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

1999 ◽  
Vol 97 (5) ◽  
pp. 539 ◽  
Author(s):  
Adriaan M. KAMPER ◽  
Peter C. CHANG
1999 ◽  
Vol 97 (5) ◽  
pp. 539-546 ◽  
Author(s):  
Adriaan M. KAMPER ◽  
Peter C. CHANG

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.


1997 ◽  
Vol 29 (Supplement) ◽  
pp. 258 ◽  
Author(s):  
B. Mahankali ◽  
J. Allen ◽  
J. Mann ◽  
A. Graves ◽  
M. Welsch

1995 ◽  
Vol 79 (3) ◽  
pp. 713-719 ◽  
Author(s):  
M. E. Tschakovsky ◽  
J. K. Shoemaker ◽  
R. L. Hughson

Simultaneous Doppler ultrasound estimates of brachial artery mean blood velocity (MBV) and venous occlusion strain-gauge plethysmography measures of forearm blood flow (FBF) were performed to determine the beat-by-beat relationship between the two methods and provide a method for flow calibration of Doppler MBV estimates. Such a calibration of Doppler MBV eliminates the need for knowledge of vessel cross-sectional area and angle of insonation while allowing for the quantification of limb blood flow. Six healthy subjects (5 men and 1 woman) performed 40 s of isometric forearm contraction at 35% maximal voluntary contraction with arterial inflow occluded. This resulted in elevated blood flow on relaxation and cuff deflation, and simultaneous beat-by-beat Doppler MBV and strain-gauge FBF measurements were then made over a period of 2–3 min as flow gradually decreased to resting levels. The r2 values for the fitted regression lines over a wide range of flows ranged from 0.87 to 0.98, and the mean square error terms ranged from 0.88 to 3.07 ml.100 ml-1.min-1. Significant day-to-day variation of the fitted regression parameters within subjects indicated that quantitative estimates of FBF from Doppler MBV require a calibration to be performed for each experiment. The finding of a strong linear relationship between Doppler MBV and venous occlusion strain-gauge plethysmography, as well as the marked beat-by-beat effect of cuff inflation on blood flow, confirms the importance of calibration on the same beats, not on adjacent segments of beats.


1996 ◽  
Vol 81 (4) ◽  
pp. 1516-1521 ◽  
Author(s):  
J. K. Shoemaker ◽  
H. L. Naylor ◽  
Z. I. Pozeg ◽  
R. L. Hughson

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.


1999 ◽  
Vol 87 (6) ◽  
pp. 2218-2224 ◽  
Author(s):  
Urs A. Leuenberger ◽  
Kris Gray ◽  
Michael D. Herr

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.


1969 ◽  
Vol 3 (2) ◽  
pp. 86-88
Author(s):  
Sidney Bloch ◽  
Brian Davies

A mercury-in-rubber strain-gauge plethysmograph was used to measure forearm blood flow in anxious and non-anxious psychiatric patients. No statistically-significant differences in forearm blood flow were found between the two groups.


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