| Background: Heart failure (HF, heart failure) is a variety of heart disease as a causeof heart failure syndrome, in most cases refers to decreased myocardial contractility,cardiac output can not meet the metabolic needs of the body, organs, tissue bloodperfusion, and pulmonary circulation and (or) circulation congestion performance.Adult prevalence of heart failure was0.9%, and0.7%for males, females was1.0%,the current35to74years, about4million adults are still the heart failure patients,and showed an increasing trend. Standardize the diagnosis and treatment of heartfailure, patients with life-saving, cost-saving medicine, is the medical professionneeds urgent problem to be solved. Movement has already proven as a treatment forheart failure in physics in the role, Research In Motion and its regulatory role in heartfailure has become the basis for the molecular mechanism of extensive researchconducted.Objective: This article based on reliable animal model and motion model, based onthe experience of previous studies of heart failure after myocardial β1-ar, β2-ar afterthe aerobic exercise intervention receptor mRNA expression and proteincharacterization density analysis of molecular biology, in order to get exerciseimproves heart function, relieve the biological mechanisms of heart failureprogression, through the movement test in rats, in order to get a reliable model ofaerobic exercise for the clinical treatment of chronic heart failure patients with newphysical treatment.Methods: Male wistar rats of clean grade80(provided by Shandong LukangPharmaceutical Experimental Animal Center),8weeks old, weighing230±32g,were housed separately, were randomly divided into four groups, there was nosignificant difference between groups in weight, natural light, free diet, the roomtemperature was controlled at20-26℃, humidity at40-50%, rats adapted to theenvironment two weeks after the start of the experiment. Based on experimentalstudies in animal models and sophisticated motion model. Experimental resultsprocessing, image processing and analysis of image processing software used by the imageJ spss19.0.Results: After ten weeks of aerobic exercise, SE rats compared with S rats, weighingslightly lighten (p<0.05), increased heart weight, cardiac index increasedsignificantly (p <0.01); M group compared with the S group, body weight decreased(p<0.05), heart weight increase in cardiac index also showed a significant increase(p<0.01); ME group comparison group M, the weight was significantly reduced heartweight slightly lower(p<0.05).cardiac index slightly increased(p<0.05).Characterization of mRNA expression of the β1receptors, SE group compared withthe S group, the expression level was significantly increased (p<0.01), compared withthe S group, the expression was significantly reduced in group M (p<0.01), ME groupand M group comparing the expression level is significantly increased, consistentwith the expression of the protein, but statistically significant decrease slightly; β2receptors although a slight change, but no statistical significance.Conclusions: Heart failure occurs after pathologic hypertrophy, β1receptorcharacterization significantly downregulated by reducing its coupled Gprotein-coupled receptor pathway, reducing the activation of protein kinase PKA,preventing apoptosis of myocardial cells; Movement normal myocardial hypertrophyproduce functional adaptation, β1receptors affected by the movement generatedincreases may be due to fans walking exercise training-induced nerve imbalancecaused by HRV, in order to maintain the body ’s ability to regulate the autonomicnervous selectively upregulated β1receptors, enhanced regulation of sympathetic;regulation of exercise on heart failure after myocardial β receptor density from the β1receptor upregulation characterization, The upgrade effect may be due to theupstream play a role of catecholamine concentration regulation of norepinephrinetransporter protein expression enhancement. |
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