Ventricular unloading causes prolongation of the QT interval and induces ventricular arrhythmias in rat hearts.

Introduction: Ventricular unloading during prolonged bed rest, mechanical circulatory support or microgravity has repeatedly been linked to potentially life-threatening arrhythmias. It is unresolved, whether this arrhythmic phenotype is caused by the reduction in cardiac workload or rather by underlying diseases or external stimuli. We hypothesized that the reduction in cardiac workload alone is sufficient to impair ventricular repolarization and to induce arrhythmias in hearts.

[Integration of natural sciences and basic medical subjects in the integrated dentistry program (iMED DENT) at the University of Hamburg].

In October 2019, an integrated dentistry program (iMED DENT) was implemented at the University of Hamburg and was the first of its kind in Germany. This model curriculum builds on didactic concepts that have been applied successfully for many years in curricula for human medicine, including interdisciplinary teaching, early clinical experience, and scientific education. The first year focuses on the healthy situation ("normal function") and aims to integrate the natural sciences (biology, chemistry, physics) and the basic medical subjects (anatomy, biochemistry, physiology, medical terminology) in the context of dental health.

The baroreceptor reflex brought to life outside the classroom - an e-learning based asynchronous laboratory class using a non-supervised modified Active Standing Test.

Background: E-learning based laboratory classes can replace or enhance in-classroom laboratories. They typically offer temporal flexibility, self-determined learning speed, repeatability and do not require supervision or face-to-face contact. The aim of this feasibility study was to investigate whether the established in-classroom laboratory class on the baroreceptor reflex (BRR) can be transformed into a new e-learning based asynchronous laboratory class for untrained, non-supervised students without medical equipment.

Human iPS cell-derived engineered heart tissue does not affect ventricular arrhythmias in a guinea pig cryo-injury model.

Human iPSC-derived engineered heart tissue (hEHT) has been used to remuscularize injured hearts in a guinea pig infarction model. While beneficial effects on cardiac remodeling have been demonstrated, the arrhythmogenic potential of hEHTs is a major concern. We investigated whether hiPSC-derived hEHTs increase the incidence of ventricular arrhythmias.

The heterotopic heart transplantation in mice as a small animal model to study mechanical unloading - Establishment of the procedure, perioperative management and postoperative scoring.

Background: Unloading of failing hearts by left ventricular assist devices induces an extensive cardiac remodeling which may lead to a reversal of the initial phenotype-or to its deterioration. The mechanisms underlying these processes are unclear.

Hypothesis: Heterotopic heart transplantion (hHTX) is an accepted model for the study of mechanical unloading in rodents.

Common microRNA signatures in cardiac hypertrophic and atrophic remodeling induced by changes in hemodynamic load.

Background: Mechanical overload leads to cardiac hypertrophy and mechanical unloading to cardiac atrophy. Both conditions produce similar transcriptional changes including a re-expression of fetal genes, despite obvious differences in phenotype. MicroRNAs (miRNAs) are discussed as superordinate regulators of global gene networks acting mainly at the translational level.

Unloaded rat hearts in vivo express a hypertrophic phenotype of cardiac repolarization.

Cardiac unloading with left ventricular assist devices is increasingly used to treat patients with severe heart failure. Unloading has been shown to improve systolic and diastolic function, but its impact on the repolarization of left ventricular myocytes is not known. Unloaded hearts exhibit similar patterns of gene expression as hearts subjected to an increased hemodynamic load.

Modulation of the transient outward K+ current by inhibition of endothelin-A receptors in normal and hypertrophied rat hearts.

Inhibition of endothelin-A (ET(A)) receptors has been shown to reduce ventricular electrical abnormalities associated with cardiac failure. In this study, we investigate the effect of ET(A)-receptor inhibition on the development of regional alterations of the transient outward K(+) current (I (to)) in the setting of pressure-induced left ventricular (LV) hypertrophy. Cardiac hypertrophy was induced in female Sprague-Dawley rats by stenosis of the ascending aorta (AS) for 7 days.

Diminished Kv4.2/3 but not KChIP2 levels reduce the cardiac transient outward K+ current in spontaneously hypertensive rats.

Objective: A reduction of the Ca(2+)-independent transient outward potassium current (I(to)) in epicardial but not in endocardial myocytes of the left ventricle has been observed in cardiac hypertrophy and is thought to contribute to the electrical vulnerability associated with this pathology.

Methods: In the present study we investigated the molecular mechanisms underlying regional alterations in I(to) in hypertrophied hearts of spontaneously hypertensive rats (SHR) using the whole-cell patch-clamp technique, quantitative RT-PCR and heterologous expression of underlying ion channel subunits.

Results: I(to) was significantly smaller in epicardial myocytes of SHR than in Wistar-Kyoto (WKY) controls (11.

A polycystin-2-like large conductance cation channel in rat left ventricular myocytes.

Objective: Several members of the PKD gene family (PKD2, PKDL and PKD2L2) are expressed in the heart. Polycystin-2 and its homologues, which are encoded by these genes, have recently been shown to form Ca(2+)-regulated nonselective cation channels in heterologous expression systems. Previously, large conductance nonselective cation channels (LCC) have been described in cardiomyocytes, however, their molecular identity remained obscure.