Aortic banding induced in 2-day-old (A2) and 6-day-old (A6) male rats increased the left ventricular (LV) weight after 60 days; right ventricular (RV) enlargement occurred in the A2 group only. The concentration of collagenous proteins in the LV was elevated in both experimental groups (more in the A2 rats) at the expenses of sarcoplasmic proteins. Aortic banding also affected the proportion of collagen types (lower collagen I, higher collagen 111, V) and myosin light chains (higher LC1/LC2) in the LV. Similar changes of proteins in the RV were less pronounced.
Endogenous regulators, such as angiotensin-II (AngII), endothelin-1 (ET-1) and urotensin-II (U-II) are released from various cell types and their plasma levels are elevated in several cardiovascular diseases. The present study evaluated a potential crosstalk between these systems by investigating if the myocardial effects of U-II are modulated by AngII or ET-1. Effects of U-II (10-8 , 10 -7 , 10 -6 M) were tested in rabbit papillary muscles in the absence and in the presence of losartan (selective AT1 receptor antagonist), PD-145065 ( nonselective ET-1 receptors antagonist), losartan plus PD-145065, AngII or ET-1. U-II promoted concentration-dependent negative inotropic and lusitropic effects that were abolished in all experimental conditions. Also, U-II increased resting muscle length up to 1.008±0.002 L/Lmax. Correcting it to its initial value resulted in a 19.5±3.5 % decrease of resting tension, indicating increased muscle distensibility. This effect on muscle length was completely abolished in the presence of losartan and significantly attenuated by PD-145065 or losartan plus PD-145065. This effect was increased in the presence of AngII, resulting in a 27.5±3.9 % decrease of resting tension, but was unaffected by the presence of ET-1. This study demonstrated an interaction of the U-II system with the AngII and ET-1 systems in terms of regulation of systolic and diastolic function., A. P. Fontes-Sousa ... [et al.]., and Obsahuje seznam literatury
Aims of the study were to compare the development of electrocardiographic responses of the ischemia-induced heterogeneities of activation and repolarization in the ventricular myocardium of normal and diabetic animals. Body surface ECGs and unipolar electrograms in 64 epicardial leads were recorded before and during 20 min after the ligation of the left anterior descending artery in diabetic (alloxan model, 4 weeks, n=8) and control (n=8) rabbits. Activation times (ATs), end of repolarization times (RTs) and repolarization durations (activation-recovery intervals, ARIs) were determined in ischemic and periischemic zones. In contrast to the controls, the diabetic rabbits demonstrated the significant prolongation of ATs and shortening of ARIs (P<0.05) during ischemia in the affected region resulting in the development and progressive increase of the ARI and RT gradients across the ischemic zone boundary. The alterations of global and local dispersions of the RTs in diabetics correlated with the Tpeak-Tend interval changes in the limb leads ECGs. In the ischemic conditions, the diabetic animals differed from the controls by the activation delay, significant repolarization duration shortening, and the increase of local repolarization dispersion; the latter could be assessed by the Tpeak-Tend interval measurements in the body surface ECGs., K. A. Sedova, M. A. Vaykshnorayte, A. O. Ovechkin, P. Kneppo, O. G. Bernikova, V. A. Vityazev, J. E. Azarov., and Obsahuje bibliografii