finger Blood Flow ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

Ten to fifteen healthy subjects, ages 18--30 yr, were used to assess the correlation of forearm blood flow with graded passive body tilts and vascular resistance and also to discern the relative effects of body tilts on finger blood flow. In the head-up tilts forearm blood flow and arterial blood pressure fell progressively, whereas forearm vascular resistance and pulse rate increased. In the head-down tilts the forearm blood flow and the arterial blood pressure increased, whereas the forearm vascular resistance and pulse rate decreased. These changes were found to be significantly correlated with the different tilt angles and with one another. In a preliminary study it was found that infrared heating of the carpometacarpal region produced finger vasodilatation similar to the forearm vasodilatation observed by Crockford and Hellon (6). However, unlike forearm blood flow, finger blood flow showed no appreciable response to either the head-up or head-down tilts. This indicates that the sympathetic tone and the volume of blood in the finger are not appreciably altered by this test procedure at least 1 min after the body tilt is assumed.

Characterization of endothelium-derived hyperpolarizing factor in the human forearm microcirculation

2001 ◽  
Vol 280 (6) ◽  
pp. H2470-H2477 ◽  
Author(s):  
Julian P. J. Halcox ◽  
Suresh Narayanan ◽  
Laura Cramer-Joyce ◽  
Rita Mincemoyer ◽  
Arshed A. Quyyumi
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Human Subjects ◽  
Epoxyeicosatrienoic Acid ◽  
Healthy Human ◽  
Human Forearm ◽  
Oxide Synthase ◽  
Cytochrome P 450

The identity of endothelium-dependent hyperpolarizing factor (EDHF) in the human circulation remains controversial. We investigated whether EDHF contributes to endothelium-dependent vasomotion in the forearm microvasculature by studying the effect of K+ and miconazole, an inhibitor of cytochrome P-450, on the response to bradykinin in healthy human subjects. Study drugs were infused intra-arterially, and forearm blood flow was measured using strain-gauge plethysmography. Infusion of KCl (0.33 mmol/min) into the brachial artery caused baseline vasodilation and inhibited the vasodilator response to bradykinin, but not to sodium nitroprusside. Thus the incremental vasodilation induced by bradykinin was reduced from 14.3 ± 2 to 7.1 ± 2 ml · min−1 · 100 g−1( P < 0.001) after KCl infusion. A similar inhibition of the bradykinin ( P = 0.014), but not the sodium nitroprusside (not significant), response was observed with KCl after the study was repeated during preconstriction with phenylephrine to restore resting blood flow to basal values after KCl. Miconazole (0.125 mg/min) did not inhibit endothelium-dependent or -independent responses to ACh and sodium nitroprusside, respectively. However, after inhibition of cyclooxygenase and nitric oxide synthase with aspirin and N G-monomethyl-l-arginine, the forearm blood flow response to bradykinin ( P = 0.003), but not to sodium nitroprusside (not significant), was significantly suppressed by miconazole. Thus nitric oxide- and prostaglandin-independent, bradykinin-mediated forearm vasodilation is suppressed by high intravascular K+ concentrations, indicating a contribution of EDHF. In the human forearm microvasculature, EDHF appears to be a cytochrome P-450 derivative, possibly an epoxyeicosatrienoic acid.

Adenosine contributes to hypoxia-induced forearm vasodilation in humans

1999 ◽  
Vol 87 (6) ◽  
pp. 2218-2224 ◽  
Author(s):  
Urs A. Leuenberger ◽  
Kris Gray ◽  
Michael D. Herr
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Brachial Artery ◽  
Adenosine Receptors ◽  
Forearm Blood Flow ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Normal Subjects ◽  
Local Release ◽  
Forearm Vascular Resistance

In humans, hypoxia leads to increased sympathetic neural outflow to skeletal muscle. However, blood flow increases in the forearm. The mechanism of hypoxia-induced vasodilation is unknown. To test whether hypoxia-induced vasodilation is cholinergically mediated or is due to local release of adenosine, normal subjects were studied before and during acute hypoxia (inspired O210.5%; ∼20 min). In experiment I, aminophylline (50–200 μg ⋅ min−1 ⋅ 100 ml forearm tissue−1) was infused into the brachial artery to block adenosine receptors ( n = 9). In experiment II, cholinergic vasodilation was blocked by atropine (0.4 mg over 4 min) infused into the brachial artery ( n = 8). The responses of forearm blood flow (plethysmography) and forearm vascular resistance to hypoxia in the infused and opposite (control) forearms were compared. During hypoxia (arterial O2 saturation 77 ± 2%), minute ventilation and heart rate increased while arterial pressure remained unchanged; forearm blood flow rose by 35 ± 6% in the control forearm but only by 5 ± 8% in the aminophylline-treated forearm ( P < 0.02). Accordingly, forearm vascular resistance decreased by 29 ± 5% in the control forearm but only by 9 ± 6% in the aminophylline-treated forearm ( P < 0.02). Atropine did not attenuate forearm vasodilation during hypoxia. These data suggest that adenosine contributes to hypoxia-induced vasodilation, whereas cholinergic vasodilation does not play a role.

Role of Nitric Oxide towards Vasodilator Effects of Substance P and ATP in Human Forearm Vessels

1997 ◽  
Vol 92 (2) ◽  
pp. 123-131 ◽  
Author(s):  
Masanari Shiramoto ◽  
Tsutomu Imaizumi ◽  
Yoshitaka Hirooka ◽  
Toyonari Endo ◽  
Takashi Namba ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Substance P ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Dependent Manner ◽  
Human Forearm ◽  
Before And After ◽  
Dose Dependent

1. It has been shown in animals that substance P as well as acetylcholine releases endothelium-derived nitric oxide and evokes vasodilatation and that ATP-induced vasodilatation is partially mediated by nitric oxide. The aim of this study was to examine whether vasodilator effects of substance P and ATP are mediated by nitric oxide in humans. 2. In healthy volunteers (n = 35), we measured forearm blood flow by a strain-gauge plethysmograph while infusing graded doses of acetylcholine, substance P, ATP or sodium nitroprusside into the brachial artery before and after infusion of NG-monomethyl-l-arginine (4 or 8 μmol/min for 5 min). In addition, we measured forearm blood flow while infusing substance P before and during infusion of l-arginine (10 mg/min, simultaneously), or before and 1 h after oral administration of indomethacin (75 mg). 3. Acetylcholine, substance P, ATP or sodium nitroprusside increased forearm blood flow in a dose-dependent manner. NG-Monomethyl-l-arginine decreased basal forearm blood flow and inhibited acetylcholine-induced vasodilatation but did not affect substance P-, ATP-, or sodium nitroprusside-induced vasodilatation. Neither supplementation of l-arginine nor pretreatment with indomethacin affected substance P-induced vasodilatation. 4. Our results suggest that, in the human forearm vessels, substance P-induced vasodilatation may not be mediated by either nitric oxide or prostaglandins and that ATP-induced vasodilatation may also not be mediated by nitric oxide.

Four weeks of cycle training increases basal production of nitric oxide from the forearm

1997 ◽  
Vol 272 (3) ◽  
pp. H1070-H1077 ◽  
Author(s):  
B. A. Kingwell ◽  
B. Sherrard ◽  
G. L. Jennings ◽  
A. M. Dart
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Protective Effects ◽  
Nitric Oxide Synthase Inhibitor ◽  
Nitrite Production ◽  
Cycle Training ◽  
Nitrate And Nitrite

The purpose of this study was to determine whether nontrained vascular beds might contribute to the beneficial effects of exercise, including reduced blood pressure by enhanced nitric oxide production. Thirteen healthy, sedentary male volunteers performed 4 wk of normal sedentary activity and 4 wk of cycle training in a randomized order. At the end of each intervention, venous occlusion plethysmography was used to study the forearm blood flow responses to intra-arterial infusions of the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA), acetylcholine, and sodium nitroprusside. Training increased the maximal work-load and maximal oxygen consumption, whereas intrabrachial blood pressure was reduced. L-NMMA caused a greater vasoconstriction after training (P = 0.004). Net nitrate and nitrite consumption by the forearm was less after training both before and after administration of L-NMMA (P = 0.04), consistent with increased nitrate and nitrite production from nitric oxide metabolism. There was no difference in the response to acetylcholine or sodium nitroprusside between the two states. Preliminary studies showed an increase in forearm blood flow and blood viscosity after cycling, suggesting that elevated shear stress in this vascular bed may contribute to endothelial adaptation and the cardiovascular protective effects of exercise training.

scholarly journals Peripheral vascular resistance increases after termination of obstructive apneas

2001 ◽  
Vol 91 (5) ◽  
pp. 2359-2365 ◽  
Author(s):  
Amit Anand ◽  
Stacia Remsburg-Sailor ◽  
Sandrine H. Launois ◽  
J. Woodrow Weiss
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Upper Airway ◽  
Blood Velocity ◽  
Peripheral Vascular ◽  
Arterial Diameter ◽  
Peripheral Vasoconstriction ◽  
Airway Obstructions ◽  
Forearm Vascular Resistance

The mechanisms by which obstructive apneas produce intermittent surges in arterial pressure remain poorly defined. To determine whether termination of obstructive apneas produce peripheral vasoconstriction, we assessed forearm blood flow during and after obstructive events in sleeping patients experiencing spontaneous upper airway obstructions. In all subjects, heart rate was monitored with an electrocardiogram and blood pressure was monitored continuously with digital plethysmography. In 10 patients ( protocol 1), we used forearm plethysmography to assess forearm blood flow, from which we calculated forearm vascular resistance by performing venous occlusions during and after obstructive episodes. In an additional four subjects, we used simultaneous Doppler and B-mode images of the brachial artery to measure blood velocity and arterial diameter, from which we calculated brachial flow continuously during spontaneous apneas ( protocol 2). In protocol 1, forearm vascular resistance increased 71% after apnea termination (29.3 ± 15.4 to 49.8 ± 26.5 resistance units, P < 0.05) with all patients showing an increase in resistance. In protocol 2, brachial resistance increased at apnea termination in all subjects (219.8 ± 22.2 to 358.3 ± 46.1 mmHg · l−1 · min; P = 0.01). We conclude that termination of obstructive apneas is associated with peripheral vasoconstriction.

Haemodynamic effects of physiological concentrations of circulating noradrenaline in man

1988 ◽  
Vol 75 (5) ◽  
pp. 469-475 ◽  
Author(s):  
Peter C. Chang ◽  
Eugene Kriek ◽  
Jacques A. Van Der Krogt ◽  
Gerard-Jan Blauw ◽  
Peter Van Brummelen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Haemodynamic Effects ◽  
Plasma Noradrenaline ◽  
Arterial Blood ◽  
Forearm Vascular Resistance ◽  
Venous Plasma

1. To define the role of circulating noradrenaline in cardiovascular regulation, threshold concentrations for haemodynamic effects were determined in arterial and venous plasma of eight healthy volunteers. 2. Five doses of noradrenaline, 0–54 ng min−1 kg−1, were infused intravenously in random order and single-blind for 15 min per dose. Changes in intra-arterial blood pressure, heart rate, forearm blood flow and forearm vascular resistance were determined, and plasma noradrenaline was measured in arterial and venous blood samples. 3. Significant increases in systolic and diastolic blood pressure were found at arterial and venous plasma noradrenaline concentrations (means ±sem) of 3.00 ± 0.23 and 1.35 ±0.12 nmol/l, respectively. A significant decrease in heart rate was found at arterial and venous plasma noradrenaline concentrations of 8.99 ± 0.69 and 3.09 ± 0.60 nmol/l, respectively. The lower doses of noradrenaline tended to increase forearm blood flow and to decrease forearm vascular resistance, whereas the higher doses had no consistent effect on forearm haemodynamics. 4. During the noradrenaline infusions 73 ± 5% of the increase in arterial plasma noradrenaline concentration was extracted in the forearm. 5. The venous plasma noradrenaline threshold concentration was found to be much lower than previously reported. It is concluded that arterial and venous plasma noradrenaline concentrations which are readily encountered in physiological circumstances elicit haemodynamic effects.

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