The influence of age and the level of arterial blood pressure on the changes in forearm blood flow resulting from sudden alterations in local vascular transmural pressure

1975 ◽  
Vol 9 (1) ◽  
pp. 56-64
Author(s):  
P. H. FENTEM ◽  
J. M. YATES
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Forearm Blood Flow ◽  
Transmural Pressure ◽  
Arterial Blood

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.

Effect of intravenous infusion of adrenaline on the cardiovascular responses to distal body subatmospheric pressure in man

1988 ◽  
Vol 75 (4) ◽  
pp. 389-394 ◽  
Author(s):  
I. W. Fellows ◽  
I. A. MacDonald ◽  
T. Bennett ◽  
D. P. O'Donoghue
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Forearm Blood Flow ◽  
Cardiovascular Responses ◽  
Saline Infusion ◽  
Subatmospheric Pressure ◽  
Arterial Blood ◽  
Adrenaline Infusion

1. On two separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline [0.27 nmol (50 ng) min−1 kg−1] or saline (154 mmol/l NaCl), plus ascorbic acid (5.68 mmol/l), over 30 min. 2. On each occasion, the subjects were exposed to distal body subatmospheric pressure (DBSP), 0 to 50 mmHg (0 to 6.65 kPa) in 10 mmHg (1.33 kPa) steps, before infusion, during the final 15 min of the infusion, and at 15 min and 30 min after the cessation of the infusion. 3. Venous adrenaline concentrations of 2.85 ±0.22 nmol/l were achieved during the adrenaline infusion, compared with 0.49 ± 0.07 nmol/l during the saline infusion (P < 0.001). At 15 min and at 30 min after cessation of the adrenaline infusion, venous adrenaline concentrations had fallen to levels similar to those achieved after the cessation of the saline infusion. 4. Heart rate rose significantly from 58 ±4 beats/min to 67 ±4 beats/min during the adrenaline infusion (P < 0.05), but there was no further significant change in response to 50 mmHg (6.65 kPa) DBSP. At 30 min after the cessation of the adrenaline infusion, heart rate rose from 60 ± 4 beats/min to 78 ± 7 beats/min in response to 50 mmHg DBSP. This increase was significantly greater than that observed before the adrenaline infusion [58 ± 4 beats/min to 69 ±7 beats/min during 50 mmHg (6.65 kPa) DBSP; P < 0.01]. 5. During the infusion of adrenaline, systolic arterial blood pressure rose and diastolic arterial blood pressure fell, but the blood pressure responses to DBSP were unaffected. 6. Forearm blood flow increased significantly during adrenaline infusion but there was no significant difference in the fall in forearm blood flow during DBSP compared with the values before infusion. At 15 min after the cessation of the adrenaline infusion, forearm vascular resistance rose proportionately more in response to DBSP than it had before the adrenaline infusion (P < 0.05). 7. These results are consistent with adrenaline-mediated facilitation of sympathetic neuronal release of noradrenaline in the heart and in the forearm vascular bed.

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.

Effect of hypovolemia on forearm vascular resistance control during exercise in the heat

1991 ◽  
Vol 71 (4) ◽  
pp. 1382-1386 ◽  
Author(s):  
T. S. Nishiyasu ◽  
X. G. Shi ◽  
G. W. Mack ◽  
E. R. Nadel
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Cycle Ergometer ◽  
Dynamic Exercise ◽  
Arterial Blood ◽  
Ergometer Exercise ◽  
Forearm Vascular Resistance

To determine the influence of hypovolemia on the control of forearm vascular resistance (FVR) during dynamic exercise, we studied five physically active men during 60 min of supine cycle ergometer exercise bouts at 35 degrees C in control (normovolemic) and hypovolemic conditions. Hypovolemia was achieved by 3 days of diuretic administration and resulted in an average decrease in plasma volume of 15.9%. Relative to normovolemia, hypovolemia caused an attenuation of the progressive rise in forearm blood flow (P less than 0.05) and an increase in heart rate (P less than 0.05) during exercise. Because mean arterial blood pressure during hypovolemic exercise was well maintained, the attenuation of forearm blood flow was due entirely to a relative increase in FVR. At the onset of dynamic exercise, FVR was increased significantly in control and hypovolemic conditions by 13.2 and 27.1 units, respectively. The increase in FVR was significantly different between control and hypovolemic conditions as well. We attributed the increased vasoconstrictor bias during hypovolemia to cardiopulmonary baroreceptor unloading and/or an increased sensitivity to cardiopulmonary baroreceptor unloading. We concluded that reduced blood flow to the periphery during exercise in the hypovolemic condition was caused entirely by an increase in vascular resistance, thereby preserving arterial blood pressure and adequate perfusion to the organs requiring increased flow.

Acute haemodynamic effects of lipolysis-induced increase of free fatty acids in healthy men

2002 ◽  
Vol 102 (5) ◽  
pp. 495-500 ◽  
Author(s):  
Mark T. KEARNEY ◽  
Philip J. CHOWIENCZYK ◽  
Sally E. BRETT ◽  
Angela SUTCLIFFE ◽  
James M. RITTER ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Blood Flow ◽  
Free Fatty Acids ◽  
Arterial Blood Pressure ◽  
Lipid Emulsion ◽  
Forearm Blood Flow ◽  
Haemodynamic Effects ◽  
Healthy Men ◽  
Arterial Blood

Circulating free fatty acids (FFA) are elevated in subjects with insulin resistance and Type II diabetes, and increase during myocardial ischaemia, but their haemodynamic effects are incompletely understood. During an investigation of the effects of FFA on endothelial function, we administered lipid emulsion (150mgċmin-1 of soybean oil) with heparin (0.2 unitċkg-1ċmin-1) intravenously to eight healthy men for 2h. This increased circulating FFA to 3.1±0.5mmol/l. Forearm blood flow was measured by venous occlusion plethysmography during brachial artery infusions of saline, acetylcholine and nitroprusside before, and at 1 and 2h. Lipid/heparin infusion had no significant effect on vasodilation to nitroprusside but progressively increased responses to acetylcholine (from 6.3±2.0 during 30μgċmin-1 before-lipid infusion to 7.9±1.3 at 1h and 12.2±1.1mlċmin-1ċ100ml-1 at 2h, P < 0.001). Basal flow increased from 2.7±0.7 to 4.7±0.8mlċmin-1ċ100ml-1 from 0 to 2h. We performed a second study to clarify this effect on basal blood flow. Healthy men (n = 8) received, on separate occasions, 4h intravenous infusions of lipid emulsion with heparin and, as a control, saline with heparin. Lipid with heparin increased mean arterial blood pressure (maximum increment 8.2±2.7mmHg, P < 0.01 compared with saline/heparin control) and forearm blood flow (from 1.7±0.2 to 2.9±0.3mlċmin-1ċ100ml-1, P < 0.01) without a significant effect on heart rate, and reduced calculated forearm vascular resistance (from 49.1±5.4 to 31.3±3.9 arbitrary units, P < 0.01). In conclusion, acute elevation of FFA in healthy men increases arterial blood pressure and reduces vascular resistance. These haemodynamic changes could be clinically relevant.

Sympathetic vascular transduction is augmented in young normotensive blacks

2002 ◽  
Vol 92 (2) ◽  
pp. 651-656 ◽  
Author(s):  
Chester A. Ray ◽  
Kevin D. Monahan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Blacks And Whites

The purpose of the present study was to determine sympathetic vascular transduction in young normotensive black and white adults. We hypothesized that blacks would demonstrate augmented transduction of muscle sympathetic nerve activity (MSNA) into vascular resistance. To test this hypothesis, MSNA, forearm blood flow, heart rate, and arterial blood pressure were measured during lower body negative pressure (LBNP). At rest, no differences existed in arterial blood pressure, heart rate, forearm blood flow, and forearm vascular resistance (FVR). Likewise, LBNP elicited comparable responses of these variables for blacks and whites. Baseline MSNA did not differ between blacks and whites, but whites demonstrated greater increases during LBNP (28 ± 7 vs. 55 ± 18%, 81 ± 21 vs. 137 ± 42%, 174 ± 81 vs. 556 ± 98% for −5, −15, and −40 mmHg LBNP, respectively; P < 0.001). Consistent with smaller increases in MSNA but similar FVR responses during LBNP, blacks demonstrated greater sympathetic vascular transduction (%FVR/%MSNA) than whites (0.95 ± 0.07 vs. 0.82 ± 0.07 U; 0.82 ± 0.11 vs. 0.64 ± 0.09 U; 0.95 ± 0.37 vs. 0.35 ± 0.09 U; P < 0.01). In summary, young whites demonstrate greater increases in MSNA during baroreceptor unloading than age-matched normotensive blacks. However, more importantly, for a given increase in MSNA, blacks demonstrate greater forearm vasoconstriction than whites. This finding may contribute to augmented blood pressure reactivity in blacks.

Contribution of prostaglandins to the dilation that follows isometric forearm contraction in human subjects: effects of aspirin and hyperoxia

2005 ◽  
Vol 99 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Thet Su Win ◽  
Janice M. Marshall
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Isometric Contraction ◽  
Forearm Blood Flow ◽  
Substantial Contribution ◽  
Isometric Handgrip ◽  
Double Blind ◽  
Arterial Blood ◽  
Peak Value

In 11 healthy volunteers, we evaluated, in a double-blind crossover study, whether the vasodilation that follows isometric contraction is mediated by prostaglandins (PGs) and/or is O2 dependent. Subjects performed isometric handgrip for 2 min at 60% maximal voluntary contraction (MVC), after pretreatment with placebo or aspirin (600 mg orally), when breathing air or 40% O2. Forearm blood flow was measured in the dominant forearm by venous occlusion plethysmography. Arterial blood pressure was also recorded, allowing calculation of forearm vascular conductance (FVC; forearm blood flow/arterial blood pressure). During air breathing, aspirin significantly reduced the increase in FVC that followed contraction at 60% MVC: from a baseline of 0.09 ± 0.011 [mean ± SE, conductance units (CU)], the peak value was reduced from 0.24 ± 0.03 to 0.14 ± 0.01 CU. Breathing 40% O2 similarly reduced the increase in FVC relative to that evoked when breathing air; the peak value was 0.24 ± 0.03 vs. 0.15 ± 0.02 CU. However, after aspirin, breathing 40% O2 had no further effect on the contraction-evoked increase in FVC (the peak value was 0.15 ± 0.02 vs. 0.16 ± 0.02 CU). Thus the present study indicates that prostaglandins make a substantial contribution to the peak of the vasodilation that follows isometric contraction of forearm muscles at 60% MVC. Given that hyperoxia similarly reduced the vasodilation and attenuated the effect of aspirin, we propose that the stimulus for prostaglandin synthesis and release is hypoxia of the endothelium.

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