Abstract
Introduction: The prevalence and incidence of cardiovascular diseases have been attracting considerable attention in recent decades. This is partly due to the fact that myocardial fibrosis is the major consequence of the most nosological units of cardiovascular diseases. We believe that early pathogenic therapy of myocardial fibrosis should be taken into consideration as a solution to this issue. The change of the connective tissue metabolism in myocardium is the central chain in pathogenesis of diffuse ischemic necrotic cardiosclerosis (DINC) occurs after repeated epinephrine injury of myocardial tissues. The aim: The present study establishes that use of metabolic therapy by trimetazidine (TM) has a protective effect on myocardium repeatedly damaged by epinephrine in hight concentration during the development of DINC in rats with different resistance to hypoxia. Materials and methods: Using the method of hypobaric hypoxia, male albino rats were divided into three groups due to their different resistance to hypoxia. Each group was divided into four equal subgroups: control group, DINC group (2 times repeated injections of epinephrine hydrotartrate (0,5 mg/kg body weight) and calcium gluconate (5 mg/ kg body weight), control group introdused with trimetazidine dihydrochloride (10 mg/kg body weight), DINC treated with TM group (2 times repeated injections of epinephrine hydrotartrate (0,5 mg/kg body weight) and calcium gluconate (5 mg/kg body weight) group introduced with TM (10 mg/kg body weight) for all period of observation. The concentration of protein-bound oxyproline in homogenate of myocardium was determined at 7, 14 and 30 days after the modelling pathology and the histological examination of Masson trichrome staining of myocardium was performed. Results: Experimental modeling of DINC increased the concentration of protein-bound oxyproline in homogenate of myocardium at 7, 14 and 30 days after the modelling pathology, as well as accompanied by metabolic imbalances in diffuse connective tissue elements, which are rich in collagens. Experimental modeling of DINC+TM increased the concentration of protein-bound oxyproline in blood serum significantly less intensive. Conclusions: The intensity of metabolic imbalances in diffuse connective tissue elements of myocardium is the highest in the low resistant animals to hypoxia. Those results are confirmed by histological examination of the myocardium of rats with different resistance to hypoxia. Fibrotic regions in myocardium are rich in collagens. It has been revealed that the most pronounced therapeutic effect of TM is observed in animals with low resistance to hypoxia, slightly less - in animals with medium resistance to hypoxia, and the lowest - in animals with high resistance to hypoxia.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have