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.

Patients with obstructive sleep apnea have an abnormal peripheral vascular response to hypoxia

1999 ◽  
Vol 87 (3) ◽  
pp. 1148-1153 ◽  
Author(s):  
Stacia Remsburg ◽  
Sandrine H. Launois ◽  
J. Woodrow Weiss
Keyword(s):  
Blood Flow ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Arterial Oxygen ◽  
Vascular Response ◽  
Peripheral Vascular ◽  
Obstructive Sleep ◽  
Forearm Vascular Resistance

Patients with obstructive sleep apnea (OSA) have been reported to have an augmented pressor response to hypoxic rebreathing. To assess the contribution of the peripheral vasculature to this hemodynamic response, we measured heart rate, mean arterial pressure (MAP), and forearm blood flow by venous occlusion plethysmography in 13 patients with OSA and in 6 nonapneic control subjects at arterial oxygen saturations ([Formula: see text]) of 90, 85, and 80% during progressive isocapnic hypoxia. Measurements were also performed during recovery from 5 min of forearm ischemia induced with cuff occlusion. MAP increased similarly in both groups during hypoxia (mean increase at 80% [Formula: see text]: OSA patients, 9 ± 11 mmHg; controls, 12 ± 7 mmHg). Forearm vascular resistance, calculated from forearm blood flow and MAP, decreased in controls (mean change −37 ± 19% at [Formula: see text]80%) but not in patients (mean change −4 ± 16% at 80%[Formula: see text]). Both groups decreased forearm vascular resistance similarly after forearm ischemia (maximum change from baseline −85%). We conclude that OSA patients have an abnormal peripheral vascular response to isocapnic hypoxia.

Vasodilation contributes to the rapid hyperemia with rhythmic contractions in humans

1998 ◽  
Vol 76 (4) ◽  
pp. 418-427 ◽  
Author(s):  
J K Shoemaker ◽  
M E Tschakovsky ◽  
R L Hughson
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Perfusion Pressure ◽  
Blood Velocity ◽  
Pulsed Doppler ◽  
Contraction Rate ◽  
Handgrip Exercise ◽  
Arterial Diameter ◽  
Exercise Tests ◽  
Rhythmic Contractions

The hypothesis that the rapid increases in blood flow at the exercise onsetare exclusively due to the mechanical effects of the muscle pump was tested in six volunteersduring dynamic handgrip exercise. While supine, each subject completed a series of eightdifferent exercise tests in which brachial artery blood pressure (BP) was altered by25–30 mmHg (1 mmHg = 133.3 Pa) by positioning the arm above or below the heart.Two different weights, corresponding to 4.9 and 9.7% of maximal voluntary isometriccontraction, were raised and lowered at two different contraction rate schedules (1s:1s and 2s:2swork–rest) each with a 50% duty cycle. Beat-by-beat measures of mean blood velocity (MBV)(pulsed Doppler) were obtained at rest and for 5 min following step increases in work ratewith emphasis on the first 24 s. MBV was increased 50–100% above rest following the firstcontraction in both arm positions (p < 0.05). The increase in MBV from rest was greaterin the below position compared with above, and this effect was observed following the first andsubsequent contractions (p < 0.05). However, the positional effect on the increase inMBV could not be explained entirely by the ~40% greater BP in this position. Also, the greaterworkload resulted in greater increases in MBV as early as the first contraction, compared withthe light workload (p < 0.05) despite similar reductions in forearm volume followingsingle contractions. MBV was greater with faster contraction rate tests by 8 s of exercise. Itwas concluded that microvascular vasodilation must act in concert with a reduction in venouspressure to increase forearm blood flow within the initial 2–4 s of exercise.Key words: Doppler, mean blood velocity, arterial diameter,handgrip exercise, perfusion pressure.

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.

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.

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.

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.

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.

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.

Impaired endothelium-mediated vasodilation is not the principal cause of vasoconstriction in heart failure

2000 ◽  
Vol 278 (1) ◽  
pp. H168-H174 ◽  
Author(s):  
Carlos E. Negrao ◽  
Michele A. Hamilton ◽  
Gregg C. Fonarow ◽  
Antoine Hage ◽  
Jaime D. Moriguchi ◽  
...  
Keyword(s):  
Heart Failure ◽  
New York ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Mental Stress ◽  
Forearm Blood Flow ◽  
Heart Association ◽  
Normal Subjects ◽  
Saline Control ◽  
Forearm Vascular Resistance

The extent to which abnormal endothelium-dependent vasodilator mechanisms contribute to abnormal resting vasoconstriction and blunted reflex vasodilation seen in heart failure is unknown. The purpose of this study was to test the hypothesis that the resting and reflex abnormalities in vascular tone that characterize heart failure are mediated by abnormal endothelium-mediated mechanisms. Thirteen advanced heart-failure patients (New York Heart Association III-IV) and 13 age-matched normal controls were studied. Saline, acetylcholine (20 μg/min), orl-arginine (10 mg/min) was infused into the brachial artery, and forearm blood flow was measured by venous plethysmography at rest and during mental stress. At rest, acetylcholine decreased forearm vascular resistance in normal subjects, but this response was blunted in heart failure. During mental stress with intra-arterial acetylcholine orl-arginine, the decrease in forearm vascular resistance was not greater than during saline control in heart failure [saline control vs. acetylcholine (7 ± 3 vs. 6 ± 3, P = NS) or vs.l-arginine (9 ± 2 units, P = NS)]. The increase in forearm blood flow was not greater than during saline control in heart failure [saline control vs. acetylcholine (1.2 ± 0.3 vs. 1.3 ± 0.3, P = NS), or vs.l-arginine (1.2 ± 0.2 ml ⋅ min−1 ⋅ 100 ml−1, P = NS)]. Furthermore, during mental stress with nitroprusside, the decrease in forearm vascular resistance was not greater than during saline control [saline control vs. nitroprusside (7 ± 3 vs. 5 ± 4 ml ⋅ min−1 ⋅ 100 g−1, P = NS)], and the increase in forearm blood flow was not greater than during saline control [saline control vs. nitroprusside (1.2 ± 0.3 vs. 1.3 ± 0.5 ml ⋅ min−1 ⋅ 100 g−1, P = NS)]. Because the endothelial-independent agent nitroprusside was unable to restore resting and reflex vasodilation to normal in heart failure, we conclude that impaired endothelium-mediated vasodilation with acetylholine-nitric oxide cannot be the principal cause of the attenuated resting- or reflex-mediated vasodilation in heart failure.

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