Peripheral vasodilatation induced by a vasopressin analogue with selective V2-agonism in dogs

1989 ◽  
Vol 256 (6) ◽  
pp. H1621-H1626 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Conscious Dogs ◽  
Hemodynamic Effects ◽  
Femoral Blood Flow ◽  
Peripheral Vasodilatation ◽  
Femoral Blood

The selective V2-agonist 4-valine-8-D-arginine vasopressin (VDAVP) increases cardiac output and heart rate and decreases total peripheral resistance in dogs. The mechanism of these hemodynamic effects was examined in the present studies. When infused into the left coronary artery of six conscious dogs for 1 h, VDAVP (10 ng.kg-1.min-1) increased cardiac output and decreased total peripheral resistance more than when given intravenously in the same animals. Administration of VDAVP into the carotid circulation elicited effects that did not differ significantly from those after intravenous infusion at the same rate in six conscious dogs. After destruction of the central nervous system in five dogs anesthetized with pentobarbital, VDAVP failed to increase cardiac output and heart rate but lowered mean arterial pressure and total peripheral resistance. Finally, infusion of VDAVP into the femoral artery of six anesthetized dogs increased femoral blood flow at rates of 1, 5, and 10 ng.kg-1.min-1, whereas none of these rates increased femoral blood flow when given intravenously. Thus the hemodynamic effects of VDAVP appear to result primarily from a peripheral vasodilatory action, with possible contribution from a positive inotropic effect. We found no evidence that central effects of VDAVP were importantly involved in its cardiovascular action.

Circulatory effects of moderately and severely increased intracranial pressure in the dog

1972 ◽  
Vol 36 (6) ◽  
pp. 721-727 ◽  
Author(s):  
Norberto C. Gonzalez ◽  
John Overman ◽  
John A. Maxwell
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Peripheral Resistance ◽  
Arterial Blood ◽  
Femoral Blood Flow ◽  
Femoral Blood

✓ Anesthetized dogs were subjected to elevated intracranial pressure (ICP) of 60 and 100 mm Hg. At 60 mm Hg, decreases in heart rate and arterial blood pressure were observed associated with an increase in femoral blood flow that suggested vasodilation in the somatic areas. Cardiac output showed little change. Subsequent elevation of ICP to 100 mm Hg was followed by an increase in arterial blood pressure; cardiac output increased, and femoral flow increased still further. Since resistance to flow did not change, the hypertension was thought to be due to an increase in flow rather than peripheral resistance. An increase in heart rate was associated with the elevation in cardiac output; the fact that femoral blood flow increased proportionately more than cardiac output suggested a redistribution of blood flow. The changes in peripheral blood flow and in cardiac output were associated with a decrease in the arteriovenous oxygen (A–VO2) difference. No signs of tissue hypoxia were observed; specifically there was no significant change in the lactate-to-pyruvate ratio; the changes in A–VO2 difference were correlated with changes in flow and the product of the two variables, namely, oxygen consumption, remained unchanged. The data show that experimental elevation of ICP restricted to moderate levels is followed by hemodynamic changes suggesting peripheral vasodilation, and that when an increase in blood pressure then occurs, it is due to an increase in blood flow despite the decrease in peripheral resistance.

Diastolic pressure and peripheral resistance during stellate ganglion stimulation

1963 ◽  
Vol 204 (1) ◽  
pp. 71-72 ◽  
Author(s):  
Edward D. Freis ◽  
Jay N. Cohn ◽  
Thomas E. Liptak ◽  
Aristide G. B. Kovach
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Diastolic Pressure ◽  
Stellate Ganglion ◽  
Peripheral Resistance ◽  
Resistance Vessels ◽  
Left Stellate Ganglion ◽  
Increased Blood Flow

The mechanism of the diastolic pressure elevation occurring during left stellate ganglion stimulation was investigated. The cardiac output rose considerably, the heart rate remained essentially unchanged, and the total peripheral resistance fell moderately. The diastolic rise appeared to be due to increased blood flow rather than to any active changes in resistance vessels.

Cardiovascular effects produced by L-glutamate stimulation of the lateral hypothalamic area

1989 ◽  
Vol 257 (2) ◽  
pp. H540-H552 ◽  
Author(s):  
S. E. Spencer ◽  
W. B. Sawyer ◽  
A. D. Loewy
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Lateral Hypothalamic Area ◽  
Hypothalamic Area ◽  
Pharmacological Blockade ◽  
Stimulation Of

L-Glutamate microinjections into the tuberal region of the lateral hypothalamic area (LHAt) caused a fall in blood pressure and heart rate in pentobarbital-anesthetized rats. The bradycardia was mediated by both beta-adrenergic and muscarinic mechanisms as demonstrated with pharmacological blockade. The hypotension was due to a decrease in cardiac output, not a decrease in total peripheral resistance. In addition, there was a reduction in coronary blood flow. If heart rate was held constant by pharmacological blockade or by electrical cardiac pacing, L-glutamate stimulation of the LHAt still caused a fall in blood pressure. When the electrically paced model was used, this hypotension was due to a fall in cardiac output. In contrast, with the pharmacological blockade of the heart, the hypotension was due to a decrease in the total peripheral resistance. The cardiac output reduction in the paced condition was not mediated solely by either beta-sympathetic or parasympathetic mechanisms as determined by pharmacological blockade. With heart rate held constant by either drugs or pacing, LHAt stimulation did not alter regional blood flow or resistance in any vascular bed, including the coronary circulation. We conclude that L-glutamate stimulation of the LHAt lowers the cardiac output and heart rate by both parasympathetic and beta-adrenergic mechanisms and elicits hypotension by lowering cardiac output in the naive and electrically paced model.

Effects of endothelin-1 and sarafotoxin S6b on regional hemodynamics in the conscious dog

1991 ◽  
Vol 260 (6) ◽  
pp. R1210-R1217 ◽  
Author(s):  
R. J. Leadley ◽  
J. L. Zhu ◽  
K. L. Goetz
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Receptor Subtypes ◽  
Regional Variability ◽  
Endothelin 1 ◽  
Regional Hemodynamics

Endothelin, a potent vasoconstrictor, also is capable of producing transient vasodilation in some situations. We examined the changes in regional hemodynamics in response to constant infusions of endothelin-1 (ET-1) at 5, 10, or 20 ng.kg-1.min-1 for 1 h into conscious dogs. The dogs were instrumented with ultrasonic flow probes for measurement of blood flow in the ascending aorta (cardiac output) and in the coronary, mesenteric, renal, and iliac arteries. A compound structurally similar to ET-1, sarafotoxin S6b (S6b), was also infused in identical experiments to determine whether the responses to these two peptides might differ. Basal plasma levels of immunoreactive ET-1 averaged approximately 6 pg/ml. After 55 min of infusion of ET-1 at 5, 10, and 20 ng.kg-1.min-1, plasma immunoreactive ET-1 increased to approximately 55, 130, and 520 pg/ml, respectively. When given at 20 ng.kg-1.min-1, ET-1 increased total peripheral resistance and arterial pressure and decreased cardiac output and heart rate. ET-1 decreased coronary, mesenteric, and renal blood flow but did not change iliac flow. In comparison with ET-1, S6b produced relatively smaller changes in total peripheral resistance, cardiac output, heart rate, and coronary, mesenteric, and renal blood flow. Iliac resistance did not change in response to ET-1, but it increased during infusions of S6b. Similar but less pronounced responses were observed when these peptides were infused at 5 and 10 ng.kg-1.min-1. The regional variability in the hemodynamic response to ET-1 and the difference in regional responses to ET-1 and S6b are consistent with the existence of heterogenous receptor subtypes for these peptides.

Hemodynamic Effects of "San-Huang-Hsieh-Hsin-Tang" in Patients with Essential Hypertension

1986 ◽  
Vol 14 (03n04) ◽  
pp. 153-156 ◽  
Author(s):  
Ho-Chan Chen ◽  
Ming-Tsuen Hsieh
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Essential Hypertension ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Contractile Force ◽  
Hemodynamic Effects ◽  
Cardiac Contractile ◽  
The Ancient Chinese

The ancient Chinese formula of "San-Huang-Hsieh-Hsin-Tang" (S-T) was originally used for patients with "epigastric fullness, flushing, restlessness, constipation and a hard pulse" (Chang 115 B.C.). All these symptoms are frequently observed in patients with essential hypertension. We assessed the antihypertensive and hemodynamic effects of this formula, and found that S-T decreased blood pressure, total peripheral resistance, heart rate and cardiac contractile force. S-T had no apparent effects on cardiac output and blood volume.

Effects of a specific antidiuretic agonist on cardiac output and its distribution in intact and anephric dogs

1988 ◽  
Vol 74 (3) ◽  
pp. 293-299 ◽  
Author(s):  
Jean-Francois Liard
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Regional Blood Flow ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Before And After

1. The specific antidiuretic agonist [4-valine, 8-d-arginine]vasopressin (VDAVP) was administered intravenously to seven conscious dogs at a rate of 10 ng min−1 kg−1. Cardiac output (aortic electromagnetic flowmeter), mean arterial pressure and regional blood flows (radioactive microspheres) were measured before and after 30 min of infusion. 2. Mean arterial pressure fell from 89.9 ± 4.5 (mean ± sem) to 82.3 ± 5.9 mmHg and cardiac output increased from 115.4 ± 8.7 to 163.0 ± 14.4 ml min−1 kg−1. Total peripheral resistance decreased from 41.6 ± 3.7 to 27.8 ± 3.6 units and heart rate increased from 79.2 ± 5.9 to 123.2 ± 5.9 beats/min. Blood flow increased significantly in the myocardium, fat and skeletal muscle vascular bed. 3. In another group of six dogs subjected to a similar protocol 24 h after bilateral nephrectomy, mean arterial pressure fell from 102.2 ± 5.3 to 82.7 ± 3.4 mmHg and cardiac output increased from 125.6 ± 3.0 to 171.2 ± 4.0 ml min−1 kg−1. Total peripheral resistance decreased from 39.3 ± 3.4 to 23.4 ± 1.3 units and heart rate increased from 84 ± 4.9 to 113.3 ± 4.3 beats/min. The increase in cardiac output and the fall in total peripheral resistance did not differ significantly between intact and anephric dogs. Regional blood flow responses differed in some respects in the two groups studied, but there was no evidence that the vasodilatory action of VDAVP depended on the presence of the kidneys. 4. These results indicate that the vasodilatation elicited by the antidiuretic agonist VDAVP in intact dogs is limited to a few vascular beds. Furthermore, this vasodilatation appears to be independent from the renal V2-vasopressin receptors.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

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.

Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (6) ◽  
pp. 1-1
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Liver Volume ◽  
Peripheral Resistance ◽  
Spleen Volume ◽  
Carotid Baroreceptor ◽  
On Line

Pages H254–H259: R. Maass-Moreno and C. F. Rothe. “Carotid baroreceptor control of liver and spleen volume in cats.” Page H254: The sentence beginning on line 11 of the abstract should read: 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 0.21 ± 0.05 mm increase in thickness). The sentence beginning on line 16 of the abstract should read: The liver volume decreased, but only by 1.6% (0.06 ± 0.02 mm decrease in thickness), a change opposite that observed in the spleen. Page H256: The sentence beginning on line 20 of the first paragraph should read: The liver thickness significantly decreased 0.06 ± 0.02 mm when increasing Pcs by 100 mmHg, whereas the spleen increased 0.21 ± 0.05 mm.

Atrial natriuretic peptide increases resistance to venous return in rats

1987 ◽  
Vol 252 (5) ◽  
pp. H894-H899 ◽  
Author(s):  
Y. W. Chien ◽  
E. D. Frohlich ◽  
N. C. Trippodo
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Total Peripheral Resistance ◽  
Venous Return ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Atrial Natriuretic

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.

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