Arterial hemodynamics in a rabbit model of atherosclerosis

1989 ◽  
Vol 257 (3) ◽  
pp. H891-H897 ◽  
Author(s):  
B. D. Zuckerman ◽  
H. F. Weisman ◽  
F. C. Yin
Keyword(s):  
Blood Pressure ◽  
Total Peripheral Resistance ◽  
Wave Reflection ◽  
Peripheral Resistance ◽  
Low Frequency ◽  
Arterial System ◽  
Base Line ◽  
Arterial Tree ◽  
Arterial Blood ◽  
Arterial Impedance

Although atherosclerosis significantly alters the structural characteristics of the arterial tree, its effect on arterial impedance, which is a means of quantifying the functional characteristics of the arterial system, has not been characterized. To assess how one type of atherosclerosis affects impedance, we studied arterial impedance in New Zealand White rabbits after 11 wk on a 2% cholesterol diet. From open-chest aortic pressures and flows, impedance data were obtained from spectral analysis of randomly paced and Fourier analysis of nonpaced beats. Compliance was calculated from the low-frequency impedance moduli by assuming a windkessel model for the arterial system. Under base-line conditions, the atherosclerotic impedance phase spectrum in the low-frequency range remained negative for higher values of frequency than in controls. There was no difference between the groups in mean arterial blood pressure, impedance modulus spectrum, characteristic impedance, compliance, or total peripheral resistance. Wave reflections were, however, increased in the atherosclerotic animals. The differences between the two groups in phase and wave reflection were completely abolished after phenylephrine (3 micrograms.kg-1.min-1). Thus this study demonstrates that under base-line conditions atherosclerosis increases wave reflection at the input to the arterial system in the absence of an alteration in global arterial compliance, total peripheral resistance, or mean blood pressure. This increase is presumably secondary to atherosclerotic changes at arterial sites, which produce local impedance mismatching.

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.

Cardiac Output by the Dye Dilution Technique Under Thiopental Sodium-Oxygen and Ether Anesthesia

1956 ◽  
Vol 186 (1) ◽  
pp. 101-104 ◽  
Author(s):  
Esther M. Greisheimer ◽  
Dorothy W. Ellis ◽  
George Stewart ◽  
Lydia Makarenko ◽  
Nadia Oleksyshyn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Stroke Index ◽  
Ether Anesthesia ◽  
Dye Dilution ◽  
Arterial Blood ◽  
Thiopental Sodium

One hundred-twenty determinations of cardiac output by the dye dilution technic utilizing the cuvette oximeter were made on 20 dogs. Of these, 60 were done under thiopental sodium-oxygen analgesia and 60 were done after supplementing with ether. Arterial blood pressure was recorded by strain gauge. Electrocardiograms were taken periodically. Concentrations of thiopental and ether in arterial blood were determined. Cardiac output began to increase under thiopental analgesia and continued to increase when ether was administered. Arterial blood pressure and heart rate decreased slightly when ether was administered. Stroke index increased when ether was administered. Total peripheral resistance decreased markedly under thiopental analgesia, and continued to decrease when ether was administered. When compared with an earlier study in which cyclopropane was used as the supplementing agent, it was found that cyclopropane and ether exert opposite effects on cardiac output and peripheral resistance despite the fact that the effect on arterial blood pressure is similar under the two agents. Increase in cardiac output was found to be parallel with decrease in total peripheral resistance in this study. Amount of dye injected did not influence cardiac output. Under the conditions of this study, cardiac output was in no way dependent on the concentration of thiopental in the blood nor on the amount injected. Level of ether in the blood did not show much effect, if any, on cardiac output. It is probable that the changes observed in this study are comparable with those which obtain clinically when thiopental-oxygen analgesia is supplemented with ether. Systolic blood pressure is not an infallible guide to other cardiovascular functions since it may remain fairly steady while cardiac output and peripheral resistance undergo marked changes under anesthesia.

Peripheral Resistance Changes and Blood Pooling After Endotoxin in Eviscerated Dogs

1958 ◽  
Vol 195 (3) ◽  
pp. 631-634 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Robert P. Gilbert ◽  
Hiroshi Kuida ◽  
Maurice B. Visscher
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Endotoxin Shock ◽  
E Coli ◽  
Arterial Blood ◽  
Later Phase

Studies were performed on eviscerated dogs maintained with a constant cardiac inflow with and without injections of lethal amounts of E. coli endotoxin. Continuous recordings of mean arterial blood pressure and total venous return permitted determination of changes in total peripheral resistance and extent of vascular pooling. A significant fall in mean arterial blood pressure occurs within 30 minutes after endotoxin in the eviscerated dog with constant cardiac inflow. There is therefore a decrease in total peripheral resistance. There is also a small but significant increase in vascular pooling exceeding that seen without endotoxin but much reduced from that observed in noneviscerated animals given endotoxin. It is concluded that a decrease in vascular tone occurs after endotoxin and that it probably plays a significant role in the later phase of endotoxin shock in the dog.

Differential effects of wave reflections and peripheral resistance on aortic blood pressure: a model-based study

1994 ◽  
Vol 266 (4) ◽  
pp. H1626-H1642 ◽  
Author(s):  
D. S. Berger ◽  
J. K. Li ◽  
A. Noordergraaf
Keyword(s):  
Blood Pressure ◽  
Left Ventricle ◽  
Direct Current ◽  
Wave Reflection ◽  
Peripheral Resistance ◽  
Arterial System ◽  
Wave Reflections ◽  
Aortic Blood ◽  
Strong Reflection ◽  
Aortic Blood Pressure

It has been generally accepted that arterial system wave reflections act to increase aortic blood pressure and the load placed on the left ventricle. Using a mathematical model of the coupled left ventricle-arterial system, we predict that this is not the case. With the model, two aspects of wave reflection, the global reflection coefficient [TG(omega)] and the pulse wave velocity (cph), were adjusted independently. In addition, TG(omega) and cph could be altered independently of the direct-current properties of the arterial system model. Reduction of TG(omega) yielded increases in stroke volume (SV) as well as in peak systolic (Ps), diastolic (Pd), and mean aortic (Pao) pressures and, hence, increased the load on the left ventricle. SV and Pao increased only in the range where strong reflection occurs. Reduced cph also yielded higher pressures, whereas increased cph resulted in reduced Pao and Pd but increased Ps. The changes in pressures and SV in response to altered TG(omega) and cph were relatively small compared with absolute levels. Simulated vasoconstriction and vasodilation further demonstrated the much greater importance of peripheral resistance on pressure and SV levels and lead to the prediction that pressure reduction in vasodilation occurs not because of, but in spite of, reduced wave reflections. We conclude that these results have not yet been observed experimentally, because reflection cannot yet be separated from the direct-current properties of the arterial system; therefore wave reflections themselves have not yet been adequately studied in the intact animal.

Studies on the Mechanism of Mineralocorticoid-Induced Blood Pressure Increase in Man

1979 ◽  
Vol 57 (s5) ◽  
pp. 303s-305s ◽  
Author(s):  
A. Distler ◽  
T. Philipp ◽  
B. Lüth ◽  
G. Wucherer
Keyword(s):  
Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Pressure Rise ◽  
Sympathetic Tone ◽  
Plasma Noradrenaline ◽  
Steroid Administration ◽  
Arterial Blood ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration

1. To gain insight into the mechanism of mineralocorticoid-induced blood pressure rise in man we performed haemodynamic studies in six normotensive volunteer subjects before and during administration of the synthetic steroid 9α-fluorocortisol (0·8 mg daily) for a period of 6 weeks. In a further study, performed in seven subjects, plasma noradrenaline concentration and reactivity to exogenous noradrenaline were determined before and during administration of the mineralocorticoid. 2. Within the first week of steroid administration an increase in mean arterial blood pressure could be demonstrated, which was due to an increase in cardiac output. After the sixth week the elevated blood pressure was the consequence of an increased total peripheral resistance. 3. Plasma noradrenaline concentration decreased and reactivity to exogenous noradrenaline increased during steroid administration. 4. The mechanism underlying the increase in total peripheral resistance during long-term mineralocorticoid administration remains unclear. Increased sympathetic tone does not seem to be a factor since plasma noradrenaline decreased considerably. Pressor response to noradrenaline increased probably due to decreased sympathetic tone.

Regional distribution of blood flow during diving in the duck (Anas platyrhynchos)

1979 ◽  
Vol 57 (5) ◽  
pp. 995-1002 ◽  
Author(s):  
David R. Jones ◽  
Robert M. Bryan Jr. ◽  
Nigel H. West ◽  
Raymond H. Lord ◽  
Brenda Clark
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Regional Distribution ◽  
Peripheral Resistance ◽  
Tissue Blood Flow ◽  
Arterial Blood ◽  
The Brain

The regional distribution of blood flow, both before and during forced diving, was studied in the duck using radioactively labelled microspheres. Cardiac output fell from 227 ± 30 to 95 ± 16 mL kg−1 min−1 after 20–72 s of submergence and to 59 ± 18 mL kg−1 min−1 after 144–250 s of submergence. Mean arterial blood pressure did not change significantly as total peripheral resistance increased by four times during prolonged diving. Before diving the highest proportion of cardiac output went to the heart (2.6 ± 0.5%, n = 9) and kidneys (2.7 ± 0.5%, n = 9), with the brain receiving less than 1%. The share of cardiac output going to the brain and heart increased spectacularly during prolonged dives to 10.5 ± 3% (n = 5) and 15.9 ± 3.8% (n = 5), respectively, while that to the kidney fell to 0.4 ± 0.26% (n = 3). Since cardiac output declined during diving, tissue blood flow (millilitres per gram per minute) to the heart was unchanged although in the case of the brain it increased 2.35 times after 20–75 s of submergence and 8.5 times after 140–250 s of submergence. Spleen blood flow, the highest of any tissue predive (5.6 ± 1.3 mL g−1 min−1, n = 4), was insignificant during diving while adrenal flow increased markedly, in one animal reaching 7.09 mL g−1 min−1. The present results amplify general conclusions from previous research on regional distribution of blood flow in diving homeotherms, showing that, although both heart and brain receive a significant increase in the proportionate share of cardiac output during diving only the brain receives a significant increase in tissue blood flow, which increases as submergence is prolonged.

Spontaneous beat-by-beat fluctuations of total peripheral and cerebrovascular resistance in response to tilt

2004 ◽  
Vol 287 (3) ◽  
pp. R670-R679 ◽  
Author(s):  
Deborah D. O'Leary ◽  
J. Kevin Shoemaker ◽  
Michael R. Edwards ◽  
Richard L. Hughson
Keyword(s):  
Blood Pressure ◽  
Transfer Function ◽  
Total Peripheral Resistance ◽  
High Frequency ◽  
Function Analysis ◽  
Peripheral Resistance ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Head Up Tilt

Beat-by-beat estimates of total peripheral resistance (TPR) can be obtained from continuous measurements of cardiac output by using Doppler ultrasound and noninvasive mean arterial blood pressure (MAP). We employed transfer function analysis to study the heart rate (HR) and vascular response to spontaneous changes in blood pressure from the relationships of systolic blood pressure (SBP) to HR (SBP→HR), MAP to total peripheral resistance (TPR) and cerebrovascular resistance index (CVRi) (MAP→TPR and MAP→CVRi), as well as stroke volume (SV) to TPR in nine healthy subjects in supine and 45° head-up tilt positions. The gain of the SBP→HR transfer function was reduced with tilt in both the low- (0.03–0.15 Hz) and high-frequency (0.15–0.35 Hz) regions. In contrast, MAP→TPR transfer function gain was not affected by head-up tilt, but it did increase from low- to high-frequency regions. The phase relationships between MAP→TPR were unaffected by head-up tilt, but, consistent with an autoregulatory system, changes in MAP were followed by directionally similar changes in TPR, just as observed for the MAP→CVRi. The SV→TPR had high coherence with a constant phase of 150–160°. Together, these data that showed changes in MAP preceded changes in TPR, as well as a possible link between SV and TPR, are consistent with complex interactions between the vascular component of the arterial and cardiopulmonary baroreflexes and intrinsic properties such as the myogenic response of the resistance arteries.

Total peripheral resistance during cardiac tamponade: adrenergic and angiotensin roles

1986 ◽  
Vol 251 (5) ◽  
pp. R916-R922
Author(s):  
T. L. Cogswell ◽  
G. A. Bernath ◽  
H. Raff ◽  
R. G. Hoffmann ◽  
H. S. Klopfenstein
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiac Tamponade ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Ang Ii ◽  
Beta Adrenergic ◽  
Renin Angiotensin ◽  
Arterial Blood

During progressive cardiac tamponade in conscious dogs, cardiac output falls continuously while arterial blood pressure is maintained until cardiovascular decompensation by increases in total peripheral resistance (TPR). Plasma renin activity (PRA) is known to increase at decompensation. We hypothesized that the increase in TPR during cardiac tamponade was mediated by alpha-adrenergic and renin-angiotensin mechanisms. Twelve adult dogs were instrumented to measure cardiac output (electromagnetic flow probe), aortic and right atrial blood pressures, and intrapericardial pressure (IPP). TPR was calculated as the conscious euvolemic animals underwent cardiac tamponade induced by intrapericardial saline infusion at 20 ml/min. Six dogs underwent cardiac tamponade in the control condition (no medications) and during independent alpha- and beta-adrenergic and angiotensin-converting enzyme (ACE) inhibition. PRA and angiotensin II (ANG II) were measured during control tamponade. We found that TPR increased continuously to levels of greater than 200% of base line as IPP rose during cardiac tamponade (P less than 0.01). This increase in TPR was unaffected by beta-adrenergic or ACE blockade but was blunted by alpha-adrenergic blockade. PRA and ANG II increased only at decompensated tamponade (P less than 0.05) when arterial blood pressure had fallen by 30%. These changes in PRA and ANG II during tamponade were not altered by beta-blockade in six separate animals. We conclude that cardiac tamponade stimulates renin release and ANG II generation by a non-beta-receptor-mediated mechanism. The increase in TPR during cardiac tamponade is primarily dependent on alpha-adrenergic mechanisms, with a limited late contribution from the renin-angiotensin system.

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