In the present study the contribution of cardiac mechanosensitive fibroblasts to the stretch-induced increase in heart rate was simulated. The results presented support the hypothesis that cardiac mechanosensitive fibroblasts could contribute to this response, functioning as an alternative mechanosensor. The pathway for the increase in heart rate is based on electrotonic interaction between pacemaker cells and fibroblasts. Stretch of the latter leads to an inwardly oriented (at diastolic potentials) depolarizing current, which increases the spontaneous depolarization rate of adjacent pacemaker cells and reduces both their maximum diastolic and maximum systolic membrane potentials. Qualitatively, this reaction of SA node cells matches the response seen experimentally . Thus, mechanosensitive fibroblasts could be a cellular substrate for a physiological form of cardiac MEF.
Investigation of the possible bioelectrical impact of mechanosensitive fibroblasts on ventricular myocyte’s function was another objective of this study. Such interaction may be expected to occur predominantly in tissue regions where fibroblasts and cardiomyocytes are heavily intermingled. A number of pathological states (such as myocardial ischemia and infarction, inflammation caused by rheumatic heart disease or other processes) are associated with fibroblast-rich growth and development of inhomogeneous tissue structures . Such inhomogeneous tissue has been reported to provide the histological substrate for fragmentation of the propagating excitation in the ventricles and could be associated with the origin of ventricular arrhythmias . This may help to explain the beneficial effect on heart rhythm of catheter ablation of scar tissue after cardiac infarction in humans. Efficient treatment has got less costly: find generic viagra canada at best online pharmacy.