Increased pulmonary vascular capacitance with β-adrenergic receptor stimulation: an experimental study of the effect of isoproterenol on the pulmonary vascular volume–pressure relationship

1988 ◽  
Vol 66 (1) ◽  
pp. 85-89 ◽  
Author(s):  
O. A. Smiseth ◽  
N. W. Scott-Douglas ◽  
D. Manyari ◽  
I. Kingma ◽  
E. R. Smith ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Diastolic Pressure ◽  
Blood Pool ◽  
Left Ventricular ◽  
Cardiac Volume ◽  
Receptor Stimulation ◽  
Vascular Volume ◽  
Vascular Capacitance ◽  
Blood Pool Scintigraphy ◽  
Β Receptor

The present study is an investigation of the effect of β-adrenergic receptor stimulation by isoproterenol on pulmonary vascular capacitance. The experiments were done in six intact-chest, anaesthetized dogs in which pulmonary and cardiac blood volumes were assessed by blood pool scintigraphy. Isoproterenol (0.150 μg∙kg−1∙min−1) significantly (p < 0.005) lowered pulmonary capillary wedge pressure (PPCW) and pulmonary artery pressure (PPA) but did not significantly change pulmonary blood volume (PBV). Left ventricular end-diastolic pressure and total cardiac volume both significantly (p < 0.005) decreased. Pulmonary vascular volume – pressure (V–P) relationships before and during isoproterenol were described by means of blood transfusions and hemorrhage. In individual dogs the PBV–PPCW and the PBV–(PPCW + PPA)/2 relationships were significantly shifted upward by isoproterenol (p < 0.05 or less); slope changes were variable. Pooled data from all dogs also showed a significant (p < 0.001) upward shift in the pulmonary vascular V–P relationship regardless of which measure of distending pressure was used. These results suggest that β-receptor stimulation by isoproterenol increases pulmonary vascular capacitance by increasing the unstressed volume.

Changes in regional vascular capacitance during prostacyclin-induced cardiac vagal reflex in pigs

1994 ◽  
Vol 267 (2) ◽  
pp. H535-H539
Author(s):  
Y. Wang ◽  
C. Drakonakis ◽  
J. L. Alderman ◽  
D. L. Rutlen
Keyword(s):  
Blood Volume ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Blood Pool ◽  
Left Ventricular ◽  
Portal Venous Pressure ◽  
Vascular Capacitance ◽  
Blood Pool Scintigraphy ◽  
Vagal Reflex ◽  
Blood Volumes

The purpose of this study was to determine the effects of the prostaglandin I2 (prostacyclin; PGI2)-induced cardiac vagal reflex on intestinal and liver blood volumes and the intestinal vascular pressure-volume (P-V) relationship. In anesthetized pigs, blood volumes were measured by blood-pool scintigraphy. Portal venous pressure was varied by graded inflation of a portal vein constrictor to determine the intestinal vascular P-V relationship. Proximal right coronary infusion of PGI2 at a rate of 0.15 micrograms.kg-1.min-1 for 6 min increased intestinal blood volume by 7.0 +/- 1.2% (P < 0.01, means +/- SE) and shifted the intestinal vascular P-V relationship away from the pressure axis (i.e., a volume increase at a given venous pressure). This change was associated with decreases in liver blood volume and left ventricular end-diastolic pressure by 4.5 +/- 1.2 (P < 0.01) and 17 +/- 2% (P < 0.05), respectively. PGI2 also reduced central venous pressure by 16 +/- 2% from 3.2 +/- 0.5 mmHg (P < 0.05) and portal venous pressure by 7.0 +/- 0.6% from 7.6 +/- 0.6 mmHg (P < 0.05). These responses were abolished by bilateral vagotomy. The results demonstrate that intracoronary PGI2 infusion increases intestinal blood volume. This increase is mediated by a cardiac vagal reflex. The PGI2-induced shift in the intestinal vascular P-V relationship suggests that intestinal blood volume increases by an active change in vascular capacitance, whereas reductions in liver blood volume and left ventricular end-diastolic pressure appear to be due to passive mechanisms related to the shift of blood volume to the intestinal circulation.

Use of the Frank-Starling mechanism during submaximal versus maximal upright exercise

1986 ◽  
Vol 251 (6) ◽  
pp. H1101-H1105 ◽  
Author(s):  
G. D. Plotnick ◽  
L. C. Becker ◽  
M. L. Fisher ◽  
G. Gerstenblith ◽  
D. G. Renlund ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Blood Pool ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Vigorous Exercise ◽  
Systolic Volume ◽  
Early Exercise ◽  
End Diastolic Volume ◽  
Blood Pool Scintigraphy ◽  
End Systolic Volume

To evaluate the extent to which the Frank-Starling mechanism is utilized during successive stages of vigorous upright exercise, absolute left ventricular end-diastolic volume and ejection fraction were determined by gated blood pool scintigraphy at rest and during multilevel maximal upright bicycle exercise in 30 normal males aged 26-50 yr, who were able to exercise to 125 W or greater. Left ventricular end-systolic volume, stroke volume, and cardiac output were calculated at rest and during each successive 3-min stage of exercise [25, 50, 75, 100, and 125–225 W (peak)]. During early exercise (25 W), end-diastolic and stroke volumes increased (+17 +/- 1 and +31 +/- 4%, respectively), with no change in end-systolic volume. With further exercise (50–75 W) end-diastolic volume remained unchanged as end-systolic volume decreased (-12 +/- 4 and -24 + 5%, respectively). At peak exercise end-diastolic volume decreased to resting level, stroke volume remained at a plateau, and end-systolic volume further decreased (-48 +/- 7%). Thus the Frank-Starling mechanism is used early in exercise, perhaps because of a delay in sympathetic mobilization, and does not appear to play a role in the later stages of vigorous exercise.

scholarly journals Adenylyl cyclase type 5 protein expression during cardiac development and stress

2009 ◽  
Vol 297 (5) ◽  
pp. H1776-H1782 ◽  
Author(s):  
Che-Lin Hu ◽  
Rachna Chandra ◽  
Hui Ge ◽  
Jayashree Pain ◽  
Lin Yan ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Adrenergic Receptor ◽  
Ventricular Hypertrophy ◽  
Cardiac Development ◽  
Mammalian Species ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Receptor Stimulation ◽  
Specific Antibodies ◽  
The Brain

Adenylyl cyclase (AC) types 5 and 6 (AC5 and AC6) are the two major AC isoforms expressed in the mammalian heart that mediate signals from β-adrenergic receptor stimulation. Because of the unavailability of isoform-specific antibodies, it is difficult to ascertain the expression levels of AC5 protein in the heart. Here we demonstrated the successful generation of an AC5 isoform-specific mouse monoclonal antibody and studied the expression of AC5 protein during cardiac development in different mammalian species. The specificity of the antibody was confirmed using heart and brain tissues from AC5 knockout mice and from transgenic mice overexpressing AC5. In mice, the AC5 protein was highest in the brain but was also detectable in all organs studied, including the heart, brain, lung, liver, stomach, kidney, skeletal muscle, and vascular tissues. Western blot analysis showed that AC5 was most abundant in the neonatal heart and declined to basal levels in the adult heart. AC5 protein increased in the heart with pressure-overload left ventricular hypertrophy. Thus this new AC5 antibody demonstrated that this AC isoform behaves similarly to fetal type genes, such as atrial natriuretic peptide; i.e., it declines with development and increases with pressure-overload hypertrophy.

Force-frequency effect is a powerful determinant of myocardial contractility in the mouse

1997 ◽  
Vol 273 (3) ◽  
pp. H1283-H1290 ◽  
Author(s):  
V. Palakodeti ◽  
S. Oh ◽  
B. H. Oh ◽  
L. Mao ◽  
M. Hongo ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Myocardial Contractility ◽  
Sinus Node ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Force Frequency ◽  
Beta Adrenergic Receptor ◽  
Receptor Stimulation ◽  
Beta Adrenergic ◽  
Open Chest

The effects of heart rate (HR) on myocardial contractility in the mouse heart in situ were first investigated in open-chest mice (n = 7) by left ventricular (LV) catheter-tip micromanometry. HR was first slowed with a sinus node inhibitor (zatebradine), and atrial pacing to progressively increase the HR caused a positive inotropic response (assessed by maximum positive first derivative of LV pressure, LV dP/dtmax) up to a HR of 282 beats/min with the onset of a descending limb of the force-frequency relation (FFR) at 332 beats/min. beta-Adrenergic receptor stimulation (dobutamine) shifted upward and significantly steepened the positive FFR and increased HR at the onset of the descending limb to 402 beats/min. HR and LV dP/dtmax were then studied in closed-chest mice without pacing during recovery from anesthesia (n = 7), and during rest and intermittent physical activity the FFR was linear and positive up to 600 beats/min. HR was then progressively slowed with zatebradine, and the points at rest and during activity fell on the same linear relation. Thus we conclude the following: 1) in the open-chest anesthetized mouse, a positive FFR was amplified by beta-adrenergic receptor stimulation, and 20 in the mouse recovering from anesthesia the sinus node rate remained a critical determinant of myocardial contractility, without a descending limb of the FFR.

scholarly journals Benefits of long-term β-blockade in experimental chronic aortic regurgitation

2008 ◽  
Vol 294 (4) ◽  
pp. H1888-H1895 ◽  
Author(s):  
Eric Plante ◽  
Dominic Lachance ◽  
Serge Champetier ◽  
Marie-Claude Drolet ◽  
Élise Roussel ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Prolonged Treatment ◽  
Adrenergic System ◽  
Lv Function ◽  
Adrenergic Blockade ◽  
Long Term Effects ◽  
Lv Remodeling

The objective of this study was to assess the long-term effects of β-blockade on survival and left ventricular (LV) remodeling in rats with aortic valve regurgitation (AR). The pharmacological management of chronic AR remains controversial. No drug has been definitively proven to delay the need for valve replacement or to affect morbidity and/or mortality. Our group has reported that the adrenergic system is activated in an animal model of AR and that adrenergic blockade may help maintain normal LV function. The effects of prolonged treatment with a β-blocker are unknown. Forty Wistar rats with severe AR were divided into 2 groups of 20 animals each and treated with metoprolol (Met, 25 mg·kg−1·day−1) or left untreated for 1 yr. LV remodeling was evaluated by echocardiography. Survival was assessed by Kaplan-Meir curves. Hearts were harvested for tissue analysis. All Met-treated animals were alive after 6 mo vs. 70% of untreated animals. After 1 yr, 60% of Met-treated animals were alive vs. 35% of untreated animals ( P = 0.028). All deaths, except one, were sudden. There were no differences in LV ejection fraction (all >50%) or LV dimensions. LV mass tended to be lower in the Met-treated group. There was less subendocardial fibrosis in this group, as well as lower LV filling pressures (LV end-diastolic pressure). β-Adrenergic receptor ratio (β1/β2) was improved. One year of treatment with Met was well tolerated. Met improved 1-yr survival, minimized LV hypertrophy, improved LV filling pressures, decreased LV subendocardial fibrosis, and helped restore the β-adrenergic receptor ratio.

Vascular β-adrenergic receptor system is dysfunctional after myocardial infarction

2001 ◽  
Vol 280 (3) ◽  
pp. H1129-H1135 ◽  
Author(s):  
Mohamed A. Gaballa ◽  
Andrea Eckhart ◽  
Walter J. Koch ◽  
Steven Goldman
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Carotid Artery ◽  
Membrane Protein ◽  
Adrenergic Receptor ◽  
Vascular Reactivity ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Receptor System

We identified abnormalities in the vascular β-adrenergic receptor (β-AR) signaling pathway in heart failure after myocardial infarction (MI). To examine these abnormalities, we measured β-AR-mediated hemodynamics, vascular reactivity, and the vascular β-AR molecular signaling components in rats with heart failure after MI. Six weeks after MI, these rats had an increased left ventricular (LV) end-diastolic pressure, decreased LV systolic pressure, and decreased rate of LV pressure change (dP/d t). LV dP/d t responses to isoproterenol were shifted downward, although the responses for systemic vascular resistance were shifted upward in heart failure rats ( P < 0.05). Isoproterenol- and IBMX-induced vasorelaxations were blunted in heart failure rats ( P< 0.05) with no change in the forskolin-mediated vasorelaxation. These changes were associated with the following alterations in β-AR signaling ( P < 0.05): decreases in β-AR density (aorta: 58.7 ± 6.0 vs. 35.7 ± 1.9 fmol/mg membrane protein; carotid: 29.6 ± 5.6 vs. 18.0 ± 3.9 fmol/mg membrane protein, n = 5), increases in G protein-coupled receptor kinase activity levels (relative phosphorimage counts of 191 ± 39 vs. 259 ± 26 in the aorta and 115 ± 30 vs. 202 ± 7 in the carotid artery, n = 5), and decreases in cGMP and cAMP in the carotid artery (0.85 ± 0.10 vs. 0.31 ± 0.06 pmol/mg protein and 2.3 ± 0.3 vs. 1.2 ± 0.1 pmol/mg protein, n = 5) with no change in Gαs or Gαi in the aorta. Thus in heart failure there are abnormalities in the vascular β-AR system that are similar to those seen in the myocardium. This suggests a common neurohormonal mechanism and raises the possibility that treatment in heart failure focused on the myocardium may also affect the vasculature.

Alpha- and beta-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system

1994 ◽  
Vol 267 (1) ◽  
pp. H201-H210 ◽  
Author(s):  
K. Shigemi ◽  
M. J. Brunner ◽  
A. A. Shoukas
Keyword(s):  
Adrenergic Receptor ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Systemic Circulation ◽  
Adrenergic System ◽  
Beta Adrenergic ◽  
Vascular Volume ◽  
Adrenergic Mechanisms ◽  
Vascular Capacitance ◽  
Carotid Sinus Baroreflex

We examined the active and passive contributions of the alpha- and beta-adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an alpha- (phentolamine) or a beta- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 +/- 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the alpha-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the beta-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

β-Receptor-mediated increase in venous return in humans

1987 ◽  
Vol 65 (8) ◽  
pp. 1658-1665 ◽  
Author(s):  
Frans H. H. Leenen ◽  
Richard A. Reeves
Keyword(s):  
Heart Rate ◽  
Sympathetic Activity ◽  
Positive Inotropic Effect ◽  
Venous Return ◽  
Left Ventricular ◽  
Receptor Stimulation ◽  
Selective Blockade ◽  
Healthy Humans ◽  
Β Receptor ◽  
Stimulation Of

To assess the involvement of β1 and β2-receptors in the regulation of venous return in humans, changes in left ventricular end-diastolic (LVED) dimension were determined during β-receptor stimulation either by exogenous catecholamines or by increased endogenous sympathetic activity after hydralazine, after placebo and during nonselective versus β1 -selective blockade. Taking changes in heart rate and LV emptying into account, the three β-agonists (isoproterenol, terbutaline, and epinephrine) as well as hydralazine increased venous return as inferred from LVED dimension. After hydralazine, nonselective and β1-selective blockade were equally effective in blunting the increases in venous return, in heart rate, and in positive inotropic response. β1-Selective blockade did not affect the increase in heart rate caused by epinephrine and partially inhibited the positive inotropic effect and the increase in venous return. Nonselective blockade not only blocked the increase in venous return owing to epinephrine but actually led to a decrease, as evidenced by a decrease in LVED dimension despite the marked bradycardia and high afterload with this combination. The present findings in healthy humans indicate that stimulation of both β1- and β2-receptors increases venous return, heart rate, and myocardial contractility. β1-Receptors appeal to predominate in the response to neuronal sympathetic activity.

Total vascular pressure-volume relationship in conscious rats with chronic heart failure

1986 ◽  
Vol 251 (3) ◽  
pp. H483-H489 ◽  
Author(s):  
R. Gay ◽  
S. Wool ◽  
M. Paquin ◽  
S. Goldman
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Blood Volume ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Venous Capacitance ◽  
Vascular Volume ◽  
Conscious Rats ◽  
Vascular Compliance ◽  
Effective Vascular Compliance

To define the changes in the venous circulation in chronic left ventricular (LV) failure, we measured the mean circulatory filling pressure (MCFP), blood volume, and effective vascular compliance in conscious rats with heart failure, 3 wk after coronary ligation. Rats with myocardial infarction and LV end-diastolic pressure (EDP) greater than 15 mmHg were considered to have chronic heart failure. Rats with chronic heart failure (n = 11) showed an increase (P less than 0.001) in LV EDP to 24 +/- 2 mmHg compared with 6 +/- 1 mmHg in sham-operated (n = 9) and 7 +/- 1 mmHg in normal (n = 6) rats. In the rats with chronic heart failure the MCFP was increased to 9.9 +/- 0.2 mmHg (P less than 0.001) compared with 7.6 +/- 0.2 mmHg in the sham-operated and 7.7 +/- 0.2 mmHg in the normal rats. Effective vascular compliance was determined from MCFP-blood volume curves. In rats with chronic heart failure, the effective vascular compliance was decreased to 2.40 +/- 0.08 ml X mmHg-1 X kg-1 from 3.34 +/- 0.16 in sham-operated rats and 3.35 +/- 0.22 ml X mmHg-1 X kg-1 in normal rats. The blood volume and the unstressed vascular volume of the rats with chronic heart failure were not statistically different from the sham-operated rats. These results suggest that venous capacitance is decreased in chronic heart failure, due to a decrease in effective vascular compliance with no significant change in unstressed vascular volume. Hexamethonium chloride did not alter the effective vascular compliance of the rats with heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document