Spatial-temporal Ca(2+) dynamics due to Ca(2+) release, buffering, and reuptaking plays a central role in studying excitation-contraction (E-C) coupling in both normal and diseased cardiac myocytes. In this paper, we employ two numerical methods, namely, the meshless method and the finite element method, to model such Ca(2+) behaviors by solving a nonlinear system of reaction-diffusion partial differential equations at two scales. In particular, a subcellular model containing several realistic transverse tubules (or t-tubules) is investigated and assumed to reside at different locations relative to the cell membrane. To this end, the Ca(2+) concentration calculated from the whole-cell modeling is adopted as part of the boundary constraint in the subcellular model. The preliminary simulations show that Ca(2+) concentration changes in ventricular myocytes are mainly influenced by calcium release from t-tubules.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179564PMC
http://dx.doi.org/10.1109/TBME.2011.2158316DOI Listing

Publication Analysis

Top Keywords

ventricular myocytes
8
realistic transverse
8
transverse tubules
8
subcellular model
8
ca2+ concentration
8
ca2+
5
multiscale modeling
4
modeling calcium
4
calcium dynamics
4
dynamics ventricular
4

Similar Publications

The combination of alcohol and a low-carbohydrate, high-protein, high-fat atherogenic diet (AD) increases the risk of lethal arrhythmias in apolipoprotein E/low-density lipoprotein receptor double-knockout (AL) mice with metabolic dysfunction-associated steatotic liver disease (MASLD). This study investigates whether left ventricular (LV) myocardial interstitial fibrosis (MIF), formed during the progression of metabolic dysfunction-associated steatohepatitis (MASH), contributes to this increased risk. Male AL mice were fed an AD with or without ethanol for 16 weeks, while age-matched AL and wild-type mice served as controls.

View Article and Find Full Text PDF

Small mammals have a higher heart rate and, relative to body mass (Mb), a higher metabolic rate than large mammals. In contrast, heart weight and stroke volume scale linearly with Mb. With mitochondria filling approximately 50% of a shrew cardiomyocyte - space unavailable for myofibrils - it is unclear how small mammals generate enough contractile force to pump blood into circulation.

View Article and Find Full Text PDF

Aim: Comparative assessment of structural changes in cardiomyocyte mitochondria of the right atrial appendage and the mitochondrial respiratory function in peripheral blood leukocytes in a cohort of patients after acute decompensated heart failure (ADHF) and with stable chronic heart failure of ischemic etiology with reduced ejection fraction (CHFrEF) or moderately reduced ejection fraction (CHFmrEF) of the left ventricle.

Material And Methods: The study analyzed 40 micrographs of right atrial appendage cardiomyocytes obtained from 12 patients with CHFrEF and CHFmrEF. The study protocol was registered on ClinicalTrials.

View Article and Find Full Text PDF

Binding of to dystrophin impairs the membrane trafficking of Nav1.5 protein and increases ventricular arrhythmia susceptibility.

Elife

January 2025

Department of Pharmacology (The Key Laboratory of Cardiovascular Research, Ministry of Education) at College of Pharmacy, Harbin Medical University, Harbin, China.

Dystrophin is a critical interacting protein of Nav1.5 that determines its membrane anchoring in cardiomyocytes. Long noncoding RNAs (lncRNAs) are involved in the regulation of cardiac ion channels, while their influence on sodium channels remains unexplored.

View Article and Find Full Text PDF

Altered Protein Kinase A-Dependent Phosphorylation of Cav1.2 in Left Ventricular Myocardium from Haploinsufficient Rat Hearts.

Int J Mol Sci

December 2024

Institute of Pharmacology and Clinical Pharmacy, Faculty of Pharmacy, Biochemical and Pharmacological Center (BPC) Marburg, University of Marburg, 35032 Marburg, Germany.

encodes the α1c subunit of the L-type Ca channel, Cav1.2. Ventricular myocytes from haploinsufficient () rats exhibited reduced expression of Cav1.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!