General and regional circulatory effects of synthetic eledoisin in man

1964 ◽  
Vol 19 (1) ◽  
pp. 113-116 ◽  
Author(s):  
Hermes A. Kontos ◽  
William Shapiro ◽  
H. Page Mauck ◽  
John L. Patterson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Normal Subjects ◽  
Average Increase ◽  
Pronounced Increase ◽  
Blood Flows ◽  
Circulatory Effects ◽  
Arterial Blood ◽  
Flow Effects

The circulatory effects of intravenous infusions of synthetic eledoisin were studied in nine normal subjects. Infusions of 0.6 μg/min of eledoisin in eight experiments on eight subjects produced a transient fall in mean arterial blood pressure, tachycardia (average 14.3 beats/min), marked increase in cardiac index (average 3.4 liters/min m2), increase in stroke volume (average 58.3 ml/beat) and fall in systemic vascular resistance (average 6 mm Hg/liter min). Blood flow to hand and forearm increased (average increase in four experiments on four subjects 7.9 and 2.9 ml/min 100 ml tissue, respectively). More marked hypotension and tachycardia and a more pronounced increase in hand and forearm blood flows were observed during infusions of 2–5 μg/min of eledoisin in four experiments on four subjects. These results indicate that eledoisin is a powerful dilator of vessels in skin and skeletal muscle, and quite probably of vessels in other vascular areas. vasodilatation; effects on cardiac output; effects on hand blood flow; effects on forearm blood flow; hypotensive agent Submitted on July 1, 1963

Age-Related Decrease in Cardiac and Peripheral Vascular Responsiveness to Isoprenaline: Studies in Normal Subjects

1981 ◽  
Vol 60 (5) ◽  
pp. 571-577 ◽  
Author(s):  
P. Van Brummelen ◽  
F. R. Bühler ◽  
W. Kiowski ◽  
F. W. Amann
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Peripheral Vascular ◽  
Chronotropic Response ◽  
Arterial Blood ◽  
Age Related ◽  
Young Subjects

1. Changes in forearm blood flow to intra-arterial infusion of isoprenaline and the chronotropic response to intravenous boluses of isoprenaline were measured in 15 healthy volunteer subjects, eight younger than 25 years and seven older than 50 years. Intra-arterial blood pressure and basal plasma renin activity, adrenaline and noradrenaline were also measured. 2. Young subjects exhibited a greater increase in forearm blood flow than old subjects, to all four doses of isoprenaline used, a greater cardiac isoprenaline responsiveness (measured by the increase in heart rate; P<0.001) and a higher renin (P<0.02). 3. Resting values of blood pressure, forearm blood flow, adrenaline and noradrenaline were not significantly different in young and old subjects. In the latter, noradrenaline correlated with forearm blood flow (r = −0.77, P<0.05), forearm vascular resistance (r = 0.86, P<0.02) and mean arterial pressure (r = 0.83, P<0.02), whereas in the younger subjects forearm blood flow was related to adrenaline (r = 0.78, P<0.05). 4. These data provide evidence for an age-related parallel reduction in cardiac, peripheral vascular and renal β-adrenoceptor-mediated responses.

The relationship of blood flow velocity fluctuations to intracranial pressure B waves

1992 ◽  
Vol 76 (3) ◽  
pp. 415-421 ◽  
Author(s):  
David W. Newell ◽  
Rune Aaslid ◽  
Renate Stooss ◽  
Hans J. Reulen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Wave Amplitude ◽  
Transcranial Doppler Ultrasound ◽  
Normal Subjects ◽  
Content Type ◽  
Arterial Blood ◽  
Flow Fluctuations

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.

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.

Maximal vascular leg conductance in trained and untrained men

1987 ◽  
Vol 62 (2) ◽  
pp. 606-610 ◽  
Author(s):  
P. G. Snell ◽  
W. H. Martin ◽  
J. C. Buckey ◽  
C. G. Blomqvist
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sedentary Subjects

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

Circulatory effects of acute or chronic endotoxemia in rats

1981 ◽  
Vol 59 (2) ◽  
pp. 204-208 ◽  
Author(s):  
R. Keeler ◽  
Anamaria Barrientos ◽  
K. Lee
Keyword(s):  
Escherichia Coli ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Gastrointestinal Tract ◽  
Peripheral Resistance ◽  
Circulatory Effects ◽  
Arterial Blood ◽  
Flow Changes ◽  
Fractional Distribution

A study was made of the effects of acute (4 h) or chronic (4 days) infusion of Escherichia coli endotoxin on cardiovascular function in rats. Rats with acute endotoxemia had a reduced cardiac output but maintained their arterial blood pressure. Fractional distribution of the cardiac output was increased to the liver and reduced to the gastrointestinal tract and skin. No changes in fractional distribution to the kidneys, lungs, or heart were observed although absolute blood flow to these areas was reduced.Rats with chronic endotoxemia had a reduced cardiac output and hypotension with no change in peripheral resistance. Other changes resembled those seen in acute endotoxemia apart from a low renal fraction of the cardiac output. Calculation and interpretation of blood flow changes in these animals was difficult because of a large fall in hematocrit and changes in organ weight.

AN EFFECT OF REDUCED BAROMETRIC PRESSURE ON THE PERIPHERAL CIRCULATION

1957 ◽  
Vol 35 (10) ◽  
pp. 777-783
Author(s):  
F. Girling ◽  
F. A. Sunahara
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Human Subjects ◽  
Arterial Oxygen Saturation ◽  
Barometric Pressure ◽  
Peripheral Circulation ◽  
Arterial Oxygen ◽  
Blood Flows ◽  
The Past

Several groups of investigators have noted in the past that exposure to a reduced barometric pressure results in a decrease in peripheral blood flow.In the present study human subjects were exposed to a pressure of 225 mm. Hg with maintenace of arterial oxygen saturation, and forearm and hand blood flows were measured plethysmographically. Forearm blood flow was not affected by the exposure whereas hand blood flow was reduced in all subjects. Blood pressure and heart rate were also measured and showed no change during the experiment.

Circulating endothelin-1 reduces splanchnic and renal blood flow and splanchnic glucose production in humans

1995 ◽  
Vol 79 (1) ◽  
pp. 141-145 ◽  
Author(s):  
G. Ahlborg ◽  
E. Weitzberg ◽  
J. M. Lundberg
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Plasma Concentration ◽  
Healthy Subjects ◽  
Glucose Production ◽  
Physiological Saline ◽  
Sepsis Syndrome ◽  
Endothelin 1 ◽  
Blood Flows ◽  
Arterial Blood

The effect of minimal changes in circulating plasma endothelin-1 (ET-1) was studied in 12 healthy subjects receiving either 60 min of ET-1 (0.2 pmol.kg-1.min-1) or physiological saline intravenously. Blood was drawn from arterial, renal, and central hepatic vein catheters. Arterial ET-1-like immunoreactivity (ET-1-LI) increased from 4.7 +/- 0.4 (SE) to 8.6 +/- 1.0 pmol/l during ET-1 infusion. After 10 min, plasma ET-1-LI had increased to 6.12 +/- 0.29 pmol/l. For comparison the plasma ET-1-LI level was 12.9 +/- 4.2 pmol/in five patients with sepsis syndrome. Mean arterial blood pressure rose from 92 +/- 3 to 99 +/- 4 mmHg. Estimated splanchnic and renal blood flows fell by 18 +/- 5 and 10 +/- 3%, respectively, and splanchnic glucose production fell by 42 +/- 6% within 10 min of the ET-1 infusion and differed compared with corresponding control values. Only estimated splanchnic blood flow had increased 60 min after the ET-1 infusion. No change in splanchnic uptake of lactate or glycerol was seen. In conclusion, we suggest that circulating ET-1 with small or no demonstrable change in plasma concentration interferes with vasoactivity and splanchnic glycogenolyses in health and possibly pathophysiological conditions.

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.

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