scholarly journals The coronary pressure-flow determinants left ventricular compliance in dogs.

1981 ◽  
Vol 49 (4) ◽  
pp. 856-865 ◽  
Author(s):  
C O Olsen ◽  
D E Attarian ◽  
R N Jones ◽  
R C Hill ◽  
J D Sink ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance

Right and left ventricular compliance in experimental acute and subacute trypanosomal myocarditis

1973 ◽  
Vol 7 (2) ◽  
pp. 202-208 ◽  
Author(s):  
D. D. MORALES ◽  
R. L. WAGNER ◽  
W. H. ABELMANN
Keyword(s):  
Left Ventricular ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance

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

2018 ◽  
Vol 315 (3) ◽  
pp. H669-H680 ◽  
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.

Effect of exercise on coronary pressure-flow relationship in hypertrophied left ventricle

1995 ◽  
Vol 269 (1) ◽  
pp. H271-H281 ◽  
Author(s):  
D. J. Duncker ◽  
J. Zhang ◽  
T. J. Pavek ◽  
M. J. Crampton ◽  
R. J. Bache
Keyword(s):  
Coronary Artery ◽  
Myocardial Perfusion ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Back Pressure ◽  
Pressure Flow ◽  
Pronounced Increase ◽  
Coronary Pressure

Left ventricular (LV) hypertrophy (LVH) secondary to chronic pressure overload is associated with increased susceptibility to myocardial hypoperfusion and ischemia during exercise. The present study was performed to determine whether exercise causes alterations in minimum coronary resistance or effective back pressure [coronary pressure at zero flow (Pzf)] that limit maximum myocardial perfusion in the hypertrophied heart. Ascending aortic banding in 7 dogs increased the LV weight-to-body weight ratio to 7.7 +/- 0.3 g/kg compared with 4.6 +/- 0.2 g/kg in 11 normal dogs (P < 0.01). Maximum coronary vasodilation was produced by intracoronary infusion of adenosine. Under resting conditions, the slope of the pressure-flow relationship (conductance) was significantly lower in the LVH animals than in the normal dogs (7.2 +/- 0.8 vs. 11.9 +/- 0.8 x 10(-2) ml.min-1.g-1.mmHg-1; P < 0.01); the slope correlated with the degree of hypertrophy r = 0.74; P < 0.001). The Pzf measured during total coronary artery occlusion (Pzf,measured) was significantly elevated in LVH compared with normal dogs (25.6 +/- 2.2 vs. 13.0 +/- 1.2 mmHg; P < 0.01); Pzf,measured was positively correlated (r = 0.78, P < 0.0005) with LV end-diastolic pressure measured during total coronary artery occlusion (9.0 +/- 1.1 mmHg in normal dogs and 22.2 +/- 3.2 mmHg in LVH dogs; P < 0.01). Graded treadmill exercise to maximum heart rates of 210 +/- 9 and 201 +/- 8 beats/min in normal and LVH animals, respectively, caused similar decreases in the slope of the pressure-flow relationship in LVH (from 7.7 +/- 0.9 to 6.1 +/- 0.8 x 10(-2) ml.min-1.g-1.mmHg-1; P < 0.01) and normal dogs (from 11.9 +/- 0.8 to 10.0 +/- 0.7 x 10(-2) ml.min-1.g-1.mmHg-1; P < 0.01). However, exercise-induced increases in Pzf,measured were significantly greater in the LVH animals (from 25.6 +/- 2.2 to 40.8 +/- 2.1 mmHg; P < 0.01) than in normal animals (from 13.0 +/- 1.2 to 24 +/- 2.1 mmHg; P < 0.01) (P < 0.01 LVH vs. normal). The greater increase in Pzf paralleled a more pronounced increase in LV end-diastolic pressure in the LVH dogs from 22.2 +/- 3.2 to 39.1 +/- 2.7 mmHg) than in normal dogs from 9.0 +/- 1.1 to 14.2 +/- 2.0 mmHg). The results suggest that exaggerated increases in filling pressure during exercise in the hypertrophied left ventricles contributed to impairment of myocardial perfusion during exercise by augmenting the back pressure, which opposes coronary flow.(ABSTRACT TRUNCATED AT 400 WORDS)

Post-reextension force decay of relaxing cardiac muscle

1987 ◽  
Vol 253 (2) ◽  
pp. H256-H261 ◽  
Author(s):  
S. U. Sys ◽  
W. J. Paulus ◽  
V. A. Claes ◽  
D. L. Brutsaert
Keyword(s):  
Cardiac Muscle ◽  
Isometric Force ◽  
Muscle Length ◽  
Wall Stress ◽  
Left Ventricular ◽  
Segment Length ◽  
Force Decay ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance ◽  
Ventricular Filling

Residual active cardiac muscle force during ventricular filling causes deviations of the pressure-volume and pressure-segment length relations from passive left ventricular compliance curves. A possible interaction at the myocardial level between muscle reextension and subsequent active force decay has not yet been investigated. We therefore studied the relation between isolated cat papillary muscle reextension, load during reextension, and isometric force decay after isotonic reextension. Both timing and extent of the isotonic muscle reextension phase were altered while load during reextension was lowered, subsequent residual isometric force was decreased. The extent of reextension or the final muscle length did not alter residual active isometric force after isotonic reextension at an identical load. Moreover, irrespective of the loading history of the shortening phase of the contraction, equal loads during reextension resulted in superimposable subsequent isometric force decay traces. From these results it therefore appears that residual isometric force after isotonic reextension is determined by the load during reextension. Extrapolation of these results to the filling ventricle implies the existence of a dynamic interaction between instantaneous extent of filling, wall stress, and residual force development.

Impact Of Arterial Stiffness On Left Ventricular Compliance In Healthy Seniors

2014 ◽  
Vol 46 ◽  
pp. 862
Author(s):  
Erin J. Howden ◽  
Graeme Carrick-Ranson ◽  
Naoki Fujimoto ◽  
Jeff L. Hastings ◽  
Paul Bhella ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
Left Ventricular ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance

Early consecutive left ventricular compliance changes after acute myocardial infarction

1973 ◽  
Vol 31 (1) ◽  
pp. 158 ◽  
Author(s):  
McKamy Smith ◽  
Robert A. Ratshin ◽  
Richard O. Russell ◽  
Charles E. Rackley
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricular ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance
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