Effects of hypertrophy on left atrial and ventricular compliance and plasma ANF levels in conscious dogs

Alterations in left atrial (LA) and left ventricular (LV) compliance and arterial and coronary sinus atrial natriuretic factor (ANF) concentrations at baseline and in response to both volume depletion and expansion were investigated in 15 conscious dogs with aortic banding-induced LV hypertrophy (LVH) (LV/body wt increased by 64%), which also induced LAH (LA/body wt increased by 61%). With volume expansion coronary sinus ANF increased more (P < 0.05) in dogs with LVH (+427 +/- 88 pg/ml) compared with control dogs (+146 +/- 45 pg/ml). Arterial ANF levels also rose more with volume expansion in LVH. In dogs with LVH, the LV end-diastolic pressure-diameter relationship was shifted to the left with a steeper slope with volume expansion, such that at any given diastolic dimension, diastolic pressure was higher. In contrast, the pressure-dimension relationship for the LA appendage was shifted in the opposite direction during both atrial systolic and diastolic phases, with a more shallow slope in hypertrophy compared with control dogs, resulting in an augmented pressure-dimension product during volume loading in LAH. In conclusion, in dogs with LVH and LAH, enhanced ANF was revealed in the coronary sinus and systemic circulation during volume expansion, which could be due, in part, to a more compliant, but hypertrophied, LA, which responded to equivalent volume loading with an augmented pressure-dimension product.

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Extent of utilization of the Frank-Starling mechanism in conscious dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1978.234.4.h338 ◽

1978 ◽

Vol 234 (4) ◽

pp. H338-H345 ◽

Cited By ~ 5

Author(s):

D. H. Boettcher ◽

S. F. Vatner ◽

G. R. Heyndrickx ◽

E. Braunwald

Keyword(s):

Coronary Artery ◽

Myocardial Ischemia ◽

Volume Expansion ◽

Left Main Coronary Artery ◽

Left Ventricular ◽

Conscious Dogs ◽

Left Main ◽

Volume Loading ◽

Conscious Animal ◽

Controlling Mechanism

The extent to which an increase in preload increases left ventricular (LV) end-diastolic (ED) diameter (D) was studied in seven conscious dogs instrumented with ultrasonic D transducers and miniature LV pressure (P) gauges. Preload was elevated by three techniques: 1) volume loading with saline infusion, 2) induction of global myocardial ischemia by constricting the left main coronary artery, and 3) infusion of methoxamine. These three interventions increased LVEDP to over 30 mmHg from a control of 10 +/- 1 mmHg. With volume loading, LVEDD rose by only 1.55 +/- 0.39 mm from a control of 44.08 +/- 1.08 mm; with ischemia LVEDD rose by only .96 +/- .29 mm from a control of 42.55 +/- 2.18 mm, while with methoxamine LVEDD rose by only 1.34 +/- 0.38 mm from a control of 43.89 +/- 2.07 mm. In contrast, in the open-chest, anesthetized dog, LVEDD was greatly reduced and volume expansion resulted in a profound increase in LVEDD. Thus, the Frank-Starling mechanism is not an important controlling mechanism in the normal, reclining, conscious animal, since LVEDD appears to be near maximal at rest and does not increase substantially despite striking increases in LVEDP.

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Acute volume expansion enhances baroreceptor discharge in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.1.h209 ◽

1992 ◽

Vol 262 (1) ◽

pp. H209-H214

Author(s):

W. Wang ◽

M. A. Weitzel ◽

J. S. Chen ◽

I. H. Zucker

Keyword(s):

Volume Expansion ◽

Carotid Sinus ◽

Diastolic Pressure ◽

Systemic Circulation ◽

Left Ventricular ◽

External Carotid ◽

A Value ◽

Flow Through ◽

The Common ◽

Circulation Volume

By recording single-unit discharge from the carotid sinus nerve of normal dogs in the control and in the volume-expanded state, both with the sinus open to the circulation and with it isolated, the effects of acute volume expansion on baroreceptor discharge sensitivity were investigated. The carotid sinus was vascularly isolated except for the common carotid and external carotid arteries. Inflation of hydraulic occluders on these vessels completely isolated the sinus from the systemic circulation. Flow and diameter changes of the carotid sinus were measured. Plasma volume was expanded with isotonic, isoncotic dextran in normal saline until the left ventricular end-diastolic pressure reached a value of 20-25 mmHg. In the group with the sinus open to the circulation, volume expansion did not depress baroreceptor discharge sensitivity; in fact, it augmented baroreceptor activity (peak discharge = 39.2 +/- 1.6 vs. 49.9 +/- 3.3 spikes/s, P less than 0.05). There was no such effect in the group with the sinus isolated from the circulation during volume expansion. In the group with the sinus open to the circulation, volume expansion significantly increased flow through the common carotid artery and shifted the carotid sinus pressure-diameter curves upward without a change in compliance. These data suggest that acute volume expansion augments baroreceptor discharge, and this phenomenon may be mediated either by some circulating substance(s) or by an increase in flow through the carotid sinus during volume expansion.

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Phylogenesis of the Bainbridge reflex

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1982.242.3.r244 ◽

1982 ◽

Vol 242 (3) ◽

pp. R244-R246 ◽

Cited By ~ 4

Author(s):

D. H. Boettcher ◽

M. Zimpfer ◽

S. F. Vatner

Keyword(s):

Heart Rate ◽

Cardiac Catheterization ◽

Diastolic Pressure ◽

Systolic Pressure ◽

Left Ventricular ◽

Conscious Dogs ◽

Volume Loading

The effects of volume loading were examined on measurements of left ventricular (LV) pressure and heart rate in patients undergoing cardiac catheterization. These data were compared to those collected in conscious dogs and subhuman primates (baboons). In man acute volume loading increased LV end-diastolic pressure by 14 mmHg, but did not increase LV systolic pressure significantly. Similar increases in LV end-diastolic pressure were observed in conscious dogs and baboons. LV systolic pressure also did not rise in baboons, but did increase (+32 mmHg) with volume loading in dogs. In man volume loading increased heart rate by 15 beats/min, significantly less (P less than 0.01) than observed in baboons (+37 beats/min), and which in turn was significantly less than that observed in dogs (+88 beats/min). Thus, the Bainbridge reflex, i.e., the tachycardia that occurs with volume loading, appears to exist in primates including man. However, the extent of utilization of this reflex decreases significantly from nonprimate mammals (dogs) to subhuman primates (baboons) to man.

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alpha-Adrenergic control of oxygen delivery to myocardium during exercise in conscious dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1982.242.5.h805 ◽

1982 ◽

Vol 242 (5) ◽

pp. H805-H809 ◽

Cited By ~ 17

Author(s):

G. R. Heyndrickx ◽

P. Muylaert ◽

J. L. Pannier

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Oxygen Consumption ◽

Coronary Blood Flow ◽

Coronary Sinus ◽

Oxygen Delivery ◽

Left Ventricular ◽

Conscious Dogs ◽

Adrenergic Blockade ◽

Adrenergic Control

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.

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Left ventricular end-diastolic pressure is associated with left atrial functional measures by echocardiography

The International Journal of Cardiovascular Imaging ◽

10.1007/s10554-021-02300-5 ◽

2021 ◽

Author(s):

Flemming Javier Olsen ◽

Rasmus Møgelvang ◽

Martina Chantal de Knegt ◽

Søren Galatius ◽

Sune Pedersen ◽

...

Keyword(s):

Left Atrial ◽

Diastolic Pressure ◽

Left Ventricular ◽

Functional Measures

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Ventricular interaction and external constraint account for decreased stroke work during volume loading in CHF

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.281.6.h2385 ◽

2001 ◽

Vol 281 (6) ◽

pp. H2385-H2391 ◽

Cited By ~ 55

Author(s):

Thomas D. Moore ◽

Michael P. Frenneaux ◽

Rozsa Sas ◽

J. J. Atherton ◽

Jayne A. Morris-Thurgood ◽

...

Keyword(s):

Diastolic Pressure ◽

Left Ventricular ◽

Negative Slope ◽

Segment Length ◽

Stroke Work ◽

Volume Loading ◽

End Diastolic Volume ◽

Pulmonary Capillary ◽

Apparent Decrease ◽

Pericardial Pressure

The slope of the stroke work (SW)-pulmonary capillary wedge pressure (PCWP) relation may be negative in congestive heart failure (CHF), implying decreased contractility based on the premise that PCWP is simply related to left ventricular (LV) end-diastolic volume. We hypothesized that the negative slope is explained by decreased transmural LV end-diastolic pressure (LVEDP), despite the increased LVEDP, and that contractility remains unchanged. Rapid pacing produced CHF in six dogs. Hemodynamic and dimension changes were then measured under anesthesia during volume manipulation. Volume loading increased pericardial pressure and LVEDP but decreased transmural LVEDP and SW. Right ventricular diameter increased and septum-to-LV free wall diameter decreased. Although the slopes of the SW-LVEDP relations were negative, the SW-transmural LVEDP relations remained positive, indicating unchanged contractility. Similarly, the SW-segment length relations suggested unchanged contractility. Pressure surrounding the LV must be subtracted from LVEDP to calculate transmural LVEDP accurately. When this was done in this model, the apparent decrease in contractility was no longer evident. Despite the increased LVEDP during volume loading, transmural LVEDP and therefore SW decreased and contractility remained unchanged.

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Acute stimulation of the soluble guanylate cyclase does not impact on left ventricular capacitance in normal and hypertrophied porcine hearts in vivo

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00510.2017 ◽

2018 ◽

Vol 315 (3) ◽

pp. H669-H680 ◽

Cited By ~ 5

Author(s):

Alessio Alogna ◽

Michael Schwarzl ◽

Martin Manninger ◽

Nazha Hamdani ◽

Birgit Zirngast ◽

...

Keyword(s):

Guanylate Cyclase ◽

Soluble Guanylate Cyclase ◽

Diastolic Pressure ◽

Aortic Pressure ◽

Left Ventricular ◽

Concentric Hypertrophy ◽

Ventricular Compliance ◽

Left Ventricular Compliance ◽

Stimulation Of

Experimental data indicate that stimulation of the nitric oxide-soluble guanylate cyclase(sGC)-cGMP-PKG pathway can increase left ventricular (LV) capacitance via phosphorylation of the myofilamental protein titin. We aimed to test whether acute pharmacological sGC stimulation with BAY 41-8543 would increase LV capacitance via titin phosphorylation in healthy and deoxycorticosteroneacetate (DOCA)-induced hypertensive pigs. Nine healthy Landrace pigs and 7 pigs with DOCA-induced hypertension and LV concentric hypertrophy were acutely instrumented to measure LV end-diastolic pressure-volume relationships (EDPVRs) at baseline and during intravenous infusion of BAY 41-8543 (1 and 3 μg·kg−1·min−1 for 30 min, respectively). Separately, in seven healthy and six DOCA pigs, transmural LV biopsies were harvested from the beating heart to measure titin phosphorylation during BAY 41-8543 infusion. LV EDPVRs before and during BAY 41-8543 infusion were superimposable in both healthy and DOCA-treated pigs, whereas mean aortic pressure decreased by 20–30 mmHg in both groups. Myocardial titin phosphorylation was unchanged in healthy pigs, but total and site-specific (Pro-Glu-Val-Lys and N2-Bus domains) titin phosphorylation was increased in DOCA-treated pigs. Bicoronary nitroglycerin infusion in healthy pigs ( n = 5) induced a rightward shift of the LV EDPVR, demonstrating the responsiveness of the pathway in this model. Acute systemic sGC stimulation with the sGC stimulator BAY 41-8543 did not recruit an LV preload reserve in both healthy and hypertrophied LV porcine myocardium, although it increased titin phosphorylation in the latter group. Thus, increased titin phosphorylation is not indicative of increased in vivo LV capacitance. NEW & NOTEWORTHY We demonstrate that acute pharmacological stimulation of soluble guanylate cyclase does not increase left ventricular compliance in normal and hypertrophied porcine hearts. Effects of long-term soluble guanylate cyclase stimulation with oral compounds in disease conditions associated with lowered myocardial cGMP levels, i.e., heart failure with preserved ejection fraction, remain to be investigated.

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Role of Diastole in Left Ventricular Function, II: Diagnosis and Treatment

American Journal of Critical Care ◽

10.4037/ajcc2004.13.6.453 ◽

2004 ◽

Vol 13 (6) ◽

pp. 453-466 ◽

Cited By ~ 18

Author(s):

Shannan K. Hamlin ◽

Penelope S. Villars ◽

Joseph T. Kanusky ◽

Andrew D. Shaw

Keyword(s):

Heart Failure ◽

Diastolic Dysfunction ◽

Left Atrial ◽

Diastolic Heart Failure ◽

Systolic Heart Failure ◽

Clinical Signs ◽

Left Ventricular ◽

Exercise Intolerance ◽

Radiographic Findings ◽

Ventricular Compliance

Left ventricular diastolic dysfunction plays an important role in congestive heart failure. Although once thought to be lower, the mortality of diastolic heart failure may be as high as that of systolic heart failure. Diastolic heart failure is a clinical syndrome characterized by signs and symptoms of heart failure with preserved ejection fraction (0.50) and abnormal diastolic function. One of the earliest indications of diastolic heart failure is exercise intolerance followed by fatigue and, possibly, chest pain. Other clinical signs may include distended neck veins, atrial arrhythmias, and the presence of third and fourth heart sounds. Diastolic dysfunction is difficult to differentiate from systolic dysfunction on the basis of history, physical examination, and electrocardiographic and chest radiographic findings. Therefore, objective diagnostic testing with cardiac catheterization, Doppler echocardiography, and possibly measurement of serum levels of B-type natriuretic peptide is often required. Three stages of diastolic dysfunction are recognized. Stage I is characterized by reduced left ventricular filling in early diastole with normal left ventricular and left atrial pressures and normal compliance. Stage II or pseudonormalization is characterized by a normal Doppler echocardiographic transmitral flow pattern because of an opposing increase in left atrial pressures. This normalization pattern is a concern because marked diastolic dysfunction can easily be missed. Stage III, the final, most severe stage, is characterized by severe restrictive diastolic filling with a marked decrease in left ventricular compliance. Pharmacological therapy is tailored to the cause and type of diastolic dysfunction.

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Positive end-expiratory pressure shifts left ventricular diastolic pressure-area curves

Journal of Applied Physiology ◽

10.1152/jappl.1980.48.4.670 ◽

1980 ◽

Vol 48 (4) ◽

pp. 670-676 ◽

Cited By ~ 44

Author(s):

J. B. Haynes ◽

S. D. Carson ◽

W. P. Whitney ◽

G. O. Zerbe ◽

T. M. Hyers ◽

...

Keyword(s):

Cardiac Output ◽

Volume Expansion ◽

Diastolic Pressure ◽

Left Ventricular ◽

Positive End Expiratory Pressure ◽

Pressure Area ◽

Radiopaque Markers ◽

Peep Ventilation ◽

Volume Characteristics ◽

Area Data

Positive end-expiratory pressure (PEEP) ventilation is frequently associated with reduction in cardiac output despite unchanged transmural left ventricular (LV) end-diastolic pressure. These findings have been interpreted to indicate decreased contractility, but could also be explained by altered LV diastolic pressure-volume characteristics. To study this possibility, radiopaque markers were inserted into a plane of the LV in nine dogs. Transmural pressure (LV-pericardial) was synchronized with LV area during ventilation with zero end-expiratory pressure and with 15 cmH2O PEEP. Mean polynomial curves derived from the diastolic pressure-area data demonstrated that PEEP shifted the curves upward so that a given diastolic area was associated with a higher transmural LV pressure (P less than 0.0001). PEEP decreased end-diastolic area and stroke area, both of which were normalized with dextran volume expansion. Restoration of stroke area by normalizing end-diastolic area with volume expansion suggests the initial changes with PEEP were due to a decrease in preload rather than in contractility.

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