Effects of arm dominance and brachial artery cannulation on forearm blood flow measured by strain-gauge plethysmography

1999 ◽  
Vol 97 (5) ◽  
pp. 539-546 ◽  
Author(s):  
Adriaan M. KAMPER ◽  
Peter C. CHANG
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Intravenous Infusion ◽  
Forearm Blood Flow ◽  
Arterial Cannulation ◽  
Flow Measurements ◽  
Artery Cannulation ◽  
Before And After ◽  
Blood Flow Ratio ◽  
Arm Dominance

The human forearm model is used extensively in physiological, pharmacological and clinical investigations. Effects of arm dominance or arterial cannulation on forearm flow measurements have never been tested formally. In the present study we tested the hypotheses that left or right arm dominance or cannulation of the brachial artery do not affect forearm haemodynamic responses to physiological or pharmacological stimuli. Results obtained in 16 volunteers showed that forearm blood flow responses to physiological stimuli are comparable before and after intra-arterial cannulation in either the dominant or the non-dominant forearm. Cannulation of a forearm brachial artery has a small effect on baseline blood flow. Responses to intra-arterially infused noradrenaline (norepinephrine) were not influenced by left or right arm dominance. Intravenous infusion of noradrenaline in eight subjects resulted in small responses in forearm blood flow that were slightly asymmetrical. During the intravenous infusion of noradrenaline, forearm blood flow or the forearm blood flow ratio did not reflect the marked increase in FVR that occurred. These results support our hypotheses (a) that either arm can be used as the control or intervention arm, and (b) that intra-arterial cannulation does not affect the results of intra-arterial infusion studies.

Selective α2-adrenergic properties of dexmedetomidine over clonidine in the human forearm

2005 ◽  
Vol 99 (2) ◽  
pp. 587-592 ◽  
Author(s):  
Shizue Masuki ◽  
Frank A. Dinenno ◽  
Michael J. Joyner ◽  
John H. Eisenach
Keyword(s):  
Blood Flow ◽  
Young Adults ◽  
Brachial Artery ◽  
Forearm Blood Flow ◽  
Adrenergic Blockade ◽  
Norepinephrine Release ◽  
Similar Extent ◽  
Human Forearm ◽  
Before And After

We tested the hypothesis that dexmedetomidine (Dex) has greater α2- vs. α1 selectivity than clonidine and causes more α2-selective vasoconstriction in the human forearm. After local β-adrenergic blockade with propranolol, forearm blood flow (plethysmography) responses to brachial artery administration of Dex, clonidine, and phenylephrine (α1-agonist) were determined in healthy young adults before and after α2-blockade with yohimbine ( n = 10) or α1-blockade with prazosin ( n = 9). Yohimbine had no effect on phenylephrine-mediated vasoconstriction but blunted Dex-mediated vasoconstriction (mean ± SE: −41 ± 5 vs. −11 ± 2%; before vs. after yohimbine) more than clonidine-mediated vasoconstriction (−39 ± 5 vs. −28 ± 4%; before vs. after yohimbine) ( P < 0.02). Prazosin blunted phenylephrine-mediated vasoconstriction (−39 ± 4 vs. −8 ± 2%; before vs. after prazosin) but had similar effects on both Dex- (−30 ± 4 vs. −39 ± 6%; before vs. after prazosin) and clonidine-mediated vasoconstriction (−29 ± 3 vs. −41 ± 7%; before vs. after prazosin) ( P > 0.7). Both Dex and clonidine reduced deep forearm venous norepinephrine concentrations to a similar extent (−59 ± 12 vs. −55 ± 10 pg/ml; Dex vs. clonidine, P > 0.6); this effect was abolished by yohimbine and blunted by prazosin. These results suggest that Dex causes more α2-selective vasoconstriction in the forearm than clonidine. The similar vasoconstrictor responses to both drugs after prazosin might be explained by the presynaptic effects on norepinephrine release.

Acute Hypertension Impairs Endothelium-Dependent Vasodilatation

1998 ◽  
Vol 94 (6) ◽  
pp. 601-607 ◽  
Author(s):  
Jonas Millgård ◽  
Lars Lind
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Acute Hypertension ◽  
Flow Measurements ◽  
Sustained Hypertension ◽  
Before And After ◽  
Normotensive Subjects ◽  
Blood Flow Measurements

1. Previous investigations have demonstrated an impaired endothelium-dependent vasodilatation (EDV) in patients with hypertension. The present study aimed to investigate if an acute rise in blood pressure to hypertensive levels impairs EDV in otherwise normotensive subjects. 2. Twenty-seven young, healthy, normotensive subjects were studied. Eight of these underwent evaluation of EDV and endothelium-independent vasodilatation (EIDV) by means of forearm blood flow measurements during local intra-arterial infusions of methacholine (2 and 4 μg/min) and sodium nitroprusside (5 and 10 μg/min), before and after 1 h of sustained hypertension, induced by noradrenaline given intravenously. Identical measurements were made in 11 subjects before and during concomitant local intra-arterial infusion of noradrenaline without change in blood pressure and eight subjects were studied during saline infusions. 3. One hour of sustained hypertension (diastolic blood pressure > 95 mmHg) significantly attenuated both forearm blood flow (17.4 ± 6.8 versus 27.4 ± 6.8 ml · min−1 · 100 ml−1 tissue at baseline, P < 0.05) and forearm vascular resistance decrease (3.2 ± 0.87 versus 7.4 ± 2.5 units at baseline, P < 0.05) during methacholine infusion. These attenuations were significantly more pronounced for methacholine than for sodium nitroprusside (P < 0.05). In contrast, local intra-arterial noradrenaline infusions impaired vasodilatation induced by methacholine and sodium nitroprusside to a similar extent. Saline infusions did not change either EDV or EIDV. 4. Thus, an acute rise in blood pressure to hypertensive levels induced by noradrenaline impaired EDV more than EIDV in otherwise normotensive subjects, while no such selective effect of local noradrenaline was seen, suggesting that a high blood pressure impairs endothelial vasodilator function.

Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans

1996 ◽  
Vol 81 (4) ◽  
pp. 1516-1521 ◽  
Author(s):  
J. K. Shoemaker ◽  
H. L. Naylor ◽  
Z. I. Pozeg ◽  
R. L. Hughson
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Time Course ◽  
Forearm Blood Flow ◽  
Voluntary Contraction ◽  
Double Blind ◽  
Rate Of Increase ◽  
Forearm Exercise ◽  
Blind Manner ◽  
Exercise In Humans

Shoemaker, J. K., H. L. Naylor, Z. I. Pozeg, and R. L. Hughson. Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans. J. Appl. Physiol. 81(4): 1516–1521, 1996.—The time course and magnitude of increases in brachial artery mean blood velocity (MBV; pulsed Doppler), diameter ( D; echo Doppler), mean perfusion pressure (MPP; Finapres), shear rate (γ˙ = 8 ⋅ MBV/ D), and forearm blood flow (FBF = MBV ⋅ π r 2) were assessed to investigate the effect that prostaglandins (PGs) have on the hyperemic response on going from rest to rhythmic exercise in humans. While supine, eight healthy men performed 5 min of dynamic handgrip exercise by alternately raising and lowering a 4.4-kg weight (∼10% maximal voluntary contraction) with a work-to-rest cycle of 1:1 (s/s). When the exercise was performed with the arm positioned below the heart, the rate of increase in MBV and γ˙ was faster compared with the same exercise performed above the heart. Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) and placebo were administered orally for 2 days before two separate testing sessions in a double-blind manner. Resting heart rate was reduced in Ibu (52 ± 3 beats/min) compared with placebo (57 ± 3 beats/min) ( P < 0.05) without change to MPP. With placebo, D increased in both arm positions from ∼4.3 mm at rest to ∼4.5 mm at 5 min of exercise ( P < 0.05). This response was not altered with Ibu ( P > 0.05). Ibu did not alter the time course of MBV or forearm blood flow ( P > 0.05) in either arm position. The γ˙ was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 s of below the heart exercise ( P < 0.05). Because PG inhibition altered the time course ofγ˙ at the brachial artery, but not FBF, it was concluded that PGs are not essential in regulating the blood flow responses to dynamic exercise in humans.

Effects of forearm bier block with bretylium on the hemodynamic and metabolic responses to handgrip

2000 ◽  
Vol 279 (2) ◽  
pp. H586-H593 ◽  
Author(s):  
Frank Lee ◽  
J. Kevin Shoemaker ◽  
Patrick M. McQuillan ◽  
Allen R. Kunselman ◽  
Michael B. Smith ◽  
...  
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Muscle Blood Flow ◽  
Reflex Responses ◽  
Muscle Ph ◽  
Before And After ◽  
Autonomic Reflex ◽  
Bier Block ◽  
Forearm Muscle ◽  
Increased Blood Flow

We tested the hypothesis that a reduction in sympathetic tone to exercising forearm muscle would increase blood flow, reduce muscle acidosis, and attenuate reflex responses. Subjects performed a progressive, four-stage rhythmic handgrip protocol before and after forearm bier block with bretylium as forearm blood flow (Doppler) and metabolic (venous effluent metabolite concentration and 31P-NMR indexes) and autonomic reflex responses (heart rate, blood pressure, and sympathetic nerve traffic) were measured. Bretylium inhibits the release of norepinephrine at the neurovascular junction. Bier block increased blood flow as well as oxygen consumption in the exercising forearm ( P < 0.03 and P < 0.02, respectively). However, despite this increase in flow, venous K+ release and H+release were both increased during exercise ( P < 0.002 for both indexes). Additionally, minimal muscle pH measured during the first minute of recovery with NMR was lower after bier block (6.41 ± 0.08 vs. 6.20 ± 0.06; P < 0.036, simple effects). Meanwhile, reflex effects were unaffected by the bretylium bier block. The results support the conclusion that sympathetic stimulation to muscle during exercise not only limits muscle blood flow but also appears to limit anaerobiosis and H+ release, presumably through a preferential recruitment of oxidative fibers.

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.

scholarly journals Improved brain perfusion after electrical cardioversion of atrial fibrillation

EP Europace ◽  
2019 ◽  
Vol 22 (4) ◽  
pp. 530-537 ◽  
Author(s):  
Marianna Gardarsdottir ◽  
Sigurdur Sigurdsson ◽  
Thor Aspelund ◽  
Valdis Anna Gardarsdottir ◽  
Lars Forsberg ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Atrial Fibrillation ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Brain Perfusion ◽  
Resonance Imaging ◽  
Flow Measurements ◽  
Before And After ◽  
Blood Flow Measurements

Abstract Aims Atrial fibrillation (AF) has been associated with reduced brain volume, cognitive impairment, and reduced cerebral blood flow. The causes of reduced cerebral blood flow in AF are unknown, but no reduction was seen in individuals without the arrhythmia in a previous study. The aim of this study was to test the hypothesis that brain perfusion, measured with magnetic resonance imaging (MRI), improves after cardioversion of AF to sinus rhythm (SR). Methods and results All patients undergoing elective cardioversion at our institution were invited to participate. A total of 44 individuals were included. Magnetic resonance imaging studies were done before and after cardioversion with both brain perfusion and cerebral blood flow measurements. However, 17 did not complete the second MRI as they had a recurrence of AF during the observation period (recurrent AF group), leaving 17 in the SR group and 10 in the AF group to complete both measurements. Brain perfusion increased after cardioversion to SR by 4.9 mL/100 g/min in the whole brain (P &lt; 0.001) and by 5.6 mL/100 g/min in grey matter (P &lt; 0.001). Cerebral blood flow increased by 58.6 mL/min (P &lt; 0.05). Both brain perfusion and cerebral blood flow remained unchanged when cardioversion was unsuccessful. Conclusion In this study of individuals undergoing elective cardioversion for AF, restoration, and maintenance of SR for at least 10 weeks after was associated with an improvement of brain perfusion and cerebral blood flow measured by both arterial spin labelling and phase contrast MRI. In those individuals where cardioversion was unsuccessful, there was no change in perfusion or blood flow.

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.

Quantitative assessment of vessel flow integrity for aneurysm surgery

1999 ◽  
Vol 91 (6) ◽  
pp. 1050-1054 ◽  
Author(s):  
Fady T. Charbel ◽  
Gabriel Gonzales-Portillo ◽  
William E. Hoffman ◽  
Lauren A. Ostergren ◽  
Mukesh Misra
Keyword(s):  
Blood Flow ◽  
Superior Cerebellar Artery ◽  
Aneurysm Surgery ◽  
Flow Measurements ◽  
Content Type ◽  
Aneurysm Clipping ◽  
Cerebellar Artery ◽  
Before And After ◽  
Vessel Flow ◽  
Improve Patient

✓ Quantitative measurement of blood flow in cerebral vessels during aneurysm surgery can help prevent ischemic injury and improve patient outcome. The authors report a case of a superior cerebellar artery (SCA) aneurysm in which perivascular microflow probes were used to measure blood flow quantitatively in both the SCA and the posterior cerebral artery before and after aneurysm clipping. Following aneurysm clipping, blood flow in the SCA was reduced to less than 25% of its initial baseline value. Prompt detection of compromised blood flow gave the surgeon the opportunity to adjust the clip and restore SCA flow to its preclipping value within 5 minutes of initial clip placement. Quantitative vessel-flow measurements were integral to the safe progression of the operation and may have prevented an adverse neurological outcome in this patient. The recommended surgical technique and the principle of operation are described.

Effect of Pentoxifylline on Cerebral Blood Flow in Patients with Chronic Cerebrovascular Disease

1981 ◽  
Vol 9 (3) ◽  
pp. 211-214 ◽  
Author(s):  
Stefano Passero ◽  
Marcello Nardini ◽  
Noé Battistini
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Disease ◽  
Pharmacological Treatment ◽  
Intravenous Infusion ◽  
Chronic Administration ◽  
Before And After ◽  
Clearance Technique

The effect of pentoxifylline on cerebral blood flow (CBF) was studied with the intravenous 133Xe clearance technique in eleven patients with chronic cerebrovascular disease. Pentoxifylline was administered orally at a dose of 1200 mg/day over a period of 30 days (eight patients) or by intravenous infusion of 100 ml saline containing 400 mg of the drug in 1 hour (three patients). CBF was measured before and after pharmacological treatment. CBF was found to be significantly increased by both acute and chronic administration of pentoxifylline.

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