Adequate assessment of the contribution of the different phases of atrial mechanical activity to the value of ejection volume and pressure developed by the ventricle is a complex and important experimental and clinical problem. A new method and an effective algorithm for controlling the interaction of isolated rat right atrial and right ventricular strips during the cardiac cycle were developed and tested in a physiological experiment. The presented functional model is flexible and has the ability to change many parameters (temperature, pacing rate, excitation delay, pre- and afterload levels, transfer length, and force scaling coefficients) to simulate different types of cardiac pathologies.
View Article and Find Full Text PDFThere are only a few studies devoted to the comparative and simultaneous study of the mechanisms of the length-dependent regulation of atrial and ventricular contractility. Therefore, an isometric force-length protocol was applied to isolated guinea pig right atrial (RA) strips and ventricular (RV) trabeculae, with a simultaneous measurement of force (Frank-Starling mechanism) and Ca transients (CaT) or transmembrane action potentials (AP). Over the entire length-range studied, the duration of isometric contraction, CaT and AP, were shorter in the RA myocardium than in the RV myocardium.
View Article and Find Full Text PDFBackground/aim: Today, stable isotopes of zinc are actively used for diagnostic purposes in oncology. However, there is extremely limited data on the attempts to apply stable zinc isotopes in cancer therapy or about the molecular mechanisms of their effects on the biology of tumor cells. Therefore, in this in vitro research, we evaluated the cytotoxic activity of stable zinc isotope (Zn) enriched compounds against malignant cells and determined the mechanisms of their action.
View Article and Find Full Text PDFThe slow force response (SFR) of a cardiac muscle to a sudden stretch is thought to be important in the regulatory adaptation of myocardial contraction. Autocrine-paracrine regulation pathways which involve angiotensin II are participating in this mechanism. On the other hand, renin-angiotensin-aldosterone system (RAS) is altered in hypertrophic or failing myocardium.
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