| Heart failure (HF) is clinic syndrome that is characterized by abnormity of heart function and decline of exercise resistance and neurohormonal activaton .Heart failure patients morbility are high and affect patients quality of life.Studys showed that apoptosis played a important role in heart failure.A important characteristic of HF were execssive action of the renin angiotensio aldosterone system(RAAS).One of the factors are increment of circulatory and local angiotensio II(ang II).Its receptions also were increased . Angiotensio II could induce cardiac remolding.There were controversies regarding the capability of Ang II to induce cardiac apoptosis and mechanism of signal transduction .Losartan were high specific ATI receptor blockade, and clinical served as a first-line drug in treating patients with hypertension. Report of its mechanism in heart failure were less.Study showed that incresed cardiomyocyte apoptosis had been demonstrated in spontaneouseously hypertensive rats (SHR) and patients with essential hypertension.Apoptosis were a continuous process and relative with ventricular remodeling.Heart failure were a chronic process.Although ratio of apoptosis were very low, it could caused plentiful cardiomyocyte loss after many months or years.Because cardiomyocyte were end-differentiation ,it could affect heart function when cardiomyocyte loss reach definite level.When knowed the role of cardiomyocyte apoptosis, intervention apoptosis were prospective direction to treat heart failure.Despite data showing major benefits of medical therapy in terms of reduced mortality in heart failure (HF), little progress had been made in improving the quality of life in these patients. Quality of life for the majority of patients were limited by two major symptoms: fatigue and shortness of breath. Fatigue were due to skeletal muscle dysfunction rather than to reduced skeletal muscle blood flow.These symptoms werepartially due to a skeletal muscle myopathy.Aim:( 1) Pathological models of heart failure (HF) were established by constriction of abdominal aorta of rats partly. To investigate the role of cardiomyocyte apoptosis and ventricular remodeling in the progress of heart failure by experiments of heart failure model in rats. ( 2 ) To explore the role and signal transduction of angiotensin lion rats with heart failure. ( 3 ) To further clarify the mechanism of losartan in decreasing cardiomyocyte apoptosis ( 4 ) To explore the role and mechanism of losartan on rats with congestive heart failure skeletal atrophy.Methods:40 rats were divided randomly into 4 groups: (1) A group: sham-operated control group(n=8),B group: heart failure group(n=12) ,C group :losarton treated group(10mg/kg/d n=12),D group :losarton treated group(30mg/kg/d n=10). Pathological models of heart failure (HF) were established by constriction of abdominal aorta of rats partly. The rats inC D group began to be treated with daily 10mg/kg/d 30mg/kg/d losartan by gavage respectively at the end of 6th week after operation, while the other rats were administered equal volume of distilled water respectively by the same way. Another 8 weeks later, all the rats were killed after measurement of hemodynamic parameters. The left and right ventricles and gastrocnemius were dissected and weighed separately.The ratio of gastrocnemius was served as degree muscle atrophy.The part of LV free wall and gastrocnemius were stored in formalin, dehydrated in ethanol, and paraffin embedded for HE immunohistochemistry and apoptosis.Another part ventricles was snap frozen in liquid nitrogen for Western blot. Apoptosis, was assessed using the immunohistochemical deoxynucleotidal transferase-mediated dUTP-digoxigenin nick-end labeling (TUNEL) method. The monitoring of Bax, and Bcl-2 protein of cardiomyocyte was determined by immunohistochemistry and Western blot.Result:(l)Abnormality of hemodynamic,histopathology were observed in rats after constriction of abdominal aorta of rats partly 14 weeks,and impoved markedly by long-term losrtan intervention. (2)The ratio of ca...
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