Relationship between Venous and Arterial Haemodynamics during Postural Changes in Venous Insufficiency

1994 ◽  
Vol 9 (2) ◽  
pp. 77-82 ◽  
Author(s):  
D. Duprez ◽  
M. De Buyzere ◽  
C. Randon ◽  
M. Dad ◽  
D. L. Clement
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Venous Insufficiency ◽  
Venous Pressure ◽  
Lower Limbs ◽  
Peripheral Vascular ◽  
Arterial Blood ◽  
Postural Changes

Objective: To study the changes in central haemodynamics and the relationship between arterial blood pressure and the venous dynamics of the lower limbs in patients with venous insufficiency. Design: Prospective haemodynamic study during postural changes in 14 patients with venous insufficiency with no other concomitant cardiovascular disease or disturbances in autonomic nervous system. Setting: Department of Cardiology and Angiology, University Hospital, Gent, Belgium. Patients: Fourteen patients with venous valve insufficiency in the lower limbs. Interventions: Measurements of arterial blood pressure, heart rate, stroke volume and cardiac output were performed in the supine position after 30 min rest and 5, 15 and 30 min after standing and during the recovery. Venous pressure at the ankle and calf circumference were also measured. Main outcome measures: Changes in cardiac output and total peripheral vascular resistance in order to maintain blood pressure during postural changes. Results: Arterial blood pressure was maintained constant owing to an increase in total peripheral vascular resistance despite a decrease in cardiac output. Venous pressure is also related to arterial blood pressure. Conclusions: The arterial and venous systems, even in venous insufficiency, are integrated to maintain blood pressure constant during postural changes.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (1) ◽  
pp. H254-H259
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Normal Brain ◽  
Spleen Volume ◽  
Arterial Blood

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.

Sympathoadrenal-circulatory regulation of arterial pressure during orthostatic stress in young and older men

1992 ◽  
Vol 263 (5) ◽  
pp. R1147-R1155 ◽  
Author(s):  
J. A. Taylor ◽  
G. A. Hand ◽  
D. G. Johnson ◽  
D. R. Seals
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Older Men ◽  
Orthostatic Stress ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Arterial Blood

Our purpose was to test the hypothesis that human aging alters sympathoadrenal-circulatory control of arterial blood pressure during orthostasis. Plasma catecholamine and hemodynamic adjustments to two different forms of orthostatic stress, lower body suction (-10 to -50 mmHg) and standing, were determined in 14 young (26 +/- 1 yr) and 13 older (64 +/- 1) healthy, normally active men. During quiet supine rest, cardiac output tended to be lower and systemic vascular resistance higher in the older men, but no other differences were observed. On average, arterial blood pressure was well maintained during both forms of orthostasis in the two groups; the older men actually demonstrated better maintenance of pressure (P < 0.05) and a lesser incidence of orthostatic hypotension than the young men during lower body suction. Despite a blunted reflex tachycardia during orthostatic stress (P < 0.05), cardiac output tended to decrease less in the older men because of a smaller decline in stroke volume (P < 0.05, suction only), whereas the reflex increases in systemic vascular resistance were not different in the two groups. The whole forearm vasoconstrictor response tended to be attenuated in the older men during lower body suction, but was identical in the two groups with standing. Forearm skin vascular resistance was unaltered during lower body suction in both groups. Orthostasis-evoked increases in antecubital venous plasma norepinephrine concentrations were similar in the young and older men, whereas little or no increases in plasma epinephrine concentrations were observed in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Circulatory responses to hypocapnia in the anesthetized dog

1965 ◽  
Vol 208 (1) ◽  
pp. 139-143 ◽  
Author(s):  
Hermes A. Kontos ◽  
H. Page Mauck ◽  
David W. Richardson ◽  
John L. Patterson
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Positive Pressure ◽  
Arterial Blood ◽  
Vasoconstrictor Effect ◽  
Anesthetized Dogs ◽  
Intact Limb

The circulatory responses to hypocapnia were studied in 40 anesthetized dogs. Hypocapnia induced without a change in ventilation caused slight increase in limb vascular resistance in six dogs and decrease in one. Hypocapnia induced by hyperventilation caused increase in limb vascular resistance in six dogs and decrease in four. Following administration of phenoxybenzamine into the femoral artery, hypocapnia induced by either method invariably caused increase in limb vascular resistance (8 dogs). These results show that hypocapnia has a direct vasoconstrictor effect on limb blood vessels. In the intact limb this response may be opposed by vasodilator effects mediated through nerves. Hypocapnia induced without change in ventilation had no significant effect on cardiac output, systemic vascular resistance or arterial blood pressure (8 dogs). Hypocapnia induced by increased ventilation was associated with significant decreases in cardiac output and systemic arterial blood pressure and significant increase in systemic vascular resistance (9 dogs). These responses were probably related to the effects of increased intermittent positive pressure used to augment ventilation.

Central and regional hemodynamic effects during infusion of Big endothelin-1 in healthy humans

1996 ◽  
Vol 80 (6) ◽  
pp. 1921-1927 ◽  
Author(s):  
G. Ahlborg ◽  
A. Ottosson-Seeberger ◽  
A. Hemsen ◽  
J. M. Lundberg
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Endothelin 1 ◽  
Healthy Humans ◽  
Arterial Blood

Big endothelin-1 (Big ET-1) was given intravenously to six healthy men to study uptakes and vascular effects. Blood samples were taken from systemic and pulmonary arterial and internal jugular and deep forearm venous catheters. Arterial Big ET-1-like immunoreactivity (Big ET-1-LI) increased from 5.43 +/- 0.60 to 756 +/- 27 pmol/l, and ET-1-LI increased from 4.67 +/- 0.08 to 6.67 +/- 0.52 pmol/l (P < 0.001). Skeletal muscle fractional extraction of Big ET-1-LI was 15 +/- 4%. ET-1-LI release did not increase in the studied vascular beds. Heart rate fell by 17% (P < 0.001), cardiac output fell by 26% (P < 0.001), and stroke volume fell by 11% (P < 0.05). Mean arterial blood pressure increased 18%, systemic vascular resistance increased 65%, and pulmonary vascular resistance increased 57% (P < 0.01-0.001). Pulmonary blood pressures, forearm blood flow, arterial pH, arterial PCO2, and systemic arterial-internal jugular venous O2 difference remained unchanged. No specific Big ET-1 receptors were found in human pulmonary membranes. The half-maximal inhibitory concentration for the receptor antagonist bosentan was 181 nM. In summary, circulating Big ET-1 elicits greater increases in mean arterial blood pressure and systemic vascular resistance and decreases in heart rate and cardiac output compared with an equimolar ET-1 infusion (26).

Postural cardiovascular reflexes: comparison of responses of forearm and calf resistance vessels

1987 ◽  
Vol 63 (5) ◽  
pp. 1801-1805 ◽  
Author(s):  
L. K. Essandoh ◽  
D. A. Duprez ◽  
J. T. Shepherd
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Valsalva Maneuver ◽  
Cardiovascular Reflexes ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Postural Changes ◽  
Change In Mean

Simultaneous measurements were made of changes in vascular resistance in the forearm and calf in response to moving from supine to sitting or to head-down tilt. The subjects were healthy male volunteers, 21–63 yr. Blood flows were measured by venous occlusion plethysmography using mercury-in-Silastic strain-gauges. The gauges were maintained at the same level relative to the heart during the postural changes. Arterial blood pressure was measured by auscultation; heart rate was counted from the plethysmograms. Changing from supine to sitting caused a decrease in forearm blood flow from 4.13 +/- 0.14 to 2.16 +/- 0.19 ml.100 ml-1.min-1. Corresponding calf flows were 4.21 +/- 0.32 and 4.40 +/- 0.59 ml.100 ml-1.min-1. There was no change in mean arterial blood pressure, and heart rate increased by 8.0 +/- 1.5 beats/min. Arrest of the circulation of both legs with occlusion cuffs on the thighs before sitting, to prevent pooling of blood in them, reduced the degree of forearm vasoconstriction. Neck suction (40 Torr) during sitting, to oppose the decrease in transmural pressure at the carotid sinuses, inhibited the vasoconstriction. During a 30 degrees head-down tilt, there was a dilatation of forearm but not of calf resistance vessels. A Valsalva maneuver caused a similar constriction of both vascular beds. Thus, when changes in vascular resistance in forearm and calf are compared, the major reflex adjustments to changes in posture take place in the forearm.

scholarly journals FIBRILLATION OF THE AURICLES: ITS EFFECTS UPON THE CIRCULATION

1912 ◽  
Vol 16 (4) ◽  
pp. 395-420 ◽  
Author(s):  
Thomas Lewis
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Initial Pressure ◽  
Ventricular Contraction ◽  
Circulatory Effects ◽  
Arterial Blood ◽  
Pressure Changes

When the auricles fibrillate, the following effects are observed. 1. The arterial blood pressure may rise, fall, or remain stationary. Usually it falls. If it falls, it generally rises again towards or to the initial pressure. 2. The venous pressure changes are the reverse of the arterial. 3. The intestinal volume and the cardiac output changes are in the same direction as those of arterial blood pressure. 4. From these observations it may be concluded that the peripheral circulatory effects are purely passive. 5. The volume of the heart decreases except in instances where there is reason to believe that the circulation is failing. All the changes described in the foregoing paragraphs, and also the variations in blood pressure reactions which occur from time to time, are attributable to alterations in the rate of ventricular contraction. Similar, though perhaps less profound changes, are seen when the heart rate accelerates in like degree in response to regular induction shocks.

Cardiovascular Effects of Chlorpromazine in the Dog

1956 ◽  
Vol 186 (3) ◽  
pp. 525-528 ◽  
Author(s):  
G. B. Spurr ◽  
Steven M. Horvath ◽  
Enid Allbaugh Farrand
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
The Mean

Chlorpromazine in doses of 2 and 5 mg/kg has been found to produce an initial hypotension in anesthetized dogs which was followed by return of the mean arterial blood pressure to near control levels. During the next 60–65 minutes there was a secondary decline in the pressure to hypotensive levels. Both an initial and secondary hypotension were the result of a decrease in peripheral vascular resistance.

Changes in cardiac output and vascular resistance during behavioral stress in the rat

1986 ◽  
Vol 251 (1) ◽  
pp. R82-R90 ◽  
Author(s):  
J. W. Hubbard ◽  
R. H. Cox ◽  
B. J. Sanders ◽  
J. E. Lawler
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Plasma Norepinephrine ◽  
Wky Rats ◽  
Arterial Blood ◽  
Behavioral Stress

Normotensive Wistar-Kyoto (WKY) rats and borderline hypertensive rats (BHR) were exposed to aversive classical conditioning procedures and chronically instrumented with arterial catheters and electromagnetic flow probes around the ascending aorta. After postoperative recovery, hemodynamic measurements and blood samples were obtained from conscious animals at rest and during aversive conditioning. The cardiovascular response to the behavioral stress consisted of a significant increase in mean arterial blood pressure, total peripheral resistance index, cardiac index, heart rate, and aortic dP/dt for both strains. However, the elevated vascular resistance seen in the BHR resulted in a significantly greater increase in mean arterial blood pressure (21 mmHg) compared with the WKY rats (14 mmHg). In addition, the BHR showed a significantly (P less than 0.05) greater plasma norepinephrine concentration (760 +/- 99 pg/ml) in response to the stress than did the WKY rats (559 +/- 53 pg/ml). These data suggest that an increase in cardiac output, elevated vascular resistance, and increased sympathetic drive may contribute to the development of stress-induced hypertension in this animal model.

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