Passive force in left ventricular human myocardium is not passive

2009 ◽  
Vol 56 (S 01) ◽  
Author(s):  
I Karliova ◽  
L Hakami ◽  
AA Peivandi ◽  
N Kayhan ◽  
U Mehlhorn ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Human Myocardium ◽  
Passive Force

scholarly journals The Role of Cardiac T-Cadherin in the Indicating Heart Failure Severity of Patients with Non-Ischemic Dilated Cardiomyopathy

Medicina ◽  
2020 ◽  
Vol 56 (1) ◽  
pp. 27
Author(s):  
Vaida Baltrūnienė ◽  
Ieva Rinkūnaitė ◽  
Julius Bogomolovas ◽  
Daiva Bironaitė ◽  
Ieva Kažukauskienė ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Experimental Studies ◽  
Left Ventricular ◽  
Human Myocardium ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cox Regression Analysis ◽  
Non Ischemic Dilated Cardiomyopathy ◽  
The Mean

Background and objectives: T-cadherin (T-cad) is one of the adiponectin receptors abundantly expressed in the heart and blood vessels. Experimental studies show that T-cad sequesters adiponectin in cardiovascular tissues and is critical for adiponectin-mediated cardio-protection. However, there are no data connecting cardiac T-cad levels with human chronic heart failure (HF). The aim of this study was to assess whether myocardial T-cad concentration is associated with chronic HF severity and whether the T-cad levels in human heart tissue might predict outcomes in patients with non-ischemic dilated cardiomyopathy (NI-DCM). Materials and Methods: 29 patients with chronic NI-DCM and advanced HF were enrolled. Patients underwent regular laboratory investigations, echocardiography, coronary angiography, and right heart catheterization. TNF-α and IL6 in serum were detected by enzyme-linked immunosorbent assay (ELISA). Additionally, endomyocardial biopsies were obtained, and the levels of T-cad were assessed by ELISA and CD3, CD45Ro, CD68, and CD4- immunohistochemically. Mean pulmonary capillary wedge pressure (PCWP) was used as a marker of HF severity, subdividing patients into two groups: mean PCWP > 19 mmHg vs. mean PCWP < 19 mmHg. Patients were followed-up for 5 years. The study outcome was composite: left ventricular assist device implantation, heart transplantation, or death from cardiovascular causes. Results: T-cad shows an inverse correlation with the mean PCWP (rho = −0.397, p = 0.037). There is a tendency towards a lower T-cad concentration in patients with more severe HF, as indicated by the mean PCWP > 19 mmHg compared to those with mean PCWP ≤ 19 mmHg (p = 0.058). Cardiac T-cad levels correlate negatively with myocardial CD3 cell count (rho = −0.423, p = 0.028). Conclusions: Univariate Cox regression analysis did not prove T-cad to be an outcome predictor (HR = 1, p = 0.349). However, decreased T-cad levels in human myocardium can be an additional indicator of HF severity. T-cad in human myocardium has an anti-inflammatory role. More studies are needed to extend the role of T-cad in the outcome prediction of patients with NI-DCM.

scholarly journals Troponin and Titin Coordinately Regulate Length-dependent Activation in Skinned Porcine Ventricular Muscle

2008 ◽  
Vol 131 (3) ◽  
pp. 275-283 ◽  
Author(s):  
Takako Terui ◽  
Munguntsetseg Sodnomtseren ◽  
Douchi Matsuba ◽  
Jun Udaka ◽  
Shin'ichi Ishiwata ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Thin Filament ◽  
Left Ventricular ◽  
Ventricular Muscle ◽  
Passive Force ◽  
Active Force ◽  
Fast Skeletal Muscle ◽  
Thin Filaments ◽  
Cross Bridges ◽  
Length Dependent Activation

We investigated the molecular mechanism by which troponin (Tn) regulates the Frank-Starling mechanism of the heart. Quasi-complete reconstitution of thin filaments with rabbit fast skeletal Tn (sTn) attenuated length-dependent activation in skinned porcine left ventricular muscle, to a magnitude similar to that observed in rabbit fast skeletal muscle. The rate of force redevelopment increased upon sTn reconstitution at submaximal levels, coupled with an increase in Ca2+ sensitivity of force, suggesting the acceleration of cross-bridge formation and, accordingly, a reduction in the fraction of resting cross-bridges that can potentially produce additional active force. An increase in titin-based passive force, induced by manipulating the prehistory of stretch, enhanced length-dependent activation, in both control and sTn-reconstituted muscles. Furthermore, reconstitution of rabbit fast skeletal muscle with porcine left ventricular Tn enhanced length-dependent activation, accompanied by a decrease in Ca2+ sensitivity of force. These findings demonstrate that Tn plays an important role in the Frank-Starling mechanism of the heart via on–off switching of the thin filament state, in concert with titin-based regulation.

Reversal of metallothionein expression is different throughout the human myocardium after prolonged left-ventricular mechanical support

2000 ◽  
Vol 19 (7) ◽  
pp. 668-674 ◽  
Author(s):  
Hideo A Baba ◽  
Florian Grabellus ◽  
Christian August ◽  
Gabriele Plenz ◽  
Atsushi Takeda ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Human Myocardium ◽  
Mechanical Support

Human cardiac myosin heavy chain isoforms in fetal and failing adult atria and ventricles

2001 ◽  
Vol 280 (4) ◽  
pp. H1814-H1820 ◽  
Author(s):  
Peter J. Reiser ◽  
Michael A. Portman ◽  
Xue-Han Ning ◽  
Christine Schomisch Moravec
Keyword(s):  
Heart Failure ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Ischemic Cardiomyopathy ◽  
Myosin Heavy Chain Isoforms ◽  
Left Ventricular ◽  
Human Myocardium ◽  
Cardiac Myosin ◽  
Fetal Stage

The goal of this study was to test the hypothesis that the relative amounts of the cardiac myosin heavy chain (MHC) isoforms MHC-α and MHC-β change during development and transition to heart failure in the human myocardium. The relative amounts of MHC-α and MHC-β in ventricular and atrial samples from fetal (gestational days 47–110) and nonfailing and failing adult hearts were determined. The majority of the fetal right and left ventricular samples contained small relative amounts of MHC-α (mean < 5% of total MHC). There was a small significant decrease in the level of MHC-α in the ventricles between 7 and 12 wk of gestation. Fetal atria expressed predominantly MHC-α (mean > 95%), with MHC-β being detected in most samples. The majority of adult nonfailing right and left ventricular samples had detectable levels of MHC-α ranging from 1 to 10%. Failing right and left ventricles expressed a significantly lower level of MHC-α. MHC-α comprised ∼90% of the total MHC in adult nonfailing left atria, whereas the relative amount of MHC-α in the left atria of individuals with dilated or ischemic cardiomyopathy was ∼50%. The differences in MHC isoform composition between fetal and nonfailing adult atria and between fetal and nonfailing adult ventricles were not statistically significant. We concluded that the MHC isoform compositions of fetal human atria are the same as those of nonfailing adult atria and that the ventricular MHC isoform composition is different between adult nonfailing and failing hearts. Furthermore, the marked alteration in atrial MHC isoform composition, associated with cardiomyopathy, does not represent a regression to a pattern that is uniquely characteristic of the fetal stage.

scholarly journals Phosphorylation of Titin Modulates Passive Stiffness of Cardiac Muscle in a Titin Isoform-dependent Manner

2005 ◽  
Vol 125 (3) ◽  
pp. 257-271 ◽  
Author(s):  
Norio Fukuda ◽  
Yiming Wu ◽  
Preetha Nair ◽  
Henk L. Granzier
Keyword(s):  
Stress Relaxation ◽  
Troponin I ◽  
Ventricular Myocytes ◽  
Left Ventricular ◽  
Dependent Manner ◽  
Passive Force ◽  
Adrenergic Stimulation ◽  
Restoring Force ◽  
Cardiac Tissues ◽  
Ventricular Compliance

We investigated the effect of protein kinase A (PKA) on passive force in skinned cardiac tissues that express different isoforms of titin, i.e., stiff (N2B) and more compliant (N2BA) titins, at different levels. We used rat ventricular (RV), bovine left ventricular (BLV), and bovine left atrial (BLA) muscles (passive force: RV &gt; BLV &gt; BLA, with the ratio of N2B to N2BA titin, ∼90:10, ∼40:60, and ∼10:90%, respectively) and found that N2B and N2BA isoforms can both be phosphorylated by PKA. Under the relaxed condition, sarcomere length was increased and then held constant for 30 min and the peak passive force, stress-relaxation, and steady-state passive force were determined. Following PKA treatment, passive force was significantly decreased in all muscle types with the effect greatest in RV, lowest in BLA, and intermediate in BLV. Fitting the stress-relaxation data to the sum of three exponential decay functions revealed that PKA blunts the magnitude of stress-relaxation and accelerates its time constants. To investigate whether or not PKA-induced decreases in passive force result from possible alteration of titin–thin filament interaction (e.g., via troponin I phosphorylation), we conducted the same experiments using RV preparations that had been treated with gelsolin to extract thin filaments. PKA decreased passive force in gelsolin-treated RV preparations with a magnitude similar to that observed in control preparations. PKA was also found to decrease restoring force in skinned ventricular myocytes of the rat that had been shortened to below the slack length. Finally, we investigated the effect of the β-adrenergic receptor agonist isoprenaline on diastolic force in intact rat ventricular trabeculae. We found that isoprenaline phosphorylated titin and that it reduced diastolic force to a degree similar to that found in skinned RV preparations. Taken together, these results suggest that during β-adrenergic stimulation, PKA increases ventricular compliance in a titin isoform-dependent manner.

scholarly journals Mechanisms of β 3 -adrenoceptor-induced eNOS activation in right atrial and left ventricular human myocardium

2004 ◽  
Vol 143 (8) ◽  
pp. 1014-1022 ◽  
Author(s):  
Klara Brixius ◽  
Wilhelm Bloch ◽  
Christian Pott ◽  
Andreas Napp ◽  
Andreas Krahwinkel ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Human Myocardium ◽  
Right Atrial

scholarly journals Gene expression of adrenomedullin in failing myocardium: comparison to atrial natriuretic peptide

2002 ◽  
Vol 92 (3) ◽  
pp. 1058-1063 ◽  
Author(s):  
Anselm T. Bäumer ◽  
Christina Schumann ◽  
Bodo Cremers ◽  
Gabi Itter ◽  
Wolfgang Linz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Normal Subjects ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Human Myocardium ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Left Ventricular Myocardium ◽  
End Stage ◽  
Atrial Natriuretic

The expression of adrenomedullin (AM) and atrial natriuretic factor (ANF) were investigated in the myocardium of a rat model of chronic ischemic heart failure (CHF) compared with sham-operated controls. In addition, human myocardium of patients with end-stage heart failure due to idiopathic dilated cardiomyopathy compared with myocardium of normal subjects (NF) was studied. In CHF, similar AM levels but increased ANF expression were observed in left ventricular myocardium, as assessed by semiquantitative PCR. Functional experiments with freshly excised papillary muscles showed no influence of AM on myocardial contractility. In NF human myocardium, the expression of AM mRNA was threefold higher in atrial compared with ventricular tissue. In analogy, ANF mRNA was increased by ∼15-fold in atrial tissue. In dilated cardiomyopathy, the expression of AM was significantly increased in right and left ventricles compared with NF. In parallel, ventricular ANF expression was enhanced.

scholarly journals Synchrony of sarcomeric movement regulates left ventricular pump function in the in vivo beating mouse heart

2021 ◽  
Vol 153 (11) ◽  
Author(s):  
Fuyu Kobirumaki-Shimozawa ◽  
Togo Shimozawa ◽  
Kotaro Oyama ◽  
Shunsuke Baba ◽  
Jia Li ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Sarcomere Length ◽  
Left Ventricular ◽  
Mouse Heart ◽  
The Novel ◽  
Passive Force ◽  
Pump Function ◽  
Average Value ◽  
Contribution Index

Sarcomeric contraction in cardiomyocytes serves as the basis for the heart’s pump functions. It has generally been considered that in cardiac muscle as well as in skeletal muscle, sarcomeres equally contribute to myofibrillar dynamics in myocytes at varying loads by producing similar levels of active and passive force. In the present study, we expressed α-actinin–AcGFP in Z-disks to analyze dynamic behaviors of sequentially connected individual sarcomeres along a myofibril in a left ventricular (LV) myocyte of the in vivo beating mouse heart. To quantify the magnitude of the contribution of individual sarcomeres to myofibrillar dynamics, we introduced the novel parameter “contribution index” (CI) to measure the synchrony in movements between a sarcomere and a myofibril (from −1 [complete asynchrony] to 1 [complete synchrony]). First, CI varied markedly between sarcomeres, with an average value of ∼0.3 during normal systole. Second, when the movements between adjacent sarcomeres were asynchronous (CI &lt; 0), a sarcomere and the ones next to the adjacent sarcomeres and farther away moved in synchrony (CI &gt; 0) along a myofibril. Third, when difference in LV pressure in diastole and systole (ΔLVP) was lowered to &lt;10 mm Hg, diastolic sarcomere length increased. Under depressed conditions, the movements between adjacent sarcomeres were in marked asynchrony (CI, −0.3 to −0.4), and, as a result, average CI was linearly decreased in association with a decrease in ΔLVP. These findings suggest that in the left ventricle of the in vivo beating mouse heart, (1) sarcomeres heterogeneously contribute to myofibrillar dynamics due to an imbalance of active and passive force between neighboring sarcomeres, (2) the force imbalance is pronounced under depressed conditions coupled with a marked increase in passive force and the ensuing tug-of-war between sarcomeres, and (3) sarcomere synchrony via the distal intersarcomere interaction regulates the heart's pump function in coordination with myofibrillar contractility.

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