Acute effect of clonidine on left ventricular pressure-volume relation in hypertensive patients with diastolic heart dysfunction

The breakdown of cardiac self-organization leads to heart diseases and failure, the number one cause of death worldwide. The left ventricular pressure–volume relation plays a key role in the diagnosis and treatment of heart diseases. Lumped-parameter models combined with pressure–volume loop analysis are very effective in simulating clinical scenarios with a view to treatment optimization and outcome prediction. Unfortunately, often invoked in this analysis is the traditional, time-varying elastance concept, in which the ratio of the ventricular pressure to its volume is prescribed by a periodic function of time, instead of being calculated consistently according to the change in feedback mechanisms (e.g., the lack or breakdown of self-organization) in heart diseases. Therefore, the application of the time-varying elastance for the analysis of left ventricular assist device (LVAD)–heart interactions has been questioned. We propose a paradigm shift from the time-varying elastance concept to a synergistic model of cardiac function by integrating the mechanical, electric, and chemical activity on microscale sarcomere and macroscale heart levels and investigating the effect of an axial rotary pump on a failing heart. We show that our synergistic model works better than the time-varying elastance model in reproducing LVAD–heart interactions with sufficient accuracy to describe the left ventricular pressure–volume relation.

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Effects of vasoactive intestinal peptide on myocardial performance

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.266.2.h399 ◽

1994 ◽

Vol 266 (2) ◽

pp. H399-H405 ◽

Cited By ~ 1

Author(s):

N. P. Xenopoulos ◽

R. J. Applegate

Keyword(s):

Vasoactive Intestinal Peptide ◽

Contractile Function ◽

Time Derivative ◽

Systolic Pressure ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Adrenergic Blockade ◽

Volume Relation ◽

First Time

It is now recognized that stimulation of the vagus releases both acetylcholine (ACh) and vasoactive intestinal peptide (VIP). Whereas ACh depresses cardiac function, recent data indicate that VIP may have a cardiostimulatory effect. Exogenously administered VIP appears to enhance left ventricular (LV) contractile function; however, whether endogenously released VIP alters LV performance is not known. Accordingly, we evaluated the effects of exogenous VIP and endogenously released VIP during vagal stimulation after muscarinic and beta-adrenergic blockade (VS-B) on LV performance using pressure-volume analysis. Eight anesthetized open-chest dogs instrumented to measure LV pressure and volume (conductance catheter) were pretreated with atropine (0.1 mg/kg) and propranolol (1 mg/kg). The cervical vagi were transected. Hemodynamic data were obtained at steady state and during transient vena caval occlusion. Exogenous intravenous VIP (0.05 microgram/kg-1 x min-1) increased HR minimally [2.1 +/- 0.9% increase; P = not significant (NS)] but significantly increased maximum first time derivative of left ventricular pressure (dP/dtmax; 29.4 +/- 19.9% increase; P < 0.05) and the slope of the end-systolic pressure-volume relation (Ees; 3.1 +/- 1.3 to 8.9 +/- 4.2 mmHg/ml; P < 0.05). Minimum first time derivative of left ventricular pressure (dP/dtmin) decreased 22 +/- 16.2% (P < 0.05), and the time constant of isovolumic relaxation (tau) decreased 38 +/- 18% (P < 0.05). During VS-B (20 Hz, 15 v, 5 min), HR increased significantly (98 +/- 11 to 130 +/- 26 beats/min; P < 0.05). Ees also increased significantly (3.3 +/- 1.6 vs. 5.2 +/- 2.8 mmHg/ml; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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Exercise-induced upward shift of diastolic left ventricular pressure-volume relation in patients with dilated cardiomyopathy. Effects of beta-adrenoceptor blockade.

Circulation ◽

10.1161/01.cir.88.5.2215 ◽

1993 ◽

Vol 88 (5) ◽

pp. 2215-2223 ◽

Cited By ~ 22

Author(s):

H Sato ◽

M Hori ◽

H Ozaki ◽

H Yokoyama ◽

K Imai ◽

...

Keyword(s):

Dilated Cardiomyopathy ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Beta Adrenoceptor ◽

Upward Shift ◽

Volume Relation ◽

Exercise Induced

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Endothelin Receptor Blockade Improves Left Ventricular Pressure-Volume Relationships Without Altering the Hypertrophic Response During Congestive Heart Failure in Rats

Journal of the American College of Cardiology ◽

10.1016/s0735-1097(97)84967-4 ◽

1998 ◽

Vol 31 (2) ◽

pp. 289A

Author(s):

E Øie

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Receptor Blockade ◽

Endothelin Receptor ◽

Hypertrophic Response

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Faculty Opinions recommendation of The relative contribution of prosthetic gradients, systemic arterial pressure, and pulse pressure to the left ventricular pressure in patients with aortic prosthetic valves.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.9881957.10592055 ◽

2011 ◽

Author(s):

Olav F Münter Sellevold

Keyword(s):

Arterial Pressure ◽

Pulse Pressure ◽

Left Ventricular Pressure ◽

Systemic Arterial Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Relative Contribution ◽

Prosthetic Valves

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Contribution of extravascular compression to reduction of maximal coronary blood flow

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.1.h68 ◽

1992 ◽

Vol 262 (1) ◽

pp. H68-H77

Author(s):

F. L. Abel ◽

R. R. Zhao ◽

R. F. Bond

Keyword(s):

Blood Flow ◽

Coronary Blood Flow ◽

Coronary Flow ◽

Perfusion Pressure ◽

Left Ventricular Pressure ◽

Coronary Perfusion Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Coronary Perfusion ◽

Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

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The crosstalk of HDAC3, microRNA-18a and ADRB3 in the progression of heart failure

Cell & Bioscience ◽

10.1186/s13578-020-00523-y ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Jingtao Na ◽

Haifeng Jin ◽

Xin Wang ◽

Kan Huang ◽

Shuang Sun ◽

...

Keyword(s):

Heart Failure ◽

Expression Patterns ◽

Systolic Pressure ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Luciferase Reporter ◽

Left Ventricular Ejection ◽

Tunel Staining ◽

Ventricular Ejection Fraction

Abstract Background Heart failure (HF) is a clinical syndrome characterized by left ventricular dysfunction or elevated intracardiac pressures. Research supports that microRNAs (miRs) participate in HF by regulating targeted genes. Hence, the current study set out to study the role of HDAC3-medaited miR-18a in HF by targeting ADRB3. Methods Firstly, HF mouse models were established by ligation of the left coronary artery at the lower edge of the left atrial appendage, and HF cell models were generated in the cardiomyocytes, followed by ectopic expression and silencing experiments. Numerous parameters including left ventricular posterior wall dimension (LVPWD), interventricular septal dimension (IVSD), left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LEVDP), heart rate (HR), left ventricular pressure rise rate (+ dp/dt) and left ventricular pressure drop rate (-dp/dt) were measured in the mice. In addition, apoptosis in the mice was detected by means of TUNEL staining, while RT-qPCR and Western blot analysis were performed to detect miR-18a, HDAC3, ADRB3, cMyb, MMP-9, Collagen 1 and TGF-β1 expression patterns. Dual luciferase reporter assay validated the targeting relationship between ADRB3 and miR-18a. Cardiomyocyte apoptosis was determined by means of flow cytometry. Results HDAC3 and ADRB3 were up-regulated and miR-18a was down-regulated in HF mice and cardiomyocytes. In addition, HDAC3 could reduce the miR-18a expression, and ADRB3 was negatively-targeted by miR-18a. After down-regulation of HDAC3 or ADRB3 or over-expression of miR-18a, IVSD, LVEDD, LVESD and LEVDP were found to be decreased but LVPWD, LVEF, LVFS, LVSP, + dp/dt, and −dp/dt were all increased in the HF mice, whereas fibrosis, hypertrophy and apoptosis of HF cardiomyocytes were declined. Conclusion Collectively, our findings indicate that HDAC3 silencing confers protection against HF by inhibiting miR-18a-targeted ADRB3.

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