An experimental method for evaluating constitutive models of myocardium in in vivo hearts

1994 ◽  
Vol 267 (2) ◽  
pp. H853-H863 ◽  
Author(s):  
L. L. Creswell ◽  
M. J. Moulton ◽  
S. G. Wyers ◽  
J. S. Pirolo ◽  
D. S. Fishman ◽  
...  
Keyword(s):  
Experimental Method ◽  
Diastolic Pressure ◽  
Constitutive Models ◽  
Fe Analysis ◽  
Small Displacement ◽  
Ventricular Wall ◽  
Canine Heart ◽  
Unknown Parameters ◽  
Tissue Tagging

A new experimental method for the evaluation of myocardial constitutive models combines magnetic resonance (MR) radiofrequency (RF) tissue-tagging techniques with iterative two-dimensional (2-D) nonlinear finite element (FE) analysis. For demonstration, a nonlinear isotropic constitutive model for passive diastolic expansion in the in vivo canine heart is evaluated. A 2-D early diastolic FE mesh was constructed with loading parameters for the ventricular chambers taken from mean early diastolic-to-late diastolic pressure changes measured during MR imaging. FE solution was performed for regional, intramyocardial ventricular wall strains using small-strain, small-displacement theory. Corresponding regional ventricular wall strains were computed independently using MR images that incorporated RF tissue tagging. Two unknown parameters were determined for an exponential strain energy function that maximized agreement between observed (from MR) and predicted (from FE analysis) regional wall strains. Extension of this methodology will provide a framework in which to evaluate the quality of myocardial constitutive models of arbitrary complexity on a regional basis.

Low-Flow Ischemia Leads to Translocation of Canine Heart GLUT-4 and GLUT-1 Glucose Transporters to the Sarcolemma In Vivo

Circulation ◽  
1997 ◽  
Vol 95 (2) ◽  
pp. 415-422 ◽  
Author(s):  
Lawrence H. Young ◽  
Yin Renfu ◽  
Raymond Russell ◽  
Xiaoyue Hu ◽  
Michael Caplan ◽  
...  
Keyword(s):  
Glucose Transporters ◽  
Low Flow ◽  
Canine Heart ◽  
Glut 1 ◽  
Glut 4

P079 In vivo FE-analysis of total hip loosening

1998 ◽  
Vol 31 ◽  
pp. 94 ◽  
Author(s):  
M. Lengsfeld ◽  
S. Werner ◽  
J. Schmitt ◽  
R. Leppek ◽  
B. Merz ◽  
...  
Keyword(s):  
Fe Analysis ◽  
Total Hip

Estimation of Left Ventricular Wall Stiffness by Analysis of Late Diastolic Pressure Components

2011 ◽  
Author(s):  
Casandra L. Niebel ◽  
Kelley C. Stewart ◽  
Takahiro Ohara ◽  
John J. Charonko ◽  
Pavlos P. Vlachos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Ventricular Wall ◽  
Ventricular Relaxation ◽  
Wall Stiffness ◽  
Ventricular Diastolic Dysfunction

Left ventricular diastolic dysfunction (LVDD) is any abnormality in the filling of the left ventricle and is conventionally evaluated by analysis of the relaxation driven phase, or early diastole. LVDD has been shown to be a precursor to heart failure and the diagnosis and treatment for diastolic failure is less understood than for systolic failure. Diastole consists of two filling waves, early and late and is primarily dependent on ventricular relaxation and wall stiffness.

Abstract 131: C-kit+ Cells Generated From Failed Heart Do Not Improve Failed Heart Function

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Liudmila Zakharova ◽  
Hikmet Nural ◽  
James R Nimlos ◽  
Snjezana Popovic ◽  
Lorraine Feehery ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Heart Function ◽  
Smooth Muscle Actin ◽  
Functional Improvement ◽  
Gene Expressions ◽  
Coronary Vein ◽  
Mesenchymal Transition

A pilot clinical study using autologous c-Kit+ cells showed improvement in cardiac functions in congestive heart failure (CHF), however, it is unclear if c-Kit+ cells isolated from CHF hearts are equally as potent as cells from controls. To test the potency of CHF c-Kit+ cells, myocardial infarction (MI) was created by permanent ligation of the left anterior descending coronary artery. Six weeks after MI, animals with left ventricle end-diastolic pressure (LVEDP) ≥20 mmHg and scar size ≥30% of left ventricle (LV) were designated as CHF rats. We found that CHF atrial explants generated less c-Kit+ cells compared to shams (15.7% vs. 11% sham vs. CHF). CHF c-Kit+ cells exhibited elevated levels of epicardial to mesenchymal transition markers, including Snail (2.5 fold) and Pai1 (3 fold), while the expression level of epithelial marker, E-cadherin was 3 fold lower in CHF c-Kit+ cells. Moreover, CHF c-Kit+ cells exhibited reduced gene expressions of pluripotency markers; 2.1 fold decrease in Nanog and 4.5 fold decrease in Sox 2 compared to sham cells. To evaluate the potency of the c-Kit+ cells, 1 x 10 6 cells isolated from CHFs or shams were delivered to 3 weeks post-MI CHF hearts. Cells were pre-labeled with GFP to enable their tracing in vivo and delivered to the infarcted myocardium via left coronary vein by a retrograde coronary sinus cell infusion (RCI). RCI delivery resulted in a cell distribution of LV (30%), right atrium (30%) and right ventricle (20%), while only 10% of cells were found in a left atrium. Three weeks after cells delivery, rats transplanted with sham c-Kit+ cells showed improved LVEDP (29.4 ± 6 vs. 11.7 ± 3.5 mmHg, CHF vs. CHF+ sham c-Kit+ cells) and a rise in peak rate of pressure (dPdt max) (3988 ± 520 vs. 5333 ± 597 mmHg/s). In contrast, no functional improvement was detected in rats transplanted with CHF c-Kit+ cells. Histological analysis demonstrated that transplanted c-Kit+/GFP+ cells were mostly incorporated into blood vessels and co-localized with endothelial marker vWf, and α-smooth muscle actin. Our results showed that left coronary vein is an efficient route for c-Kit+ cell delivery and that c-Kit+ cells isolated from CHF rats are less potent when transplanted in chronic heart failure rat model compared to those isolated from control.

Use of pulse pressure method for estimating total arterial compliance in vivo

1999 ◽  
Vol 276 (2) ◽  
pp. H424-H428 ◽  
Author(s):  
N. Stergiopulos ◽  
P. Segers ◽  
N. Westerhof
Keyword(s):  
Pulse Pressure ◽  
Diastolic Pressure ◽  
Arterial Compliance ◽  
Aortic Pressure ◽  
Lower Limbs ◽  
Pressure Method ◽  
Total Arterial Compliance ◽  
The Difference ◽  
Pulse Pressure Method

We determined total arterial compliance from pressure and flow in the ascending aorta of seven anesthetized dogs using the pulse pressure method (PPM) and the decay time method (DTM). Compliance was determined under control and during occlusion of the aorta at four different locations (iliac, renal, diaphragm, and proximal descending thoracic aorta). Compliance of PPM gave consistently lower values (0.893 ± 0.015) compared with the compliance of DTM (means ± SE; r = 0.989). The lower compliance estimates by the PPM can be attributed to the difference in mean pressures at which compliance is determined (mean pressure, 81.0 ± 3.6 mmHg; mean diastolic pressure, over which the DTM applies, 67.0 ± 3.6 mmHg). Total arterial compliance under control conditions was 0.169 ± 0.007 ml/mmHg. Compliance of the proximal aorta, obtained during occlusion of the proximal descending aorta, was 0.100 ± 0.007 ml/mmHg. Mean aortic pressure was 80.4 ± 3.6 mmHg during control and 102 ± 7.7 mmHg during proximal descending aortic occlusion. From these results and assuming that upper limbs and the head contribute as little as the lower limbs, we conclude that 60% of total arterial compliance resides in the proximal aorta. When we take into account the inverse relationship between pressure and compliance, the contribution of the proximal aorta to the total arterial compliance is even more significant.

Method for Incorporating Three-Dimensional Residual Stresses Into Patient-Specific Simulations of Arteries

2013 ◽  
Author(s):  
David M. Pierce ◽  
Thomas E. Fastl ◽  
Hannah Weisbecker ◽  
Gerhard A. Holzapfel ◽  
Borja Rodriguez-Vila ◽  
...  
Keyword(s):  
Medical Imaging ◽  
Three Dimensional ◽  
Constitutive Models ◽  
Abdominal Aortic Aneurysms ◽  
Aortic Aneurysms ◽  
Patient Specific ◽  
Abdominal Aortic ◽  
Model Geometry ◽  
Reconstructed Model

Through progress in medical imaging, image analysis and finite element (FE) meshing tools it is now possible to extract patient-specific geometries from medical images of, e.g., abdominal aortic aneurysms (AAAs), and thus to study clinically relevant problems via FE simulations. Medical imaging is most often performed in vivo, and hence the reconstructed model geometry in the problem of interest will represent the in vivo state, e.g., the AAA at physiological blood pressure. However, classical continuum mechanics and FE methods assume that constitutive models and the corresponding simulations start from an unloaded, stress-free reference condition.

scholarly journals How affinity of the ELT-2 GATA factor binding to cis-acting regulatory sites controls Caenorhabditis elegans intestinal gene transcription

Development ◽  
2020 ◽  
Vol 147 (14) ◽  
pp. dev190330
Author(s):  
Brett R. Lancaster ◽  
James D. McGhee
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Binding Affinity ◽  
Experimental System ◽  
Quantitative Relationship ◽  
Gata Factor ◽  
Unknown Parameters ◽  
Cis Acting ◽  
Complicated Model

ABSTRACTWe define a quantitative relationship between the affinity with which the intestine-specific GATA factor ELT-2 binds to cis-acting regulatory motifs and the resulting transcription of asp-1, a target gene representative of genes involved in Caenorhabditis elegans intestine differentiation. By establishing an experimental system that allows unknown parameters (e.g. the influence of chromatin) to effectively cancel out, we show that levels of asp-1 transcripts increase monotonically with increasing binding affinity of ELT-2 to variant promoter TGATAA sites. The shape of the response curve reveals that the product of the unbound ELT-2 concentration in vivo [i.e. (ELT-2free) or ELT-2 ‘activity’] and the largest ELT-XXTGATAAXX association constant (Kmax) lies between five and ten. We suggest that this (unitless) product [Kmax×(ELT-2free) or the equivalent product for any other transcription factor] provides an important quantitative descriptor of transcription-factor/regulatory-motif interaction in development, evolution and genetic disease. A more complicated model than simple binding affinity is necessary to explain the fact that ELT-2 appears to discriminate in vivo against equal-affinity binding sites that contain AGATAA instead of TGATAA.

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.

IN VIVO PRODUCTION OF NITRIC OXIDE IN THE CANINE HEART IN IgE-MEDIATED ANAPHYLAXIS

Shock ◽  
1996 ◽  
Vol 6 (1) ◽  
pp. 66-70 ◽  
Author(s):  
Jin Saitoh ◽  
Hiromasa Mitsuhata ◽  
Haruhiko Takeuchi ◽  
Naoki Hasome ◽  
Reiju Shimizu
Keyword(s):  
Nitric Oxide ◽  
Canine Heart ◽  
Ige Mediated

Effect of human urotensin-II infusion on hemodynamics and cardiac function

2003 ◽  
Vol 81 (2) ◽  
pp. 125-128 ◽  
Author(s):  
Ghada S Hassan ◽  
Fazila Chouiali ◽  
Takayuki Saito ◽  
Fu Hu ◽  
Stephen A Douglas ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Diastolic Pressure ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Urotensin Ii ◽  
Ventricular Systolic Pressure ◽  
Wide Range ◽  
Dose Dependent Decrease

Recent studies have shown that the vasoactive peptide urotensin-II (U-II) exerts a wide range of action on the cardiovascular system of various species. In the present study, we determined the in vivo effects of U-II on basal hemodynamics and cardiac function in the anesthetized intact rat. Intravenous bolus injection of human U-II resulted in a dose-dependent decrease in mean arterial pressure and left ventricular systolic pressure. Cardiac contractility represented by ±dP/dt was decreased after injection of U-II. However, there was no significant change in heart rate or diastolic pressure. The present study suggests that upregulation of myocardial U-II may contribute to impaired myocardial function in disease conditions such as congestive heart failure.Key words: urotensin-II, rat, infusion, heart.

Sign in / Sign up

Export Citation Format

Share Document