Sympathetic stimulation alters left ventricular relaxation and chamber size

1993 ◽  
Vol 264 (1) ◽  
pp. R1-R7 ◽  
Author(s):  
I. G. Burwash ◽  
D. E. Morgan ◽  
C. J. Koilpillai ◽  
G. L. Blackmore ◽  
D. E. Johnstone ◽  
...  
Keyword(s):  
Stellate Ganglion ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Wall Stress ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Ventricular Contractility ◽  
Cross Sectional ◽  
Stress Changes ◽  
Neuronal Stimulation

Alterations in left ventricular (LV) contractility, relaxation, and chamber dimensions induced by efferent sympathetic nerve stimulation were investigated in nine anesthetized open-chest dogs in sinus rhythm. Supramaximal stimulation of acutely decentralized left stellate ganglia augmented heart rate, LV systolic pressure, and rate of LV pressure rise (maximum +dP/dt, 1,809 +/- 191 to 6,304 +/- 725 mmHg/s) and fall (maximum -dP/dt, -2,392 +/- 230 to -4,458 +/- 482 mmHg/s). It also reduced the time constant of isovolumic relaxation, tau (36.5 +/- 4.8 to 14.9 +/- 1.1 ms). Simultaneous two-dimensional echocardiography recorded reductions in end-diastolic and end-systolic LV cross-sectional chamber areas (23 and 31%, respectively), an increase in area ejection fraction (32%), and increases in end-diastolic and end-systolic wall thicknesses (14 and 13%, respectively). End-systolic and end-diastolic wall stresses were unchanged by stellate ganglion stimulation (98 +/- 12 to 95 +/- 9 dyn x 10(3)/cm2; 6.4 +/- 2.4 to 2.4 +/- 0.3 dyn x 10(3)/cm2, respectively). Atrial pacing to similar heart rates did not alter monitored indexes of contractility. Dobutamine and isoproterenol induced changes similar to those resulting from sympathetic neuronal stimulation. These data indicate that when the efferent sympathetic nervous system increases left ventricular contractility and relaxation, concomitant reductions in systolic and diastolic dimensions of that chamber occur that are associated with increasing wall thickness such that LV wall stress changes are minimized.

Severe myocardial dysfunction induced by ventricular remodeling in aging rat hearts

1990 ◽  
Vol 259 (4) ◽  
pp. H1086-H1096 ◽  
Author(s):  
J. M. Capasso ◽  
T. Palackal ◽  
G. Olivetti ◽  
P. Anversa
Keyword(s):  
Ventricular Remodeling ◽  
Volume Fraction ◽  
Diastolic Pressure ◽  
Structural Characteristics ◽  
Myocardial Dysfunction ◽  
Pressure Rise ◽  
Wall Stress ◽  
Left Ventricular ◽  
Cross Sectional

To determine if aging engenders alterations in the functional properties of the myocardium and ventricular remodeling, the hemodynamic performance and structural characteristics of the left ventricle of male Fischer 344 rats at 4, 12, 20, and 29 mo of age were studied by quantitative physiology and morphology. In vivo assessment of cardiac pump function showed no change up to 20 mo, whereas left ventricular end-diastolic pressure was increased at 29 mo. Moreover, peak rates of pressure rise and decay, stroke volume, ejection fraction, and cardiac output were depressed at the later age interval, demonstrating the presence of ventricular failure at this time. The measurements of chamber size and wall thickness showed that ventricular end-diastolic and end-systolic volumes progressively increased with age with the greatest change occurring at 20-29 mo. Aging was also accompanied by a marked augmentation in the volume fraction of fibrotic areas in the ventricular myocardium that was due to an increase in their number and cross-sectional area with time. These architectural rearrangements, in combination with the abnormalities in ventricular function, resulted in an elevation in the volume of wall stress throughout the cardiac cycle. Wall stress increased by 64, 44, and 50% from 4 to 12, 12 to 20, and 20 to 29 mo of age. In conclusion, aging leads to a continuous rise in wall stress that is not normalized by ventricular remodeling. These two independent processes appear to be responsible for the onset of heart failure in the senescent rat.

Assessment of slope of end-systolic pressure-volume line of in situ dog heart

1986 ◽  
Vol 250 (4) ◽  
pp. H685-H692 ◽  
Author(s):  
Y. Igarashi ◽  
H. Suga
Keyword(s):  
Systolic Pressure ◽  
Electromagnetic Flowmeter ◽  
Left Ventricular ◽  
Aortic Occlusion ◽  
Atrial Pacing ◽  
Ventricular Contractility ◽  
Dog Heart ◽  
End Diastolic Volume ◽  
Isovolumic Contraction

The purpose of this study was to establish a new method of assessment of the slope (Emax) of the end-systolic pressure-volume line (ESPVL) of the in situ heart. In anesthetized open-chest dogs, an isovolumic contraction was produced by an aortic occlusion after steady-state ejecting contractions in the left ventricle. We plotted ventricular pressure measured with a catheter-tip manometer against time integral of aortic flow measured with an electromagnetic flowmeter of the last ejecting and the first isovolumic contraction, assuming the same end-diastolic volume. ESPVL was drawn from the peak isovolumic pressure-volume point tangential to the left upper corner of the +/- 3.0 (SE) mmHg/ml (n = 9 dogs) in control run and was increased by 59 +/- 19% under isoproterenol and decreased by 47 +/- 9% after propranolol. Emax was little changed by atrial pacing. We conclude that Emax by this aortic occlusion method is useful for assessment of left ventricular contractility of the in situ dog heart.

Histamine decreases left ventricular contractility in normal human subjects

1992 ◽  
Vol 73 (6) ◽  
pp. 2530-2537 ◽  
Author(s):  
D. J. Cooper ◽  
C. R. Thompson ◽  
K. R. Walley ◽  
R. P. Gillis ◽  
P. E. Wolinski-Walley ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Human Subjects ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
H1 Receptor ◽  
Wide Range

To determine whether histamine alters human left ventricular contractility we measured heart rate, calibrated carotid arterial pressure, and left ventricular dimensions (echocardiogram) in nine healthy volunteers. We assessed baseline contractility using the end-systolic pressure-dimension relationship and the end-systolic meridional wall stress-rate-corrected velocity of circumferential fiber shortening relationship determined over a wide range of afterloads using phenylephrine and nitroprusside infusions. We then infused histamine for 3–5 min at a dose predetermined to decrease mean arterial pressure by 20%, both before and after H1 receptor antagonist pretreatment (diphenhydramine 50 mg i.v.). Histamine decreased end-systolic pressure but, unlike an equally hypotensive infusion of nitroprusside, did not decrease end-systolic dimension or increase fractional shortening. Histamine also decreased velocity of circumferential fiber shortening at the same end-systolic meridional wall stress as controls (P < 0.05). These effects of histamine were inhibited by H1 antagonist pretreatment. We conclude that the dominant effect of histamine on the human heart is to decrease left ventricular contractility and that this decrease in contractility is dependent, at least partially, on H1-receptor activation.

scholarly journals A simulation study of left ventricular decompression using a double lumen arterial cannula prototype during a veno-arterial extracorporeal membrane oxygenation

2019 ◽  
Vol 42 (12) ◽  
pp. 748-756
Author(s):  
Filip Ježek ◽  
Svitlana Strunina ◽  
Brian E Carlson ◽  
Jiří Hozman
Keyword(s):  
Extracorporeal Membrane Oxygenation ◽  
Cardiogenic Shock ◽  
Cardiovascular System ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Double Lumen ◽  
Membrane Oxygenation ◽  
Arterial Cannula

Background: Veno-arterial extracorporeal membrane oxygenation can be vital to support patients in severe or rapidly progressing cardiogenic shock. In cases of left ventricular distension, left ventricular decompression during veno-arterial extracorporeal membrane oxygenation may be a crucial factor influencing the patient outcome. Application of a double lumen arterial cannula for a left ventricular unloading is an alternative, straightforward method for left ventricular decompression during extracorporeal membrane oxygenation in a veno-arterial configuration. Objectives: The purpose of this article is to use a mathematical model of the human adult cardiovascular system to analyze the left ventricular function of a patient in cardiogenic shock supported by veno-arterial extracorporeal membrane oxygenation with and without the application of left ventricular unloading using a novel double lumen arterial cannula. Methods: A lumped model of cardiovascular system hydraulics has been coupled with models of non-pulsatile veno-arterial extracorporeal membrane oxygenation, a standard venous cannula, and a drainage lumen of a double lumen arterial cannula. Cardiogenic shock has been induced by decreasing left ventricular contractility to 10% of baseline normal value. Results: The simulation results indicate that applying double lumen arterial cannula during veno-arterial extracorporeal membrane oxygenation is associated with reduction of left ventricular end-systolic volume, end-diastolic volume, end-systolic pressure, and end-diastolic pressure. Conclusions: A double lumen arterial cannula is a viable alternative less invasive method for left ventricular decompression during veno-arterial extracorporeal membrane oxygenation. However, to allow for satisfactory extracorporeal membrane oxygenation flow, the cannula design has to be revisited.

Congestive Heart Failure in Copper-Deficient Mice

2003 ◽  
Vol 228 (7) ◽  
pp. 811-817 ◽  
Author(s):  
Laila Elsherif ◽  
Raymond V. Ortines ◽  
Jack T. Saari ◽  
Y. James Kang
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Experimental Models ◽  
Left Ventricular ◽  
Mouse Heart ◽  
Total Period

Copper Deficiency (CuD) leads to hypertrophic cardiomyopathy in various experimental models. The morphological, electrophysiological, and molecular aspects of this hypertrophy have been under investigation for a long time. However the transition from compensated hypertrophy to decompensated heart failure has not been investigated in the study of CuD. We set out to investigate the contractile and hemodynamic parameters of the CuD mouse heart and to determine whether heart failure follows hypertrophy in the CuD heart. Dams of FVB mice were fed CuD or copper-adequate (CuA) diet starting from the third day post delivery and the weanling pups were fed the same diet for a total period of 5 weeks (pre- and postweanling). At week 4, the functional parameters of the heart were analyzed using a surgical technique for catheterizing the left ventricle. A significant decrease in left ventricle systolic pressure was observed with no significant change in heart rate, and more importantly contractility as measured by the maximal rate of left ventricular pressure rise (+dP/dt) and decline (−dP/dt) were significantly depressed in the CuD mice. However, left ventricle end diastolic pressure was elevated, and relaxation was impaired in the CuD animals; the duration of relaxation was prolonged. In addition to significant changes in the basal level of cardiac function, CuD hearts had a blunted response to the stimulation of the β-adrenergic agonist isoproterenol. Furthermore, morphological analysis revealed increased collagen accumulation in the CuD hearts along with lipid deposition. This study shows that CuD leads to systolic and diastolic dysfunction in association with histopathological changes, which are indices commonly used to diagnose congestive heart failure.

scholarly journals Novel Neuromodulation Approach to Improve Left Ventricular Contractility in Heart Failure

2020 ◽  
Vol 13 (11) ◽  
Author(s):  
Vivek Y. Reddy ◽  
Jan Petrů ◽  
Filip Málek ◽  
Lee Stylos ◽  
Steve Goedeke ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Diastolic Pressure ◽  
Acute Decompensated Heart Failure ◽  
Systolic Pressure ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Right Pulmonary Artery ◽  
The Right

Background: Morbidity and mortality outcomes for patients admitted for acute decompensated heart failure are poor and have not significantly changed in decades. Current therapies are focused on symptom relief by addressing signs and symptoms of congestion. The objective of this study was to test a novel neuromodulation therapy of stimulation of epicardial cardiac nerves passing along the posterior surface of the right pulmonary artery. Methods: Fifteen subjects admitted for defibrillator implantation and ejection fraction ≤35% on standard heart failure medications were enrolled. Through femoral arterial access, high fidelity pressure catheters were placed in the left ventricle and aortic root. After electro anatomic rendering of the pulmonary artery and branches, either a circular or basket electrophysiology catheter was placed in the right pulmonary artery to allow electrical intravascular stimulation at 20 Hz, 4 ms pulse width, and ≤20 mA. Changes in maximum positive dP/dt (dP/dt Max ) indicated changes in ventricular contractility. Results: Of 15 enrolled subjects, 5 were not studied due to equipment failure or abnormal pulmonary arterial anatomy. In the remaining subjects, dP/dt Max increased significantly by 22.6%. There was also a significant increase in maximum negative dP/dt (dP/dt Min ), mean arterial pressure, systolic pressure, diastolic pressure, and left ventricular systolic pressure. There was no significant change in heart rate or left ventricular diastolic pressure. Conclusions: In this first-in-human study, we demonstrated that in humans with stable heart failure, left ventricular contractility could be accentuated without an increase in heart rate or left ventricular filling pressures. This benign increase in contractility may benefit patients admitted for acute decompensated heart failure.

Increased cardiac contractility in acute uremia: interrelationships with hypertension

1975 ◽  
Vol 229 (2) ◽  
pp. 501-505 ◽  
Author(s):  
T Nivatpumin ◽  
T Yipintsoi ◽  
S Penpargkul ◽  
J Scheuer
Keyword(s):  
Blood Pressure ◽  
Systolic Hypertension ◽  
Diastolic Pressure ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Ventricular Systolic Pressure ◽  
Inotropic State ◽  
Left Ventricular Systolic Pressure

To study the effects of acute uremia on the inotropic state of the rat heart, we subjected rats to bilateral nephrectomy and studied their hearts in the open chest 24 h later. Uremic rats had significantly higher systolic blood pressure than sham-operated animals. Left ventricular systolic pressure and maximum dP/dt, both during ejection and isovolumic contrations, were higher for any given end-diastolic pressure in hearts of uremic rats than in sham-operated animals. This difference in performance charcteristics was not abolished by doses of propranolol that blocked the heart rate response to isoproterenol. The administration of phenoxybenzamine during the 24 h of uremia abolished the blood pressure rise in uremic rats, but the increased contractile state persisted. Treatment of sham-operated animals with methoxamine to produce the same course of blood pressure as observed in uremic rats was also associated with an increased inotropic state. These results indicate that in the rat, acute uremia is associated with an increased inotropic state that is not mediated by beta-adrenergic mechanisms. The systolic hypertension of acute uremia is not the major cause of the increased contractility, although systolic hypertension without uremia can mimic the performance characteristics found in hearts of uremic rats.

Influence of pacing site on canine left ventricular contraction

1986 ◽  
Vol 251 (2) ◽  
pp. H428-H435 ◽  
Author(s):  
D. Burkhoff ◽  
R. Y. Oikawa ◽  
K. Sagawa
Keyword(s):  
Right Ventricular ◽  
Time Course ◽  
Peak Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Free Wall ◽  
Ventricular Pacing ◽  
Right Ventricular Free Wall ◽  
Isolated Hearts

We investigated the influence of pacing site on several aspects of left ventricular (LV) performance to test the hypothesis that "effective ventricular muscle mass" is reduced with direct ventricular pacing. All studies were performed on isolated supported canine hearts that were constrained to contract isovolumically. To determine the influence of pacing site on magnitude and time course of isovolumic LV pressure (P) generation, LVP waves were recorded in eight isolated hearts paced at 130 beats/min. Pacing was epicardially from atrium, LV apex, LV free wall, right ventricular free wall (RVF), and endocardially from right ventricular endocardium. In a given heart, peak LVP was greatest with atrial pacing and smallest with RVF pacing, the difference being on average 26 +/- 10% (mean +/- SD) of the former pressure. The other pacing sites produced intermediate peak LVPs. When instantaneous LVP waves, obtained while pacing from each of the five sites, were normalized by their respective amplitudes, they were virtually superimposable up to the time of peak pressure and only slightly different during the remainder of the cardiac cycle. With changes in pacing site there was a linear negative correlation (r = 0.971) between changes in peak pressure and changes in duration of the QRS complex of a bipolar epicardial electrogram with an average slope of -0.51 mmHg/ms. Compared with atrial pacing, the slope of the end-systolic pressure-volume relation, Ees, was decreased with ventricular pacing, but Vo, the volume axis intercept, was relatively constant.(ABSTRACT TRUNCATED AT 250 WORDS)

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