Haemodynamic Abnormalities in Hypertensive Patients: A Review of the Influence of Vasodilating Drugs

1986 ◽  
Vol 14 (6) ◽  
pp. 289-298
Author(s):  
U Abshagen ◽  
E von Möllendorff
Keyword(s):  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Progressive Increase ◽  
Left Ventricular ◽  
Arterial System ◽  
Organic Nitrates ◽  
Moderate Increase ◽  
Ventricular Performance ◽  
Venous Capacitance

Mean arterial pressure is determined primarily by cardiac output and total peripheral resistance, in addition to blood volume and compliance of the arterial system. The regulation of these determinants occurs via reflex neurogenic mechanisms and metabolic or humoral mechanisms. The haemodynamic situation in the early stages of arterial hypertension is characterized by a slight hypercirculatory state due to a moderate increase in heart rate and cardiac output, whereas the total peripheral resistance is increased only moderately, if at all. In later stages, however, a progressive increase in total peripheral resistance prevails, accompanied by a decrease in left ventricular performance due to the development of left ventricular hypertrophy, changes in ventricle geometry and coronary heart disease. A pharmacologically-induced decrease of total peripheral resistance by means of vasodilators, therefore, represents a logical approach to therapy, at least of advanced hypertension. Vasodilators can be classified into three categories: (1) those with preferential activity on the arterial resistance vessels, eg hydralazine, diazoxide, minoxidil; (2) those with preferential activity on venous capacitance vessels, eg organic nitrates; and (3) those with activities on both branches, eg sodium nitroprusside, urapidil, prazosin and other α-blockers. Brief reference is made to new and possibly more acceptable vasodilators – in particular carvedilol and prizidilol.

Effects of dihydroergotamine on hemodynamic molsidomine actions in anesthetized dogs

1984 ◽  
Vol 62 (6) ◽  
pp. 634-639 ◽  
Author(s):  
Volker B. Fiedler ◽  
Helmut Göbel ◽  
Rolf-Eberhard Nitz
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Venous Capacitance ◽  
Heart Performance ◽  
Dose Dependent Fashion ◽  
Anesthetized Dogs

In pentobarbital-anesthetized mongrel dogs the intravenous actions of 0.50 mg/kg molsidomine on pulmonary artery and left ventricular (LV) end-diastolic pressures and internal heart dimensions (preload), left ventricular systolic and peripheral blood pressures, and total peripheral resistance (afterload), as well as on heart rate, dP/dt, stroke volume, and cardiac output (heart performance) were studied for 2 h. Hemodynamic molsidomine effects were influenced by increasing amounts of intravenously infused dihydroergotamine solution (DHE, 1–64 μg∙kg−1∙min−1). Molsidomine decreased preload, stroke volume, and cardiac output for over 2 h but decreased ventricular and peripheral pressures for 45 min. Systemic vascular resistance showed a tendency to decrease while heart rate and LV dP/dtmax were not altered. DHE infusion reversed molsidomine effects on the preload and afterload of the heart. The diminished stroke volume was elevated so that cardiac output also increased. Total peripheral resistance increased while heart rate fell in a dose-dependent fashion. The LV dP/dtmax remained unchanged until the highest dose of 64 μg∙kg−1∙min−1 DHE elevated the isovolumic myocardial contractility. These experiments indicate that DHE can reverse the intravenous molsidomine effects on hemodynamics. Most likely, this is mediated through peripheral vasoconstriction of venous capacitance vessels, thereby affecting moldisomine's action on postcapillary beds of the circulation.

Serial study of factors influencing changes in cardiac output during human pregnancy

1989 ◽  
Vol 256 (4) ◽  
pp. H1060-H1065 ◽  
Author(s):  
S. C. Robson ◽  
S. Hunter ◽  
R. J. Boys ◽  
W. Dunlop
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
First Trimester ◽  
Progressive Increase ◽  
Left Ventricular ◽  
Cross Sectional ◽  
Ventricular Performance ◽  
Orifice Area ◽  
Mitral Valves ◽  
Ventricular Wall Thickness

Serial hemodynamic measurements were performed in 13 women on two occasions before conception and then at monthly intervals throughout pregnancy. Cardiac output (CO) was measured by Doppler and cross-sectional echocardiography at the aortic, pulmonary, and mitral valves. Cardiac chamber size and ventricular function were investigated by M-mode echocardiography. CO increased from a mean of 4.88 l/min before the conception to a maximum of 7.21 l/min at 32 wk, the increase being significant by 5 wk after the last menstrual period. Heart rate and left ventricular performance increased during the first trimester. Heart rate increased further during the second trimester, during which left atrial and left ventricular end-diastolic dimensions increased, suggesting an increase in venous return. Derived values of total peripheral vascular resistance fell during the first 20 wk. These changes were associated with a progressive increase in valve orifice area and left ventricular wall thickness during pregnancy.

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.

scholarly journals Elevated Blood Pressure in Adolescence Is Attributable to a Combination of Elevated Cardiac Output and Total Peripheral Resistance

Hypertension ◽  
2018 ◽  
Vol 72 (5) ◽  
pp. 1103-1108 ◽  
Author(s):  
Chloe Park ◽  
Abigail Fraser ◽  
Laura D. Howe ◽  
Siana Jones ◽  
George Davey Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Elevated Blood Pressure ◽  
Elevated Blood

RSR-13, an allosteric effector of hemoglobin, increases systemic and iliac vascular resistance in rats

1996 ◽  
Vol 271 (2) ◽  
pp. H602-H613 ◽  
Author(s):  
M. P. Kunert ◽  
J. F. Liard ◽  
D. J. Abraham
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Experimental Models ◽  
Metabolic Demand ◽  
Flow Probe ◽  
Inositol Hexaphosphate ◽  
Control Value ◽  
Allosteric Effector

Tissue O2 delivery in excess of metabolic demand may be a factor in the development of high vascular resistance in experimental models of volume-expanded hypertension. This hypothesis was previously tested in rats with an exchange transfusion of red blood cells treated with inositol hexaphosphate or an intravenous infusion of RSR-4, allosteric effectors of hemoglobin. The binding of these drugs with hemoglobin effect a conformational change in the molecule, such that the affinity for O2 is reduced. However, in both preparations, the changes in vascular resistance could have been nonspecific. The present studies used intravenous infusions of RSR-13, which did not share some of the problematic characteristics of RSR-4 and inositol hexaphosphate. Conscious instrumented rats (an electromagnetic flow probe on ascending aorta or an iliac, mesenteric, or renal Doppler flow probe) were studied for 6 h after an RSR-13 infusion of 200 mg/kg in 15 min. This dose significantly increased arterial P50 (PO2 at which hemoglobin is 50% saturated) from 38 +/- 0.8 to 58 +/- 1.4 mmHg at 1 h after the start of the infusion. In the 3rd h cardiac output fell significantly from a control value of 358 +/- 33 to 243 +/- 24 ml.kg-1.min-1 and total peripheral resistance significantly increased from 0.31 +/- 0.03 to 0.43 +/- 0.04 mmHg.ml-1.kg.min. Cardiac output and P50 returned toward control over the next few hours. Neither cardiac output nor total peripheral resistance changed in the group of rats receiving vehicle alone. In a separate group of rats, iliac flow decreased significantly to 60% of control and iliac resistance increased to 160% of control. Iliac flow increased significantly in the group of rats that received vehicle only. Although the mechanism of these changes has not been established, these results suggest that a decreased O2 affinity leads to an increased total peripheral resistance and regional vascular resistance and support the hypothesis that O2 plays a role in the metabolic autoregulation of blood flow.

Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep

1988 ◽  
Vol 254 (4) ◽  
pp. H811-H815 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. G. McDougall ◽  
B. A. Scoggins
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Blood Volume ◽  
Total Peripheral Resistance ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The hemodynamic and metabolic effects of long-term (5 day) infusion of human atrial natriuretic factor (ANF) were examined in conscious chronically instrumented sheep. Infusion of ANF at 20 micrograms/h, a rate below the threshold for an acute natriuretic effect, decreased blood pressure by 9 +/- 1 mmHg on day 5, associated with a fall in calculated total peripheral resistance. On day 1, ANF reduced cardiac output, stroke volume, and blood volume, effects that were associated with an increase in heart rate and calculated total peripheral resistance and a small decrease in blood pressure. On days 4 and 5 there was a small increase in urine volume and sodium excretion. On day 5 an increase in water intake and body weight was observed. No change was seen in plasma concentrations of renin, arginine vasopressin, glucose, adrenocorticotropic hormone, or protein. This study suggests that the short-term hypotensive effect of ANF results from a reduction in cardiac output associated with a fall in both stroke volume and effective blood volume. However, after 5 days of infusion, ANF lowers blood pressure via a reduction in total peripheral resistance.

Plotting cardiac output versus total peripheral resistance

1981 ◽  
Vol 9 (2) ◽  
pp. 129-130
Author(s):  
Heinz Mrochen ◽  
Ullrich Hieronymi ◽  
Werner Kuckelt
Keyword(s):  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance

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.

Sepsis-induced diastolic dysfunction in chronic canine peritonitis

1990 ◽  
Vol 258 (3) ◽  
pp. H625-H633 ◽  
Author(s):  
T. J. Stahl ◽  
P. B. Alden ◽  
W. S. Ring ◽  
R. C. Madoff ◽  
F. B. Cerra
Keyword(s):  
Heart Rate ◽  
Cecal Ligation ◽  
Strain Analysis ◽  
High Volume ◽  
Canine Model ◽  
Progressive Increase ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Leukocyte Counts ◽  
Hyperdynamic Sepsis

A chronic canine model of hyperdynamic sepsis was achieved by cecal ligation and puncture (SEP) in conjunction with continuous high-volume fluid resuscitation. Cardiac function was evaluated using ultrasonic cardiac crystals placed across the major, minor, and wall thickness axes of the left ventricle, together with simultaneous arterial and ventricular pressure measurement. Seven to 10 days after crystal implantation, animals were randomized to either SEP (n = 10) or sham laparotomy control (n = 7). SEP dogs became febrile and lethargic, with elevated leukocyte counts and positive blood cultures for enteric organisms. They were also hyperdynamic, with significant increases in heart rate and cardiac output and a fall in systemic vascular resistance. Systolic blood pressure, stroke volume, and ejection fraction remained stable. Relative to control, the SEP group demonstrated a significant reduction in intrinsic contractility during systole, as measured by the heart rate and load-independent index of left ventricular performance Emax (P less than 0.01), confirming the observations of others. In addition, however, diastolic function also became markedly abnormal with a progressive increase in unstressed and end-diastolic ventricular volumes (P less than 0.05) and a significant decrease in myocardial compliance as quantitated by transmural pressure vs. volume-strain analysis. It is hypothesized that this increase in diastolic volume helps to maintain global cardiac performance during the hyperdynamic response to sepsis in the presence of adequate volume support.

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.

Sign in / Sign up

Export Citation Format

Share Document